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• Published: 04 May 2020

Non-vector-borne transmission of lumpy skin disease virus

• Kononov Aleksandr 1 ,
• Byadovskaya Olga 1 ,
• Wallace B. David 2 , 3 ,
• Prutnikov Pavel 1 ,
• Pestova Yana 1 ,
• Kononova Svetlana 1 ,
• Nesterov Alexander 1 ,
• Rusaleev Vladimir 1 ,
• Lozovoy Dmitriy 1 &
• Sprygin Alexander 1  

Scientific Reports volume  10 , Article number:  7436 ( 2020 ) Cite this article

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• Animal disease models
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The transmission of “lumpy skin disease virus” (LSDV) has prompted intensive research efforts due to the rapid spread and high impact of the disease in recent years, especially in Eastern Europe and Balkan countries. In this study, we experimentally evaluate the vaccine-derived virulent recombinant LSDV strain (Saratov/2017) and provide solid evidence on the capacity of the virus for transmission in a vector-proof environment. In the 60-day long experiment, we used inoculated bulls (IN group) and two groups of in-contact animals (C1 and C2), with the former (C1) being in contact with the inoculated animals at the onset of the trial and the latter (C2) being introduced at day 33 of the experiment. The infection in both groups of contact animals was confirmed clinically, serologically and virologically, and viremia was demonstrated in blood, nasal and ocular excretions, using molecular tools. Further studies into LSDV biology are a priority to gain insights into whether the hypothesized indirect contact mode evidenced in this study is a de novo -created feature, absent from both parental stains of the novel (recombinant) LSDV isolate used, or whether it was dormant, but then unlocked by the process of genetic recombination. Author summary: In global terms, LSD has been termed a “neglected disease” due to its historic natural occurrence of being restricted to Africa and, occasionally, Israel. However, after its slow spread throughout the Middle East, the disease is now experiencing a resurgence of research interest following a recent and rapid spread into more northern latitudes. Given the dearth of solid findings on potential transmission mechanisms, no efficient or reliable control program currently exists, which does not involve the use of live attenuated vaccines or stamping out policies – both of which are controversial for implementation in non-endemic regions or countries. The vector-borne mode is the only working concept currently available, but with scarce evidence to support the aggressive spread northwards – except for human-assisted spread, including legal or illegal animal transportation. The emergence of outbreaks is not consistently linked to weather conditions, with the potential for new outbreaks to occur and spread rapidly. Here, for the first time, we provide evidence for indirect contact-mode transmission for a naturally-occurring recombinant LSDV isolated from the field. In an insect-proof facility, we obtained solid evidence that the novel LSDV strain can pass to in-contact animals. Given the recombinant nature of the virus utilised, its genetic background relating to the observed transmission pattern within the study needs to be delineated.

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Introduction.

Lumpy skin disease (LSD) virus belongs to the genus Capripoxvirus within the family Poxviridae (Buller et al ., 2005). It contains a double-stranded, covalently-linked linear DNA genome enveloped by a lipid bilayer. Mature capripox virions have an oval profile and large lateral bodies, and they are 320 ×260 nm on average in size 1 . The viral genome is approximately 151 kb in size, encoding 156 putative genes 2 . LSD virus (LSDV) genes share a high degree of co-linearity and amino acid identity (average of 65%) with genes of other known mammalian poxviruses, particularly suipoxvirus, yatapoxvirus, and leporipoxvirus. Within the genus Capripoxvirus , which also includes sheep pox and goat pox viruses, genetic identities are at least 96% 3 . Generally, based on full-genome sequences deposited in GenBank, LSDV exists as two genetic lineages: field isolates and live attenuated vaccine strains, although evidence for a naturally occurring recombinant between a vaccine strain and field strain has also been reported 4 .

Displaying a strict and narrow host range, LSDV mainly infects cattle and water buffaloes 5 , with one documented isolation from sheep 6 , 7 , although a limited number of other ruminant species, such as antelope, also appear to be susceptible. In recent decades, the disease has been documented in both Southern and Northern hemispheres due to a rapid expansion of its range, although historically, it was restricted to the African continent 8 , 9 , 10 . The unprecedented incursions into new territories and resurgence of LSD creates an objective need for joint efforts to investigate the obscure nature of LSDV transmission 11 .

Initial evidence and studies suggested that direct or indirect contact (without vectors) are ineffective routes for LSDV transmission 12 , whereas the predominant transmission pathway for sheep pox and goat pox viruses is via aerosols. However, importantly, other poxviruses are most commonly spread by direct contact rather than by transmission by arthropod vectors such as by contaminated insects during biting of their hosts. Moreover, poxvirus infection can also occur through ingestion, parenteral inoculation, or droplet or aerosol exposure to mucous membranes or broken skin. Some poxviruses can be transmitted by fomites (inanimate objects). Transmission pathways may vary among poxviruses even within a genus 13 . For orthopoxviruses that infect humans, infection occurs via exposure to aerosols or droplets (variola virus) or through close personal contact. Poxviruses from the Parapoxvirus genus (e.g. orf virus or milker’s nodule virus) can pass from one animal to another through direct or indirect contact. Unfortunately, there are no available studies addressing the issue whether closely related capripoxviruses actually employ different routes of spread.

Transmission of LSDV is surmised to occur through mechanical vector-borne spread via insect or tick bites as most outbreaks occur during the warmer (and, often, wetter) summer months when potential vector species numbers are high 11 , 14 , 15 . Unfortunately, transmission studies conducted to date using arthropod species which may be involved in transmission are mostly species which are restricted to the Southern hemisphere (e.g. Rhipicephalus appendiculatus ticks), which complicates analysis of transmission potential of local species in climatically new geographic areas in the Northern hemisphere. Moreover, LSD outbreaks are not only reported within the warmer summer period, optimal for arthropod blood meal search activity, but also outside of it.This observation thus points to a possible non-vector-borne route for spread of the virus (WAHIS, 2019). Studies using a small cohort of animals were conducted in the past to show that direct contact transmission between infected and naïve animals is possible, but at an extremely low efficiency rate 12 , 16 . New work to replicate the findings has not yet been encouraged. Nevertheless, field evidence suggests that successful transmission can be achieved when naïve animals are allowed to share a drinking trough with severely infected animals 17 , 18 .

This supports the common hypothesis that direct contact does not appear to be an effective route for LSDV transmission. In addition, recent experiments with various field strains did not result in successful contact transmission 19 , 20 , 21 . Attenuated vaccine strains have also been claimed to be devoid of transmission capacity, but recent field evidence argues to the contrary 22 , 23 .

In this environment of uncertainty for LSD spread, elucidation of the exact transmission mode/s could contribute significantly towards improving control and eradication programs.

In this paper, we report on work performed to evaluate transmission of the naturally occurring vaccine-derived virulent recombinant strain of LSDV Saratov/2017 4 , in an experimental setting and for the first time conclusively demonstrate non-vector-borne transmission of the virus.

Materials and methods

The vaccine-derived virulent recombinant LSDV strain, LSDV Saratov/2017, was isolated by FGBI ARRIAH researchers from a cow presenting with severe clinical signs of LSD 22 . The strain was obtained from the FGBI ARRIAH depository and refreshed using two rounds of passaging in goat testis cells. To prepare the final inoculum virus, the refreshed virus was subjected to polymerase chain reaction (PCR) amplification of different loci of vaccine and field strain genomes to confirm the identity of this virus strain 4 .

Ethics statement

The animal experiment, as well as the euthanasia procedure, were approved by the Ethics Committee of the Federal Center for Animal Health, Russia (Permit Number: №2/1-21082018) and conducted in strict accordance with Directive 2010/63/EU on the protection of animals used for scientific purposes.

Experimental design

The initial experimental group consisted of 10 bulls of the Russian Black Pied breed aged 6-8 months. The animals were consecutively numbered from 1 to 10 in a random fashion and maintained in Animal Biosafety Level 3 housing with a 12-hourly light-dark cycle, relative humidity of 30% to 70%, temperature of 23 to 26 °C and all animals were monitored twice daily by the veterinary staff. Water and feed were provided ad libitum . The experiment was carried out in an insect-proof facility. To detect any possible dipteran presence, indoor blood-feeding insect UV light traps and sticky traps were mounted at regular intervals on the walls of the facility. The animals were also examined for the presence of ticks.

The five animals with even numbering (2, 4, 6, 8, 10) each received 2 ml of 5 log TCID 50 /ml of the recombinant virus, LSDV Saratov/2017, intravenously (called the infected/inoculated group – IN) and the remaining five animals with odd numbers were mock inoculated (called C1 - in-contact group 1, also acting as negative controls) with phosphate-buffered saline (PBS) (Table  1 ). The animals were placed in a row along a shared trough according to their consecutive numbering. Their mobility was restricted using tethering, although contact between adjacent animals was possible. At post-inoculation (p.i.) day 33, when there were clear signs of infection in the C1 animals (e.g. crusts, shedding), another group of five bulls (C2 group) was introduced, and positioned between the clinically ill animals, including infected and in-contact animals (Table  2 ).

The animals were monitored daily for the presence of fever until day 52 and clinical signs of LSD until the end of the experiment. To evaluate the time course of virus shedding and viremia, nasal and ocular discharges, skin scabs, blood and semen were collected and tested for virus presence using PCR until day 50.

To assess the clinical picture and collect samples, all experimental animals were first stunned using a penetrative captive bolt to induce unconsciousness, followed by the administration of “Adilinum super” (Federal Center for Toxicological, Radiation and Biological Safety, Kazan, Russia) at day 61 p.i. at a recommended dose of 5 mg/kg according to the drug use instruction approved by the Russian Federal Service for Veterinary and Phytosanitary Surveillance in 2008. At the recommended dose, the Adilinum mechanism of action provides painless and rapid euthanasia: cerebral death commences first followed by circulatory collapse.

Virus isolation in cell culture

Only skin lesions were used for virus isolation and culture. They were ground finely and added to sterile saline at a mass/volume (m/v) ratio of 1:10, followed by repeated freeze–thaw cycles at −80 °C and room temperature (3 times) to disrupt cell membranes. The processed samples were clarified at 1,500 rpm for 15 minutes (min). The supernatant was removed, mixed with antibiotics (penicillin and streptomycin at final concentrations of 2000 IU/mL and 2 mg/mL, respectively) at room temperature for 90 min and then inoculated onto ovine testis or goat gonad cells (70–80% confluency for both), as follows: after removal of the growth medium from flasks containing the cell cultures and washing twice with Hanks’ medium, a 0.1 mL volume of inoculum was added. The flasks were incubated at 37 °C for 90 min to ensure virus adhesion. Once the incubation period was completed, 10 mL of maintenance medium supplemented with 1.0 mL fetal bovine serum was added. The flasks were again incubated at 37 °C. The inoculated cell cultures were observed daily for cytopathic effect (CPE). The cells were then harvested when 80% CPE was observed and lysed to release the virus, using repeated freeze- thaw cycles (3×). The presence of LSDV was confirmed using real-time PCR.

Virus neutralization

Virus neutralization in flat-bottomed microplates (96 wells) was conducted using the protocol described previously 24 , with a few modifications. The test was performed on ovine testis cells using 2 replicates. The volume of inocumlum virus was 100 µl into each well. The neutralization index was considered negative if less than or equal to1:8.

ELISA testing

A double-antigen ELISA for the detection of antibodies against capripoxviruses, including lumpy skin disease virus (LSDV), sheeppox virus (SPPV) and goatpox virus (GTPV) in serum or plasma from cattle, sheep, goats or other susceptible species (IDvet, France), was used to confirm exposure of the bulls to LSDV infection. Serum samples were collected from infected (IN) and in-contact animals (C1 and C2) (all animals per group) showing clinical signs at 0, 42 and 60 days p.i. The ELISA was performed according to the manufacturer’s recommendations. Reactions were measured as optical density (OD) readings at 450 nm using a Tecan Sunrise absorbance microplate reader (Switzerland). The antibody responses were represented as sample-to-positive (S/P) ratios (percentages), calculated as follows: S/P% ratio = (sample OD– negative control OD)/(positive control OD– negative control OD) × 100%. S/P ratios ≥ 30% were considered as being positive.

DNA extraction

The samples were aseptically handled and processed as 10% homogenates in PBS. A 200 μL aliquot was used for total nucleic acid extraction using the QIAamp DNA Mini Kit (Qiagen, Germany), following the manufacturer’s recommendations.

Real-time PCR (quantitative [q] PCR)

Sample extracts were analyzed using real-time PCR for the presence of LSDV DNA, as previously described by Sprygin et al . 25 . The fluorogenic probe was labeled at the 5′ end with the FAM reporter dye and with BHQ as a quencher at the 3′ end. Selected primers and probes were synthesized by Syntol (Moscow, Russia). PCR was performed using a Rotor-Gene Q (Qiagen, Germany) instrument and the following thermal-cycling profile: 95 °C for 10 min, followed by 45 cycles at 95 °C for 15 seconds (s) and 60 °C for 60 s. The final reaction volume was 25 μL containing 10 pmol of each primer, as well as 5 pmol of the probe, 25 mM MgCl 2 , 5 μL 5× PCR Buffer (Promega, USA), 1 μL of 10 pmol dNTPs (Invitrogen, USA), and deionized water to make up the final volume. Samples were tested and results interpreted according to the protocol, as previously described 25 .

Clinical observations

Body temperature.

The baseline average temperature for the animals before the trial was 38.4 °C. All animals infected with LSDV at the outset of the trial (group IN) had fevers up to 40.7 °C (range 39.0 °C to 40.7 °C) on p.i. day 3, indicating virus replication and circulation. By day 8 p.i., the body temperatures of all the inoculated bulls rose above 39.6 °C and their temperatures remained high until p.i. day 20, and thereafter moderate declines were measured to within the range of 38.1 to 39.6 °C in most of the infected animals up to around day 40 p.i. – thereafter a second bout of fever (bi-phasic) was measured in most of the group (except for NI-8) with temperatures rising to a high of 41.5 °C (IN-2) on day 41 p.i., tailoring off to close to normal levels from day 48 p.i. (Fig.  1 and S 1 Table ).

Average body temperature measurements per group over the course of the trial (orange – IN bulls, blue – C1 bulls, grey – C2 bulls).

On the other hand, the control (C1) in-contact animals that did not receive virus at initial inoculation, maintained normal body temperatures of around 38.6 °C until day 19 p.i., and thereafter their temperatures also showed increases up to 41.1 °C (C1-9, day 46 p.i.), which decreased slightly on day 46 p.i., but then rising again (bi-phasic fever) in most animals (except C1-1) up until the end of the trial, i.e., day 61.

In C2 animals, which were introduced from day 33 p.i., their body temperatures increased from as early as five days post-introduction (day 38 of the trial), also showing a bi-phasic pattern of fever, with the second phase starting around day 49 p.i. (16 days post-introduction), with a high of 40.9 °C being recorded for animal C2-3.

There was a significant level of edema in the inoculated bulls (IN group) in their subscapular axillary and popliteal lymph nodes, except in bull IN-6 – this animal exhibited edema in its dewlap area and joints, accompanied by lesions on its muzzle, and general weakness (Figs. 2 and 3 ). In the C1 group, edema appeared late, between days 28–30 p.i., in the areas under the jaw, corresponding with the detectable viremia and elevated body temperatures in all the bulls in this group (up to 40.6 °C, in C1-5) (Figs. 5  and 6 ). In the C2 group, elevated temperatures were recorded in all animals within a week following their inclusion in the trial (day 33 p.i.), found to be associated with slightly enlarged lymph nodes and edema in the jaw (for C2-3), and the C2-1 bull displayed a mild edema in its dewlap.

Lesions in the muzzle (red arrows) of IN-6 at day 21 p.i.

Edematous joints in IN-6 bull at day 21 p.i.

In-contact bull C1-9 with swollen submandibular space (red arrow) at day 28 p.i.

C1-5 bull with hyperaemic muzzle epithelium at day 28 p.i.

Viremia dynamics (averaged per group) (blue – IN, pink – C1, orange – C2).

Viremia, as assessed using qPCR on blood samples, was evident as early as p.i. day 7 in the infected animals (IN-6), peaking by p.i. days 11-13 (only detectable on day 13 in IN-8), followed by a slow decline after p.i. day 20, until p.i. day 38 in all animals in this group (with no detection in IN-8, indicating a very low level of viremia in this animal) (Fig. 6 , S1 Table ).

In the C1 control (in-contact) animals (except in C1-1), which were not inoculated, viremia was measurable using qPCR only after p.i. day 27, to a varying extent, and reached a plateau between p.i. day 38 and 41 (4 out of 5 bulls), which corresponds to days 25–28 following the peak viremia in infected (IN) bulls. Viremia in IN and C1 animals became undetectable after p.i. day 43 (except in C1-3, day 47).

For the C2 group, except for a low-level detectable viremia five days post-introduction in C2-3, no viremia was detectable in blood for the remaining animals, or at any other time point during the trial for this group, even though a low-level bi-phasic fever was measured. However, low levels of viral DNA was detectable from nasal and/or ocular secretions from all animals from this group at some point during their inclusion in the trial ( S1 Table ).

Virus shedding

Virus shedding in inoculated bulls was initially observed as early as p.i. day 11 in nasal discharges, and this lasted intermittently, at least until p.i. day 38. Ocular shedding was also observed in nos. 2, 4, 6 and 10, starting from day 13 p.i. ( S1 Table , Fig.  7 ). Nasal shedding was observed in bull nos. 2, 4, 6 and 10 by day 11 p.i. ( S1 Table and Fig.  8 ).

Dynamics of ocular shedding (averaged per group) (blue – IN, pink – C1, yellow – C2).

Dynamics of nasal shedding (averaged per group) (blue – IN, pink – C1, yellow – C2).

The dynamics of virus shedding in the two groups in contact with each other at the outset of the trial (IN and C1) showed no statistically significant differences (p > 0.05). The nasal shedding was more durable in IN bulls versus C1 animals with no statistical significance in virus loads. The ocular shedding was comparable in time between the two groups and did not differ statistically (Figs.  7 and 8 ).

Skin lesions

In the inoculated bulls, by p.i. day 11, there was a significant appearance of lesions (0.5 to 1 cm diameter) on the shoulders of three of them (bull nos. 4, 6 and 10). In addition, in these bulls in this group, except IN-2, the scrotum and ventral aspects of the abdomen showed typical foci of erosions. Bull IN-2 showed erosions in only the groin and scapula areas, with the temperature remaining steady at an average of 40 °C. By day 15, there was fulminating disease presentation in infected bull nos. 4, 6 and 10 with symptoms of multiple lumps, coalescing together over the entire body (up to 3 cm in diameter), erosions in the foci up to 2 cm in diameter, and lesions in the scapula and sides as large as 1.5 cm in diameter. Erosions were also observed on their muzzles and associated epithelia. Bull no. 8 displayed similar symptoms, but their appearance was delayed. By p.i. day 21, the size of the lesions had enlarged to 2.5 cm in diameter in inoculated bull nos. 4, 6 and 10, and their nasal epithelia were hyperaemic. Also, there were isolated foci of necrotic lesions in the scrota of these animals.

For the C1 bulls, by day 28 p.i., three of them exhibited small erosions in their nasal epithelia and in their muzzles (Fig.  9a ), during which period their viremia was significant, with high body temperatures (40.6 °C in C1-5). Importantly, no erosions were evident towards the rear half of their bodies (scrotum or inner sides of their legs), as opposed to small skin lesions present on their necks. Three out of five C1 animals (C1-5, C1-7, C1-9) developed characteristic signs of viral infection by day 35, with the symptoms including: enlarged lymph nodes (predominantly prescapular, paratracheal and head lymph glands) and multiple lumps over their bodies, from their heads to their tails, 0.5 to −4 cm in diameter (Fig.  9b ). However, there was no pronounced pathology in popliteal or groin lymph glands as compared to the inoculated animals, and also there were no erosions in their scrotums.

C1 bulls with lesions. ( a ) In-contact bull (C1-3) at day 35 p.i., indicating a lesion in the muzzle (arrow). ( b ) C1-7 bull with skin lumps (lesions) on the back and ventral side.

Blood, nasal and ocular discharges were positive for LSDV DNA from these animals, as assessed using qPCR. Even though bull C1-1 was asymptomatic, it was positive for the presence of virus using qPCR analysis. The presence of virus in ocular shedding became detectable only from p.i. day 28 (nos. 3, 5, 7 and 9), while virus shedding in nasal excretions was evident mostly after 35 days p.i. (S 1 Table , Figs.  6 – 8 ). Ocular shedding was more pronounced in C1 bulls as compared to the inoculated bulls (IN group), although, in general, the inoculated bulls displayed longer and more intense shedding.

From day 38 of the experiment, i.e., five days after introducing the C2 animals, viral DNA was detectable from them in blood (viremia), ocular and nasal discharges ( S1 Table , Figs.  6 – 8 ). Shedding in C2 bulls was weak and lasted intermittently for 12 days, from day 5 to day 17 post-introduction. There were variable clinical symptoms in the C2 animals: C2-1 displayed a mild edema in its dewlap, whereas C2-5 developed a few foci of erosion in its scrotum (Table 2 ). At post-introduction day 21 (i.e., day 54 of the experiment), the C2-3 bull displayed a few small lumps in the scapular region. By post-introduction day 26, these lumps had increased in number and size, between 2.0 and 2.5 cm in diameter (Fig.  10a,b ).

C2-3 bull: ( a ) at day 20 post-introduction - lumps developing on the neck; ( b ) at day 26 post-introduction – lump development progressing towards the tail.

Recovery from infection

Inoculated (IN) animal nos. 4, 6 and 10 had persistent clinical symptoms, with virus shedding in secretions, till p.i. day 37. But, the inoculated bulls nos. 2 and 8 were asymptomatic, without fever, despite delivering positive PCR results for the presence of virus. All the infected (inoculated) bulls stopped shedding the virus thereafter, with erosions displaying complete scarring and their edemas being cleared, but with their lymph nodes remaining enlarged (as detectable to the touch) up to p.i. day 45.

On the other hand, most of the C1 bulls (nos. 3, 5, 7, 9) displayed clinical signs until day 54. Their skin lesions became necrotic and erupted, with persistent fever between 39 and 40 °C. At p.i. day 50, these bulls developed additional skin lesions, hyperemic nasal epithelia, mild edema in their jaws and dewlaps, and enlarged lymph nodes in their necks. They also had enlarged lymph nodes that were painful to the touch. There was still detectable virus shedding, at this time.

ELISA and VNT

ELISA testing was conducted to assess the levels of seropositivity of the animals to the virus, and it was confirmed that at day 0 before the inoculation, all animals were seronegative (Table  3 ). By p.i. day 42, the five IN bulls seroconverted, whereas, only three out of the five in-contact group (C-1) showed a weak seropositive response (Table  3 ). By p.i. day 60, all IN bulls were strongly seropositive, which was also verified using virus neutralization testing (VNT), as were all C1 animals. However, C2 animals were seronegative throughout the experiment, until day 60, even though there was the detectable presence of virus in their nasal and ocular discharges (and, on one day, day 38, in the blood of bull C2-3).

Recombination is key towards molecular evolution of viruses. Many viruses appear to have diverged from a common ancestor through genetic exchanges and reassortments to expand their diversity, likely including capripoxviruses 26 . However, novel features arising in new chimeric progeny as a result of these events may include drastic phenotypic changes such as a shift in host range, pathogenicity and in transmission pathways 27 . The first field evidence of capripoxvirus recombination between a virulent and vaccine strain was published recently, with the new virus clustering outside both distinct groups of vaccine and field strains 4 . Despite the genome delineation, the degree to which the genome rearrangements contributed to new phenotypic characteristics remains to be elucidated. In this study, we follow up on the novel recombinant strain, LSDV Saratov/2017, in susceptible hosts (bulls) and demonstrate clearly for the first time non-vector in-contact transmission of this isolate with a focus on the time course of viremia and virus shedding in different groups of experimental animals.

The experiment was designed to gain an insight into whether the novel vaccine-derived virulent recombinant LSDV strain, with some genes restored to the yet unknown wild-type parental strain, such as the KSGP-like LSDV isolate, could exert new features surmised to be absent in the normal field parental strains (e.g. Dagestan/2015 20 ) – in this case, efficient non-vector-assisted transmission. Previous experiments with field strains never showed convincing proof that LSDV can transmit to susceptible hosts through air-borne or other non-vector contact modes 20 , 21 . By contrast, the findings of the current study showed that the recombinant virus was able to transmit horizontally without arthropod assistance, as neither flying insects nor ticks were detected throughout the trial period in the indoor containment facility. The first group of in-contact animals (C1) possibly became infected via indirect contact through sharing food and water troughs, while actual physical contact with adjacent animals to their left and right was also possible and may have resulted in direct contact transmission via the mucosa resulting from virus shedding. Drinking troughs have already been blamed for indirect transmission of LSDV in an insect-free setting 17 , however the complexity of transmission is far from being fully comprehended 11 , 18 .

Interestingly, the viremia in the IN bulls was observed between 7 and 22 days p.i., up to 38 days p.i., whereas Babiuk et al . (2008) previously showed that DNA in blood was detectable between 6 and 15 days p.i., only. In the same study, oral and nasal shedding was reported between 12 and 18 days p.i., whereas in our study this window was from 11 to 38 days p.i., which is much longer.

Importantly, virus loads in blood (viremia), nasal and ocular shedding did not differ significantly between IN and C1 animals (p > 0.05), but the duration of viremia and nasal shedding was twice as long in IN animals versus C1 animals, except for ocular shedding where the duration was comparable (S 1 Table ). It is likely that the intravenous route, which closely imitates an insect bite, promotes a more aggressive disease pattern as evidenced by experimental studies 20 , 21 . However, the presumed indirect contact (air-borne or alimentary [mucosa]) route as evidenced by C1 bulls in this study deserves further attention in experimental settings to delineate the complex nature of LSDV transmission. The first evidence of viremia in C1 bulls was observed at day 29 p.i. (S 1 Table ), which is eight days after the IN animals started showing the last signs of their detectable viremia (day 21 p.i.). To confirm the infection, in support with the PCR results, C1 animals did seroconvert, with three of them (C1-1, C1-3 and C1-9) showing antibodies to LSDV by day 42 p.i. (Table  3 , ELISA results), with the remaining animals having all seroconverted by day 60 p.i. (Table  3 ).

Concerning the C2 group, these animals also became infected via an in-contact mode as evidenced by clinical signs, PCR and virus isolation. Although this group had a significantly lower virus load (viremia) versus the IN and C1 groups (p < 0.05), the nasal and oral discharge loads in this group did not differ significantly from either of the other groups (p > 0.05) (Figs.  6 – 8 ). As the number of days and duration of detectable virus was also generally lower, it is surmised that there was possible environmental contamination of the swabs with virus from the IN and/or C1 animals.

Of note is that the ELISA and VNT results indicate that the C2 group did not seroconvert, even after 27 days, possibly due to the shorter time available for antibodies to be elicited in this group compared to the other groups (Table  3 ), whereas virus shedding was detected within the time frame of the experiment (S 1 Table ). The presence of the virus in nasal and ocular discharges in these animals can be explained by the profound shedding of the virus from the skin erosions in the IN and C1 groups contributing to a more rapid infection of the C2 group. In this regard, the importance of the crusts and erosions in virus transmission, be it vector-borne or in-contact, may be significant. However, as judged by the virus dynamics in nasal and ocular discharges (Figs.  7 and 8 ), the virus shedding in terms of titers did not differ statistically (p > 0.05), but, when considering the generalized disease presentation in IN bulls with fulminating skin lesions, containing high concentrations of virus, it is proposed that the skin lesions may have contributed to the virus transmission to the C1 in-contact animals, although to a lesser degree in C2 animals. This may suggest that the amount of virus shed by infected animals is key to virus spread. However, the limitation of the reported evidence is that the mechanism of virus entry cannot be conclusively established on account of the observations made during the experiment - this could be either through the alimentary and/or digestive tracts.

In addition, the localization and dissemination of skin lesions merits further discussion. From our experience, inoculated animals usually develop generalized disease with lesions breaking out evenly over the entire body, including scrotum, muzzle and epithelium, and within the same basic time period. This observation was also true for the IN bulls in this study. The C1 animals, in contrast, displayed a dramatically different pattern, where skin lesions first appeared and were initially restricted to the neck and head regions only, with no lesions in the scrotum or remainder of the body. However, eventually new lesions did develop, spreading throughout the remainder of the animals, down to the tail (Fig.  10a,b ). This is an interesting observation which may provide clues as to the gateway for LSDV infection through contact. In this scenario it is likely that the virus entered C1 animals through their lungs or other mucosa from where it travelled to the closest skin areas – head and neck - then spreading from there to the rest of the animal via the lymphatic system. Since upon intravenous inoculation the virus skips the skin barrier (such as is the case for an insect bite), it infects macrophages and settles in secondary sites, such as lymph nodes and testicles, whereas upon proposed inhalation and/or contact with conjunctiva, it needs to make its way through respiratory barriers. It is also likely that if the C1 and C2 animals had been given more time, their antibody responses would have likely been more pronounced. Moreover, C2 animals displayed no viremia, although they were in contact with virus-shedding cattle - this may also argue for the virus load factor in LSDV transmission, wherein a certain threshold needs to be surpassed.

Another important aspect of the current findings begs the question as to which genomic loci of the recombinant virus likely contributed to enhanced severity and improved capacity for contact transmission. Although identification of the particular genetic targets determining the virus phenotype was outside the scope of the current study, a number of the vaccine-derived genes within the recombinant virus, which reverted to the wild-type genotype following recombination, warrant further study 4 . Since this virus clearly showed contact transmission, it follows that all LSDVs should be capable of spreading by the same mode to varying degrees. Along with the anticipated vector-borne mode of transmission, with no single vector species yet clearly identified as being responsible for transmission, the direct or indirect contact modes have far reaching implications regarding control and eradication. The previously pursued intravenous pathway resulting from vector blood-feeding, has failed to explain outbreaks occurring when cold or dry weather conditions do not permit potential vector flight activity 1 . The likely reality is that a number of modes probably come into play, with the dominant one leading to an outbreak dependent on the specific circumstances and environmental and biological factors present immediately prior to the onset of the outbreak. This aspect warrants urgent attention and research efforts in the context of the current low-level research base on LSD, especially in non-endemic countries, to gain better insights to enable more adequate and targeted control practices to be developed and implemented.

Assimilating the evidence gained from this study, a contact mode of LSDV transmission has been clearly demonstrated for a novel recombinant LSDV recently recovered in the field. Coupled to other alternative modes like vector-assisted spread, these findings may contribute to future risk analysis and complement approaches to combating the threat this disease poses. The findings presented herein will lay a justifying basis for revisiting the control strategies currently in place, considering the danger from the emergence of hybrids, should the use of live vaccines be resorted to, especially in non-endemic countries. Further studies into LSDV biology are warranted to delineate the reasonable question if the contact mode demonstrated here is a de novo -created feature absent from both parental stains of the novel LSDV or whether it maintained a low profile, but was activated by genetic alterations following recombination.

Overall, the current approach to combat LSD and the virus, generally looks at insect vector control, besides vaccination and restriction of cattle movement, while food, water or litter are often overlooked as being ineffective sources of infection. In this scenario, control strategies need to be revisited for development of a more complex approach involving new parameters to consider in risk analyses. Moreover, contact transmission mitigates the factor of seasonality, which is linked to insect activity and widens the possibilities for spread regardless of the presence of biting insects.

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K.A., B.O., P.P., P.Y., K.S. and N.A. designed the experiments and collected the data. K.A., W.D., L.D., R.V. and S.A. analyzed the data and wrote the manuscript. All authors read and approved the final version of the manuscript.

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Aleksandr, K., Olga, B., David, W.B. et al. Non-vector-borne transmission of lumpy skin disease virus. Sci Rep 10 , 7436 (2020). https://doi.org/10.1038/s41598-020-64029-w

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Lumpy skin disease virus (LSDV) belongs to the genus Capripoxvirus and family Poxviridae . LSDV was endemic in most of Africa, the Middle East and Turkey, but since 2015, several outbreaks have been reported in other countries. In this study, we used whole genome sequencing approach to investigate the origin of the outbreak and understand the genomic landscape of the virus. Our study showed that the LSDV strain of 2022 outbreak exhibited many genetic variations compared to the Reference Neethling strain sequence and the previous field strains. A total of 1819 variations were found in 22 genome sequences, which includes 399 extragenic mutations, 153 insertion frameshift mutations, 234 deletion frameshift mutations, 271 Single nucleotide polymorphisms (SNPs) and 762 silent SNPs. Thirty-eight genes have more than 2 variations per gene, and these genes belong to viral-core proteins, viral binding proteins, replication, and RNA polymerase proteins. We highlight the importance of several SNPs in various genes, which may play an essential role in the pathogenesis of LSDV. Phylogenetic analysis performed on all whole genome sequences of LSDV showed two types of variants in India. One group of the variant with fewer mutations was found to lie closer to the LSDV 2019 strain from Ranchi while the other group clustered with previous Russian outbreaks from 2015. Our study highlights the importance of genomic characterization of viral outbreaks to not only monitor the frequency of mutations but also address its role in pathogenesis of LSDV as the outbreak continues.

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The Lumpy Skin Disease is caused by Lumpy Skin Disease Virus (LSDV) [ 1 ] which is a double-stranded DNA virus of genome size 150 kb and belongs to the genus Capripoxvirus , sub-family Chordopoxviridae and family Poxviridae [ 2 ]. The other members of the genus are Goat poxvirus (GTPV) and Sheep poxvirus (SPPV). LSDV is very similar to all the members of the Poxvirdae family in morphological characteristics, such as being very similar to the vaccinia virus under electron microscopy [ 3 ]. LSDV is non-zoonotic and is known to infect specific hosts, including cattle ( Bos indicus , Bos taurus ) and domestic water buffaloes ( Bubalus bubalis ) [ 4 , 5 , 6 ]. In recent years, reports have emerged that LSDV can also infect camel, giraffe, and wildebeest in the wild [ 7 , 8 , 9 ]. It spreads via contact through skin lesions, milk, and blood-sucking insects such as biting flies, ticks and mosquitoes [ 10 , 11 , 12 , 13 ]. The infection spreads more in the warm and wet periods as compared to the winters due to the increased insect population and its mobility in summers [ 14 ].

LSD virus was first reported in 2019 from India and has since caused several outbreaks. In the recent outbreak, cases started to appear in May 2022. Around 1 lakh cows have died as per recent reports in the current outbreak [ 15 ]. In a developing country like India, livestock production constitutes one of the important ways of earning a livelihood, and a deadly disease such as Lumpy Skin Disease has caused direct loss to the economy and poor production of livestock [ 15 ]. India has a cattle population of 308 million; therefore, controlling the spread of infectious diseases is important [ 16 ].The direct loss includes deaths of cattle, a decrease in milk production while the indirect losses include movement restriction of cattle across the country [ 15 ]. Earlier studies have reported pathological changes in most of the organs and tissues of infected animals such as cow mastitis, necrotic hepatitis, lymphadenitis, orchitis and also in some cases, myocardial damage [ 17 ].

World Organization of Animal Health (WOAH) has now identified lumpy skin disease as a notifiable disease [ 18 ]. Since its first discovery in Zambia in 1931 [ 19 ], this disease was initially confined to the Sub-African region until 1989 and then it started spreading across boundary to Middle East Asia [ 20 , 21 ]. LSDV was reported in 2016 in Russia and other Southeast European nations [ 21 ]. The disease first appeared in India along with other Asian countries such as China, Nepal, Thailand, Bangladesh, Bhutan in November 2019 [ 22 , 23 ]. While LSD has been reported in India since 2019, it has caused significant damage during 2022 outbreak by infecting more than 2 million cows. The symptoms of LSD vary in individual animals depending on the severity of the infection. An animal takes 1–4 weeks to develop symptoms such as high fever, ocular and nasal discharge, loss of appetite, nodular lesion on skin [ 24 ]. According to the data available, a mortality rate of 5–45% was observed [ 4 , 25 , 26 , 27 ]. The major states affected in terms of mortality and morbidity are Rajasthan, Gujarat, Uttar Pradesh, Punjab, Haryana, Karnataka, West Bengal and Maharashtra [ 28 ]. Due to the lack of treatment options, only way of preventing infection is vaccination and by separating the infected animals. The Indian government has taken several measures to control the spread of LSD, including mass vaccination campaigns (goatpox vaccine), setting up quarantine facilities and restricting the movement of infected and susceptible animals. However, the disease continues to be a challenge due to a lack of awareness about its transmission and control, as well as the difficulty in detecting infected animals in the early stages of the disease.

It is generally recognized that the LSDV may have originated from one of the earlier pox virus species and then evolved by spreading in different kind of hosts. Double-stranded DNA viruses are known to use homologous recombination for evolution towards expanding their host range and virulence [ 29 ]. In this study, we have utilized genome sequencing to identify the variants of LSDV circulating in India. Through the phylogenetic analysis we found there are two different classes of variants in India. We then performed mutation (SNP) analysis and found the groups differ significantly in the number of mutations.

Analysis of LSDV cases in the field reveal varied signs and clinical outcomes

Samples of blood, oral swab and skin scab from infected cows were collected from Karnataka, Maharashtra, Rajasthan, and Jhansi during August-November 2022 while the outbreak was going on in India. The animals were showing typical clinical signs such as reduced milk yield, loss of body mass, raised body temperature upto 40–41 °C, nasal and lachrymal discharge, lost appetite, and skin nodules observed on the body of both young and adult cows. The skin nodules burst open when the viral titre is high, exposing the internal layers of the skin which leads to open wounds and eventually secondary bacterial infection if not timely treated (Figure 1 A). The villages observed mortality rate as high as 40% for infected cows, and higher mortality was evidenced in young cows as compared to the adults.

Vectors such as flies, blood-sucking ticks, and mosquitoes were also observed in the vicinity of the animals. Due to the lack of proper ventilation and isolation facilities for cattle, LSDV managed to infect over 20 million cows in 15 different states, and the outbreak is still ongoing.

PCR-based detection strategy for LSDV

The diagnosis for Lumpy skin disease mainly depends on the typical clinical signs and differential diagnosis. The severe form of the disease has characteristic symptoms while the early signs of LSDV overlaps with other diseases like bovine herpes mammillitis, bovine papular stomatitis and foot and mouth disease [ 30 ]. Agar gel precipitation is also used to detect viral antigen in a serum or tissue sample. But this test is not specific and cannot be used for LSDV because the antigens of LSDV are shared with other poxviruses. Therefore, molecular diagnosis by using PCR is the most effective method to detect LSDV.

Samples including blood, oral swab, skin scabs were collected from different parts of India and transported to the ICAR and IISc laboratory to confirm LSDV infection. Conserved regions in the virus genome were identified using multiple sequence alignment and then primers were designed for detecting LSDV. LSDV specific primers were used for fusion gene LSDV0117, which helps the viral envelope fusion with the host membrane as described in method section. Conventional PCR was performed and the amplicon size of 472 bp was confirmed (Fig.  1 B), full image (Supplementary Fig.  1 ). All the samples collected from symptomatic cows were positive for Lumpy Skin Disease Virus.

Clinical signs and molecular diagnostics. ( A ) Animal showing severe skin lesions and nodules on body and appearance of swollen lymph nodes ( B ) PCR-based confirmation of LSDV by using partial viral fusion gene amplification

Amplification of Indian LSDV strain genome to develop amplicon-based whole genome sequencing

DNA extracted from 22 samples (including twelve skin scab/nodule samples from cows and ten virus samples collected after cell culture passage) was used for further processing. The whole genome of LSDV is approximately 150 kb, so it was necessary to generate smaller amplicons (3 kb) to achieve full genome coverage for Oxford Nanopore Technology and overlapping primers were designed. Nanopore sequencing produces long reads, which are useful for characterizing complex genomic regions.

A total of 1,126,683 reads were obtained, ranging in size from 105 bp to 54,253 bp, with a median size of 10,000 bp. Reads smaller than 1.5 kb were filtered out to avoid non-specific reads. The coding sequences of 156 genes were obtained using GeneMarkS2 for ab initio gene prediction. The genome was assembled from the raw sequencing data, and the location of the genes was identified. Additional 12 samples collected from Jamnagar, Anand, and Surat were sequenced using Illumina sequencing, covering over 90% of the genome sequence.

Phylogenetic analysis using whole genome sequences of LSDV reveals multiple strains

Multiple sequence alignment of the LSDV whole genome sequences from different regions of the world was performed and then used to construct a maximum likelihood-based phylogenetic tree, which shows the evolutionary relationships among different LSDV strains and other pox viruses. Goat poxvirus was used as outgroup, as shown in Fig.  2 .

Phylogenetic analysis of LSDV. Maximum-likelihood Bayesian phylogenetic tree based on whole genome sequences showing the relationship in Capripox virus family including Sheep poxvirus, Goat poxvirus and complete genome sequences of LSDV strains sequenced from many parts of India during 2022 outbreak as well as sequences available on NCBI from previous outbreaks. The genomes sequenced in this study are highlighted in red text

The genome sequences from 2022 outbreak (India) lie on two separate branches on the phylogenetic tree, which has been labelled as low-mutation and high-mutation (Fig.  2 ). Low-mutation genomes closely resemble the Ranchi sequence from 2019 outbreak and Hyderabad sequence from 2020 outbreak. This group has lesser number of variations in their genome sequences as compared to the reference Neethling LSDV sequence. The other group, high-mutation, with higher number of variations per sequence, lies separately, grouping with Russian 2015 LSDV outbreaks. This observation suggests that the current 2022 LSDV outbreak in India is a result of two different group of strains circulating together in the same region.

The Indian LSDV sequences from 2022 are distinct from the vaccine strains of LSDV, confirming that the recent outbreak in India is unlikely to be the result of vaccine spillover. All the Neethling virus-based vaccine strains and vaccine-derived recombinant strains, characterized by combined genetic sequences [ 31 ], form a separate group. The close resemblance of samples from recent outbreak to the 2019 Ranchi strain suggests that infections were occurring, although not very severe, in cows for a few years. However, the higher number of mutations in high mutation group indicates the circulation of another strain with an increased mutation rate in genes involved in host cell binding and immune evasion.

The Indian LSDV sequences are 99.98% identical to the neethling strain and 97.38% identical with Goat poxvirus. LSDV is known to code for 156 proteins, and most of the genes are common between these viruses. The differences in LSDV and goatpox sequences lies in the terminal region of the genome. These terminal regions contain genes important for virulence such as ankyrin repeat-domain containing proteins which helps the virus to bind to the host cell.

SNP analysis in the genome sequence reveals genetic variants with potential to cause severe infection

We performed mutation analysis using nucmer and found a total of 1819 variations in the 22 sequenced genomes compared to the reference sequence LSDV Neethling strain (NC003027.1). These variations at the amino acid level were dominated by silent SNPs (synonymous), followed by extragenic, SNPs (non-synonymous), deletion frameshift, and insertion frameshift mutations (Fig.  3 A). High-mutation group sequences exhibit the highest number of SNPs at the amino acid level (Fig.  3 B). Among the LSDV genes, 38 genes have more than two variations per gene, with the gene encoding Interleukin-10-like protein having the highest number of variations [ 10 ]. This is followed by the virion core protein gene with 7 variations, DNA ligase-like protein, B22R-like protein, and Ankyrin-like protein with 6 and 5 variations, respectively (Fig.  4 ). Other genes, such as Kelch-like proteins, RNA polymerase subunit, EV glycoprotein, DNA helicase transcriptional elongation factor, and early transcription factor large subunit, important for virus binding to host cells and virus replication, have three to four variations in each gene. Additionally, 25 genes have two mutations, including several hypothetical protein-coding genes, and 34 genes show one variation only. Twenty out of 22 genomes sequenced in this study showed non-synonymous changes at amino acid level (Fig.  3 C).

The variations in 22 LSDV genome sequences from India were classified into mutation classes ( A ) All classes of variations present in a total of 22 genomes, most of the variations belong to SNP_Silent followed by extragenic mutations ( B ) Total number of variations identified in LSDV strains from 2022 outbreak. The colors in the graph used are for various regions in India ( C ) Single Nucleotide Polymorphisms (SNPs) on amino acid level across all LSDV genomes sequenced

( A ) Graph showing number of variations in protein-coding genes in LSDV, with more than 2 variations per gene represented. ( B ) The graph represents the most common mutation on amino acid level in 22 LSDV genome sequences upon analysis

The most mutated protein-coding gene, namely LSDV005, coding for Interleukin-10-like protein is a functional viral cytokine homolog that plays a role in regulating host immune response, as inferred from UniProt. This protein has 4 helix cytokine-like core. Viral interleukins have been shown to activate cellular signalling cascades that enhance viral replication [ 32 ]. Previous gene knockout studies have shown that LSDV005 is one of the important protein-coding genes which is responsible for the virulence of the LSD virus in host cells. LSDV005 is similar to cellular IL-10 in the carboxyl terminus part and affects the immune system similarly [ 33 ].

Another highly mutated gene is LSDV094, which codes for virion core protein. LSDV genome consists of 10 virion core protein-coding genes throughout the genome which make up the core/nucleoprotein of the LSD virus. One common SNP in this gene in High-mutation leads to R578M transition, that is from basic to non-polar amino acid. Other variations inlude R581Q. Virion core proteins are one of the largest families of poxvirus proteins, many of which have been correlated as virulence factors [ 34 ].

Other genes with major variations include LSDV134, which encodes for variola virus (VV) B22R like protein. It is a VV immunomodulating gene with sequence homology to serine protease inhibitors (serpins) that possess antiapoptotic and anti-inflammatory properties. B22R has been shown to reduce the host’s immune response to the virus and rabbitpox equivalent of VV B22R has been shown to inhibit apoptosis in a caspase-independent manner and increase host range as well [ 35 ].

Another important gene which is mutated on protein level is LSDV036 which encode for RNA polymerase subunit. Poxviruses encode a multi-subunit DNA-dependent RNA-polymerase that carries out viral gene expression in host cytoplasm. There were two silent mutations, and 2 SNPs observed in High-mutation genome sequences. The SNP leads to F130S, V297A substitution and given its role in the regulating transcription, any mutations in this gene can lead to altered ability to proliferate and cause symptoms.

Gene LSDV140 encoding for Ring finger host range protein or p28-like protein was also found to be mutated with N203K transition in low-mutation while high-mutation showed SNPs T132M and S152F. P28-like protein is a part of Ub system and acts as Ubiquitin ligase. Similar mutation was reported earlier also in this protein [ 36 ]. These findings highlight the importance of consistent monitoring of genetic variations among LSDV variants. Rest of the SNPs belong to hypothetical proteins, whose functions are yet to be identified in poxviruses. Out of 156 genes of LSDV, more than 40 protein coding genes are hypothetical, and their function remains unknown. 26 of these hypothetical protein coding genes were found to have variations. A total of 399 extragenic mutations are present in 22 genome sequences, and most of the variations were observed in 3’UTR. Since 3’UTRs are involved in post-transcriptional regulation, and mRNA stability and degradation, these variations might affect gene expression and regulation in the host cell. Supplementary File 1 presents the number of mutations found in different proteins in 22 genomes reported in this study.

Many unique mutations were also identified in the genomes sequenced in the current study, such as N1 sample collected from Jamnagar, Gujarat in 2022 has K114I in gene LSDV005 coding for Interleukin-10-like protein; West Bengal sample showed unique SNP Y418F in gene LSDV116 coding for RNA polymerase subunit; Banswara, Rajasthan 2021 genomes sequence showed Y194C in LSDV057 coding for putative virion core protein. Mutations in these proteins can be one of the sophisticated mechanisms for enhancing the spread of virus and these mutations can affect the virulence and host range of the virus. These mutations can arise spontaneously or due to selection pressure from the host immune system and from the use of vaccines.

The most common mutations found in Indian LSDV 2022 sequence include changes in the viral envelope protein, which can alter the ability of virus to evade the host immune response, or in the viral polymerase gene, which can affect the replication and spread of the virus. It is important to monitor the genetic variation in LSDV in India, as it can help to understand the evolution and transmission of the virus and to design effective control strategies, including diagnostic tests.

The frequency in the occurrence of the outbreak and spread of the virus from its original geographic range has led to increased research. The first major outbreak in India happened in 2019, most of the sequences deposited for that outbreak are closely related to Neethling reference strain harbouring a few mutations. But the recent outbreak in India shows presence of at least two types of variants circulating in India.

To gain a comprehensive understanding of the variants of LSDV and their circulation patterns, samples were collected from different parts of India. The phylogenetic analysis of these sequences revealed two major groups. Analysis of the sequence composition at the nucleotide and protein levels demonstrated significant differences in the occurrence of single nucleotide polymorphisms (SNPs) between the two groups. The group that is closer to the neethling strain exhibited less variation, while the other group displayed a higher number of mutations, most of which did not result in amino acid changes. Generally, the poxviruses are not fast evolving viruses, such as Variola virus is estimated to be evolving at ˜ 0.9–1.2 × 10 − 6 substitutions/site/year [ 37 ]. But they can undergo mutations due to mechanisms such as homologous and nonhomologous recombination, gene duplications, gene loss, and the acquisition of new genes through horizontal gene transfer.

Recently, Schalkwyk et al. established the substitution rate of 7.4 × 10 − 6 substitutions/site/year in Lumpy skin disease virus [ 38 ]. Therefore, it is possible that the high severity in the recent outbreaks has increased due to the increased number of mutations, as seen in high-mutation, containing sequences from Indian regions with high-severity cases such as Rajasthan, Gujarat, and Maharashtra, which enables the virus to replicate more and cause more clinical symptoms and resulting in high mortality. Similarity in mutations of high-mutation strains with Nigeria 2021 and Russian 2015 outbreak suggests that there might have been a transboundary migration of an infected animal as both groups show higher number of similar mutations. Some SNPs caused changes in amino acids within proteins, particularly in genes like Interleukin 10-like protein, virion core-like protein, and GPCR-like protein. These mutations could be due to the evolutionary pressure on the virus resulting from the widespread use of vaccines that are not very effective, leading to mutations in important viral immune response genes.

Field analysis of LSD cases revealed a wide range of clinical signs and outcomes in infected cattle, including reduced milk production, weight loss, elevated body temperature, nasal and lachrymal discharge, loss of appetite, and the development of skin nodules. When these nodules burst open, they can lead to open wounds and bacterial infections. The high mortality rate, especially among young cattle, highlights the severity of LSDV infection. The increased severity observed in samples from Gujarat, Maharashtra, and Rajasthan may be a result of the high number of variations in those regions. Analysis of LSDV genomes identified numerous genetic variations, including silent SNPs, extragenic mutations, deletion and insertion frameshift mutations, and SNPs leading to amino acid changes. Several genes with multiple variations were found, including those encoding Interleukin-10-like protein, virion core protein, RNA polymerase subunit, and B22R-like protein. These variations can influence virulence and host range of the virus. Recently, there have been reports of LSDV infection in yaks [ 39 ], camels, free ranging gazelles in India, and giraffes in Vietnam [ 8 , 9 , 40 ], indicating that LSDV can undergo transmission across species with an increased number of mutations. A total of 230 variations were observed in the LSDV strain sequenced from camel hosts. These SNPs were similar to the strains in High-mutation sequenced from cow hosts. Mutations in proteins like B22R, coded by LSDV134, which have been shown to reduce the host’s immune response to the virus and increase host range, were also found in the LSDV strain from camels [ 35 ]. Therefore, it becomes important to identify and vaccinate other hosts which can act as reservoirs for the virus. Monitoring genetic variations in LSDV is crucial for understanding its evolution, developing control strategies, and detecting new outbreaks. The easy spread of LSDV through direct contact, vectors, and bodily fluids emphasizes the importance of proper animal management and biosecurity measures to prevent and control the disease.

Sheep poxvirus and Goat poxvirus, both belonging to the genus Capripoxvirus , have been endemic in India. However, LSDV outbreaks only started recently in Southeast Asian countries in 2019 [ 41 ]. Another poxvirus of the Poxviridae family, Smallpox virus, which caused significant damage to human health and life, has been globally eradicated in the last century through large-scale vaccination campaigns using live vaccinia vaccines [ 42 ]. Therefore, most effective way to prevent and eliminate disease is vaccination. While there are vaccines for LSD based on the Neethling strain. However, animals sometimes develop clinical symptoms such as the formation of nodules and a drop in milk yield even after vaccination. This adverse effect is known as ‘Neethling disease’ [ 43 ]. The commonly used Goat poxvirus vaccine is often employed to prevent LSDV, due to its antigenic similarity to LSDV. The fact that some outbreaks are occurring in vaccinated animals raises about the complete effectiveness of the vaccine. Possible reasons for this include the vaccination method being ineffective, flaws in the administration methods, or issues with vaccine storage.

Some studies report that the commonly used LSDV vaccine is not a pure viral culture of LSDV virus but instead contains a mix of quasi-species, which raises the chances of homologous recombination in the genome of viruses [ 31 ]. It has been reported that LSDV can also undergo recombination [ 29 ]. Therefore, while using live attenuated viruses, it is important to analyze the quality and nature of variation. Previously, several vaccine-like recombinant LSDV strains were discovered in Kazakhstan, neighbouring of Russia and China from 2017 to 2019 [ 44 ]. In our study, we analyzed the current LSDV outbreak clusters and observed that both the groups lie away from the vaccine strains as well as the recombination-derived strains. Therefore, the current outbreak is not a result of vaccine spillover. The 22 LSDV genomes sequenced in this study are separate from the recombinant LSDV strains from Southeast Asia and the Russian vaccine spillover LSDV strains, as clearly depicted in the phylogenetic analysis.

A Ranchi strain-based homogenous live-attenuated LSD vaccine, Lumpi-Pro VacInd (an experimental vaccine) has been developed to prevent the outbreaks. The ‘Neethling disease’ event in which animals develop a reaction against vaccination such as skin nodule formation was not observed in field animals and the vaccine was shown to be 100% effective till January 2023 [ 45 ]. The SNP analysis of this vaccine strain showed that it belongs to the LSDV sequences of Low-mutation in the phylogram which has lesser number of mutations. It has been shown that it neutralizes LSDV strains from 2022 outbreak [ 45 ]. Continued monitoring of vaccinated animals for extended periods will be important to assess the vaccine’s efficacy.

To prevent future outbreaks of LSDV, it is crucial to identify the possible reasons behind these outbreaks and strategize accordingly. It is important to identify all potential hosts for LSDV beyond cattle and arthropod vectors. Regulating the transboundary migrations of animals is necessary to prevent all possible pathways for LSDV introduction. Regarding vaccines, live attenuated LSDV strain vaccines should only be used after undergoing quality testing.

The analysis of LSDV cases in India during the 2022 outbreak highlighted the severe impact of the disease on cows and the significant economic losses incurred in the agricultural sector. Developing a molecular detection strategy using PCR allowed for accurate diagnosis of LSDV, overcoming the challenges posed by clinical signs overlapping with other diseases. Whole genome sequencing provided valuable information on the origin and evolution of the LSDV strains circulating in India. The phylogenetic analysis revealed the presence of two distinct groups, suggesting multiple introductions of the virus. SNP analysis identified genetic variations in essential genes, potentially affecting virulence and antigenicity.

These findings contribute to a better understanding of LSDV and provide valuable information for developing effective control strategies, such as development of diagnostic tests. Monitoring genetic variations and protein expression patterns is crucial for detecting new outbreaks, tracking the virus’s evolution, and guiding the development of targeted interventions. Overall, this research enhances our knowledge of LSDV and its impact on cow’s health, supporting efforts to mitigate its spread and minimize economic losses in the future.

Material and method

Sample collection.

Biological specimens including saliva swab, blood sample, skin lesion scabs were collected from infected cattle as per the standard practices without using any anaesthesia by veterinarians in Karnataka in India. An informed consent was taken from the cows owners before collection of samples. The animals presented symptoms such as fever, nasal discharge and characteristic pox nodular skin lesions. Blood samples were collected in EDTA vacutainers (Becton-Dickenson) and the skin lesions were collected and transported to the laboratory in 50% glycerol (Qualigens). All samples from the previous outbreaks (2019–2021) were available as cell cultures. For the 2022 samples, some were directly processed for DNA extraction, while others were first propagated in either Vero or Lamb testis cell cultures before proceeding with DNA extraction. The samples were used to extract DNA and remaining samples were stored in -80 °C for further use.

Processing of samples

For molecular diagnosis, 200 µl of Blood sample was used to extract DNA by using Nucleic acid extraction kit (HL-NA-100) from Huwel, and the DNA concentration was estimated using a nanophotometer (Implen).

A total of 22 samples of LSDV were used for sequencing (Table  1 ). Seven samples were from the outbreaks during 2020–2021, 1 sample from Ranchi outbreak in 2019, and 14 samples were from 2022 outbreak in different parts of India, as mentioned in the table below. Out of 22 samples, 12 were taken from skin nodules from cattle and 10 were taken from cell-infected viral cultures [ 39 ].

Molecular diagnostics

The primers were designed for the viral Fusion gene to confirm LSDV in the collected samples, forward primer- 5’ ATGGACAGAGCTTTATCA, reverse primer- 5’ TCATAGTGTTGTACTTCG (10pM/µl) with Tm 55 °C. The conventional PCR was carried out in 25 µl reaction with the following conditions used: 94 °C for 5 min for initial denaturation, 30 cycles for 94 °C for 1 min denaturation, 55 °C for 30 s annealing, 72 °C for 45 s extension and a final extension step of 72 °C for 5 min. The PCR result was visualized on 1% agarose (Himedia) gel having Ethidium Bromide (Amresco, Cole-Parmer) and analyzed against 100 bp DNA ladder (G-Biosciences) [ 46 ].

Individual PCR for sequencing

A total of 55 overlapping primer sets for 3 kbp amplicons with Tm 66 °C were designed by using PrimalScheme [ 47 ], a tool which is used to design primers for multiplex PCR, especially for viral outbreak strains. The complete genome sequence of LSDV from previous outbreak with GenBank ID: OK422493.1 was used to design primers. The DNA extracted from the skin scab sample collected from India was used to amplify the LSDV DNA. The 2-step PCR was performed using Phusion polymerase (Thermofisher Scientific) with the following conditions: 98 °C for initial denaturation, 98 °C for denaturation, 66 °C for annealing and extension, and 72 °C for 3 min for the final extension step. The PCR results were analyzed on 1% agarose (Himedia) gel having Ethidium Bromide (Amresco, Cole-Parmer) and analyzed against 1 kb plus DNA ladder (G-Biosciences).

Sequencing using Oxford-nanopore technology

The amplified LSDV DNA amplicons of 3 kbp size were pooled together, and the DNA concentration was determined by using a Qubit 3 fluorometer (Invitrogen) after calibrating with the standards, provided by manufacturer. The samples were processed for genome sequencing on MinION (Oxford Nanopore Technologies, Oxford, United Kingdom) with the ligation sequencing kit SQK-LSK109 Oxford Nanopore Technologies (ONT). Samples were sequenced on flow cell R10.3 version (FLO-MIN111) with 1570 active pores. For the MinION, the Barcode 01–09 from the native barcoding kit (ONT) were used. The DNA was cleaned up using KAPA Hyperpure beads (Roche) after every step during sample preparation, and DNA concentration was recorded. The DNA library was prepared as per the ONT protocol by adopting the following steps: end prep of the LSDV amplicons followed by Barcoding and adapter ligation. The flow cell was primed by using the EXP-FLP002 Flow cell priming kit (ONT). Around 300 fmol of DNA library was loaded along with the sequencing buffer and loading beads on the Spot ON MinION sequencer and was run for 11 h on R10.3 flow cell. Base calling and demultiplexing was performed by using Guppy v5.0 command-line software. The reads were aligned to the LSDV whole genome sequence GenBank ID: OK422493 (Ranchi, India, 2019). The alignment-based consensus was generated using a protocol adapted using Artic pipeline v1.2.1 developed for SARS-COV-2, and the gaps were filled by sequencing missing regions using same protocol.

Sequencing using Illumina NGS technology

NGS library preparation for LSDV whole genome sequencing was done using an in-solution tagmentation-based Illumina Nextera XT DNA Library Prep kit (Illumina) with starting DNA concentration of 1 ng/µl. Prepared libraries were quantified using Qubit 1X ds DNA HS kit (Invitrogen) and the quality check was done on Agilent 2100 bioanalyzer using High sensitivity DNA reagent kit (Agilent). All the libraries were normalized up to 4 nM and pooled. The equimolarized pool of library was processed for the denaturation with 1% PhiX library spike-in as the control library (Illumina). Sequencing was performed on Illumina NovaSeq 6000 SP Reagent Kit v1.5 (300 cycles) paired-end chemistry. Isolated Viral DNA library was sequenced on Illumina MiSeq using MiSeq reagent kit v2 (500 Cycles). The data generated was subject to reference-based assembly using CLC Genomics Workbench v22.0.2 against LSDV reference sequence (NC003027.1). The consensus of each sample were obtained using an inbuilt consensus sequence caller in CLC Genomics Workbench. The variants were visualized using IGV v 2.4.14.

Phylogenetic analysis and SNP analysis

The newly generated consensus sequence was used along with other LSDV complete genome sequences retrieved from the public domain database NCBI virus, accessed on Dec 25, 2023. The sequences used for phylogeny were aligned using Mafft v7.49, and a maximum likelihood phylogenetic tree was constructed using Iqtree2 version 2.0.7 with 1000 bootstrap value. The tree was visualized using interactive Tree Of Life (iTOL) v6.8.1. Nucmer v3.1 was used to generate SNPs in comparison to the Reference sequence of LSDV (NC003027.1). Nucmer does pairwise alignment to identify SNPs in query sequences compared to reference genome sequence. The table with SNPs was further analyzed using R script in R v4.3.1. The script [ 48 ] is available on GitHub (R script link Github).

Data availability

The data that supports the findings of this study is available in the NCBI (BioProject ID PRJNA998208 and PRJNA1004082).

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UT acknowledges funding from IISc-DBT partnership and IOE grant. AK acknowledges financial support from CSIR. PY acknowledges financial support from IISc. GR, BG acknowledges funding from ICAR-NIVEDI, Bangalore. CJ acknowledges funding from Government of Gujarat State and NK acknowledges funding from ICAR-NRC on Equines, Hisar.

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UT, GR, BG and CJ conceived and designed the study. PY, AK performed the ONT-based sequencing, analysed the data, and wrote the manuscript. YD helped in analysing sequencing data. AP, SS, JR, RP, PC prepared samples and performed NGS Illumina sequencing. MJ, DP, FT, NK helped in coordinating with team. SN, SN, YR and RSK diagnosed the cattle. SN, JR, AK, NK collected samples from field. UT, GR, BG, CJ reviewed the manuscript.

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Institute Bio-Safety certificate (IBSC) with Reference number IBSC/IISc/UT/16/2023 was obtained from the ethics committee to work on LSDV. The utilization of animal sample was undertaken as per ARRIVE guidelines. The LSDV samples were collected by the veterinarians as per the approved protocols and guidelines.

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Supplementary File 1.

SNPs in different proteins of 22 genomes of LSDV reported in the study

Supplementary Fig. 1.

Complete agarose-gel image for PCR confirmation of LSDV in clinical samples (Figure 1B)

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Yadav, P., Kumar, A., Nath, S.S. et al. Unravelling the genomic origins of lumpy skin disease virus in recent outbreaks. BMC Genomics 25 , 196 (2024). https://doi.org/10.1186/s12864-024-10061-3

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Lumpy skin disease: a systematic review of mode of transmission, risk of emergence and risk entry pathway.

1. Introduction

2. materials and methods, 3.1. selection process, 3.2. description of the retrieved articles, 3.3. host of lumpy skin disease virus, 3.4. modes of transmission, 3.4.1. direct transmission, 3.4.2. indirect transmission via vectors, 3.5. emergence of vaccine-like recombinant strains, 3.6. risk factors of lumpy skin disease outbreaks and spread, 3.7. risk analysis of introduction of lumpy skin disease to a free-area, 4. discussion, 5. conclusions, author contributions, institutional review board statement, informed consent statement, data availability statement, conflicts of interest.

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Bianchini, J.; Simons, X.; Humblet, M.-F.; Saegerman, C. Lumpy Skin Disease: A Systematic Review of Mode of Transmission, Risk of Emergence and Risk Entry Pathway. Viruses 2023 , 15 , 1622. https://doi.org/10.3390/v15081622

Bianchini J, Simons X, Humblet M-F, Saegerman C. Lumpy Skin Disease: A Systematic Review of Mode of Transmission, Risk of Emergence and Risk Entry Pathway. Viruses . 2023; 15(8):1622. https://doi.org/10.3390/v15081622

Bianchini, Juana, Xavier Simons, Marie-France Humblet, and Claude Saegerman. 2023. "Lumpy Skin Disease: A Systematic Review of Mode of Transmission, Risk of Emergence and Risk Entry Pathway" Viruses 15, no. 8: 1622. https://doi.org/10.3390/v15081622

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• DOI: 10.1016/j.virusres.2019.05.015
• Corpus ID: 173187984

Transmission of lumpy skin disease virus: A short review.

• A. Sprygin , Y. Pestova , +2 authors A. Kononov
• Published in Virus Research 1 August 2019
• Environmental Science, Medicine

112 Citations

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A Recombinant Vaccine-like Strain of Lumpy Skin Disease Virus Causes Low-Level Infection of Cattle through Virus-Inoculated Feed

Molecular characterization of lumpy skin disease virus from recent outbreaks in pakistan, 65 references, lumpy skin disease, an african capripox virus disease of cattle., evidence of vertical transmission of lumpy skin disease virus in rhipicephalus decoloratus ticks., epidemiological characterization of lumpy skin disease outbreaks in russia in 2016, detection of vaccine‐like lumpy skin disease virus in cattle and musca domestica l. flies in an outbreak of lumpy skin disease in russia in 2017, mechanical transmission of lumpy skin disease virus by rhipicephalus appendiculatus male ticks, a potential role for ixodid (hard) tick vectors in the transmission of lumpy skin disease virus in cattle., the detection of lumpy skin disease virus in samples of experimentally infected cattle using different diagnostic techniques., molecular detection and seasonal distribution of lumpy skin disease virus in cattle breeds in turkey, an investigation of possible routes of transmission of lumpy skin disease virus (neethling), epidemiological and molecular studies on lumpy skin disease outbreaks in turkey during 2014–2015, related papers.

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Molecular characterization of lumpy skin disease virus from recent outbreaks in Pakistan

• Original Article
• Published: 25 November 2023
• Volume 168 , article number  297 , ( 2023 )

Cite this article

• Shumaila Manzoor   ORCID: orcid.org/0000-0002-3623-9086 1 ,
• Muhammad Abubakar 1 ,
• Aziz Ul-Rahman 2 ,
• Zainab Syed 3 ,
• Khurshid Ahmad 1 &
• Muhammad Afzal 3  

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Lumpy skin disease (LSD) is a contagious viral transboundary disease listed as a notifiable disease by the World Organization of Animal Health (WOAH). The first case of this disease was reported in Pakistan in late 2021. Since then, numerous outbreaks have been documented in various regions and provinces across the country. The current study primarily aimed to analyze samples collected during LSD outbreaks in cattle populations in the Sindh and Punjab provinces of Pakistan. Phylogenetic analysis was conducted using partial sequences of the GPCR, p32, and RP030 genes. Collectively, the LSDV strains originating from outbreaks in Pakistan exhibited a noticeable clustering pattern with LSDV strains reported in African, Middle Eastern, and Asian countries, including Egypt, the Kingdom of Saudi Arabia, India, China, and Thailand. The precise reasons behind the origin of the virus strain and its subsequent spread to Pakistan remain unknown. This underscores the need for further investigations into outbreaks across the country. The findings of the current study can contribute to the establishment of effective disease control strategies, including the implementation of a mass vaccination campaign in disease-endemic countries such as Pakistan.

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Acknowledgments

The authors would like to thank the veterinary field staff and Livestock & Dairy Development Department Pakistan, for their support during sample collection.

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Shumaila Manzoor, Muhammad Abubakar & Khurshid Ahmad

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Manzoor S, Abubakar M, and Afzal M conceived the study; Abubakar M, Syed Z, and Ahmad K collected data from field outbreaks; Ul-Rahman A did data analysis; and Manzoor S, Abubakar M, and Ul-Rahman A wrote the manuscript and edited the final draft.

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Manzoor, S., Abubakar, M., Ul-Rahman, A. et al. Molecular characterization of lumpy skin disease virus from recent outbreaks in Pakistan. Arch Virol 168 , 297 (2023). https://doi.org/10.1007/s00705-023-05925-0

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What Is Lumpy Skin Disease, Can It Infect Humans? Symptoms And Causes of LSD

The Lumpy Skin Disease (LSD) is caused by a virus called the Capripoxvirus and is one of the biggest threats to livestock worldwide. This virus genetically belongs to the goatpox and sheeppox virus family.

Lumpy Skin Disease (LSD) is spreading rapidly in India. In the latest data, the health officials have confirmed that the viral disease has infected over 5,000 cattle in Uttar Pradesh, which has disrupted milk production as well. Not just in UP, the viral disease has entered other states too. Over the last few weeks, nearly 3,000 cattle have died in Rajasthan and Gujarat. Focusing on the seriousness of the disease and its high transmission rate, many states have also put a ban on the movement of cattle. Now, to know more about this disease which is killing cattle across India, let's understand this virus. How does it transmit from one person to another, what are the symptoms that it can cause and everything else related to it.

What Is The Lumpy Skin Disease?

Who is the carrier of this virus.

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Some of the other symptoms of LSD include excessive nasal and salivary secretion. One of the severe effects of LSD also includes miscarriage. Experts say that pregnant cows and buffaloes often suffer miscarriage and in some cases, infected cattle/animals can die due to the infection as well.

Can Lumpy Skin Disease Infect Humans?

Lumpy Skin Disease (LSD) is not a new disease, according to the available data, this disease was already endemic in most African countries, and since 2012it is spreading across the Middle East, Southeast Europe and West and Central Asia. Also, when it comes to Asia, LSD has been infecting cattle since 2019. In May 2022, Pakistan's Punjab reported the deaths of over 300 cows due to LSD. Currently, the concerning part is that the virus is not only spreading across the country but also killing cattle.

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Can we drink milk, trending now, how can one stop the viral disease from spreading further.

This viral disease spread among animals, however, it is important to save the cattle also. In order to do so, the first thing that is required is proper vigilance of the virus, which include - early detection, followed by a rapid and widespread vaccination campaign. The next few steps can include sanitising cattle sheds, isolating the infected animals, and contacting the nearest veterinarian for treatment of the infected animal.

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TALK WITH SHIVI

10 lines on Lumpy Virus in English / What is Lampi Virus?

10 lines on lumpy virus.

Hello friends in this video we are presenting a 10 line essay on “ Lumpy Virus ” & “ Lampy Virus “. We hope this is helpful for you.

What is lumpy Virus?/ Short essay on Lampy Virus

• The lumpy virus is spreading in cows in many states of the country.
• According to the Global Alliance for Vaccines and Immunization (GAVI), the lumpy virus is a disease transmitted by cows and buffaloes.
• This is a type of skin disease which is caused by a virus called Capripoxvirus . It spreads from one animal to another.
• Due to this disease, lumps start appearing in the skin of infected cows and buffaloes.
• This virus is spreading so fast that thousands of animals have died in Rajasthan, UP, Bihar and MP.
• The main symptoms of lumpy disease are fever, loss of weight, watery eyes, drooling, rash on the body, loss of appetite and giving less milk.
• It is a disease that spreads through direct contact with cattle and also through contaminated food and water.
• To prevent lumpy disease, keep the infected animal isolated and clean the living space properly. Also regularly spray mosquitoes and get the infected animal vaccinated.
• When the animal dies, do not leave it uncovered and spray the entire area with disinfectants.
• This virus especially affects cows with weak immunity. Only a vaccine can control and prevent this disease.
• While milking a cow-buffalo infected with lumpy virus, take these measures to protect yourself –  do milking by wearing a mask, sanitize your hands after milking, cleaning your hands before and after milking.

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Lumpy skin disease: A newly emerging disease in Southeast Asia

Kanokwan ratyotha.

1 Faculty of Veterinary Sciences, Mahasarakham University, Maha Sarakham 44000, Thailand

Suksanti Prakobwong

2 Department of Biology, The Parasitology, Geoinformatics, Environment and Health Science Research Group, Faculty of Science, Udon Thani Rajabhat University, Udon Thani 41000, Thailand

Supawadee Piratae

3 One Health Research Unit, Faculty of Veterinary Sciences, Mahasarakham University, Maha Sarakham 44000, Thailand

Lumpy skin disease (LSD) is caused by LSD virus (LSDV). This virus has been classified in the genus Capripoxvirus , family Poxviridae which generally affects large ruminants, especially cattle and domestic water buffalo. The first outbreak of LSD was found in 1929 in Zambia, then spreading throughout Africa and with an ongoing expanding distribution to Asia and Europe. In 2020, LSD was found from Southeast Asia in Vietnam and Myanmar before reaching Thailand and Laos in 2021. Therefore, LSD is a newly emerging disease that occurs in Southeast Asia and needs more research about pathology, transmission, diagnosis, distribution, prevention, and control. The results from this review show the nature of LSD, distribution, and epidemic maps which are helpful for further information on the control and prevention of LSD.

Introduction

Lumpy skin disease (LSD) is caused by LSD virus (LSDV), a virus in the family Poxvirus, genus Capripoxvirus as well as sheep pox virus (SPPV) and goat pox virus (GTPV) [ 1 ]. This virus can cause infection mainly in cattle ( Bos spp.) and buffaloes ( Bubalus spp.); there are also reports in other wild ruminant species, such as giraffes, bulls, and springboks [ 2 ]. This arbovirus is probably transmitted by mechanical transmission through blood–sucking arthropods, including mosquitoes, ticks, and flies [ 3 ]. This virus can also be transmitted to susceptible animals through direct contact with the secretions of other infected animals and indirect contact from contaminants of the owner of the animals and objects (vehicle, equipment, etc.) [ 1 , 4 ]. Infected animals may present variations of clinical signs ranging from subclinical to high morbidity and mortality. The clinical signs are fever (40.0°C–41.5°C), lacrimation, nasal discharge, hypersalivation, lethargy, anorexia, and weakness, followed by the development of nodular lesions in the skin and mucous membranes of the whole body. In addition, these lesions may develop into the muscular layer [ 3 , 4 ]. The resulting wound lesions can develop necrotic tissue and scarring, which may occur with secondary infection with other types of complications such as bacteria, viruses, or myiasis and cause severe clinical symptoms [ 5 ]. In general, prevalence of LSD ranges from 1%–2% to 80%–90% in different situations in the endemic region [ 2 ]. Mostly LSD can cause low mortality and the differences in the mortality rate may be explained by differing susceptibility of hosts (strain, age, and host immune response).

The first reported case of LSD occurred in 1929 in Zambia and after that, it spread throughout South Africa with sporadic outbreaks in some areas [ 5 ]. At present, this disease is an endemic disease in Africa. Lumpy skin disease has recently spread in Asia during 1988–1989 following outbreaks in Europe and the Middle East in 1990 [ 6 ]. The disease emerged in South Asia in 2019 and then rapidly spread throughout Southeast Asia in 2020 [ 1 ]. Infection with LSDV could affect not only the health status of ruminants, but furthermore, might impact the economic activity of ruminants, especially cattle.

Here, we review the general information about LSD and show where research is needed for a better understanding of the biology, pathology, transmission, diagnosis, distribution, prevention, and control of this newly emerging disease in Southeast Asia.

Virus and Classification

Lumpy skin disease virus (LSDV) is a virus in the family Poxviridae, subfamily Chordopoxviridae, genus Capripoxvirus . The genus Capripoxvirus comprises three viruses; SPPV, GTPV, and LSDV. Lumpy skin disease virus is large–sized (230–260 nm) enclosed in a lipid enveloped with a genome of approximately 150 kilobase pairs (kbp) and shared 97% identity in the nucleotide sequences with SPPV and GTPV genome ( Figure-1 ). The LSDV genome included at least 146 putative genes, which displayed proteins that play roles in virion structure, DNA replication, transcription and metabolism, protein processing and assembly, virus stability, and evading host immune response [ 7 ]. Lumpy skin disease virus can cause infection mainly in large ruminants; specifically in cattle, buffaloes, and other wild ruminant species. However, the disease is not contagious from animals to humans. Signs and symptoms of LSDV vary widely and depend on many factors, such as status of the host’s immune response, strain of the virus, and the environment. Severe clinical signs of disease may occur in young animals, lactating animals, or animals with lower immunity than healthy animals. European beef cattle strains ( Bos taurus ) are more susceptible to LSD than tropical or Indian beef cattle strains ( Bos indicus ). Moreover, domestic buffalo ( Bubalus bubalis ) have a lower incidence rate than cattle [ 1 , 4 , 8 ]. The LSDV genome can be detected in nodules, ulceration, blood, secretions, and semen in both vertebrate (ruminant) ( Table-1 ) [ 1 , 2 , 4 ] and invertebrate animals (arthropods) ( Table-2 ) [ 9 – 19 ].

Schematic diagram of the poxvirus structure. (a) cross-section; (b) longitudinal section. (Figure prepared by Kanokwan Ratyotha).

Vertebrate hosts susceptible to LSDV infection.

LSDV=Lumpy skin disease virus

LSDV genome detected in vertebrate animals.

transmission, Spread, and Virus Stability

Lumpy skin disease is a vector-borne disease transmitted by mosquitoes ( Aedes aegypti, Anopheles stephensi, Culex quinquefasciatus , and Culicoides nubeculosus ), ticks ( Rhipicephalus appendiculatus, Rhipicephalus decoloratus , and Amblyomma hebraeum ), and Diptera ( Haematopota spp. and Stomoxys calcitrans ). The LSDV can survive in skin nodules for 1 month and at least 3 weeks in air–dried hides. The virus is excreted in the blood, nasal secretions, saliva, ear notches, semen, and milk and can be transmitted to suckling calves [ 20 – 22 ]. In general, vectors enhance the distribution of LSDV by mechanical and biological transmissions. Many studies have reported that after blood-sucking vectors (mosquitoes, ticks, glimpse, and flies) take a blood meal from infected cattle (viremia stage), the virus can propagate and shed in the salivary glands, head, body, and feces of insects. This allows the infected insects to become a reservoir for further transmission [ 15 ]. The infectivity of LSDV has been studied in both egg and juvenile of ticks ( R. decoloratus ) in which it was found that the disease can be transmitted by transovarial transmission [ 14 ]. In addition, the mechanical contact of flies is also a way they can be carriers of disease. Direct contact between cattle in a cage has been commonly found in endemic areas. However, the viral transmission was also accomplished by the contamination of veterinary equipment and vehicles as well as stockholders from a farm translocating to distant areas [ 1 , 23 ]. Most LSD infections have been found in the summer when vectors are active; it may designate the blood–feeding insects and the virus spread. The enhancement of risk factors was associated with a warm and humid climate that supported the reproduction of vector populations. The introduction of new animals to a herd is one of the risk factors.

Lumpy skin disease virus is well tolerated in the environment in the pH range of 6.3–8.3 and it can survive in dry scabs on the skin for up to 3 months [ 1 ]. Lumpy skin disease virus can grow in cell cultures at 4°C for up to 6 months, in phosphate buffer saline at 28°C for up to 35 days, in skin nodule lesions collected from frozen at –80°C for up to 10 years. However, it can be destroyed by ultraviolet heat for an exact time, for example, 55°C for 2 h, 60°C for 1 h, and 65°C for 30 min. Moreover, this virus is sensitive to excess acid or base and therefore, it can be destroyed by common disinfectants [ 9 ].

Pathogenesis and Clinical Signs

In some outbreaks that occurred in Africa and middle Asia countries, the mortality rate was generally low (1%–3%) but may reach 40% in some regions. After infection, the incubation period ranges from 4 to 7 days, as determined experimentally, but for naturally occurring infections, the incubation period is 28 days or is prolonged to 35 days [ 1 , 4 ]. Lumpy skin disease virus infection by intradermal replication in fibroblasts, macrophage, pericytes, and endothelial cells leads to viremia causing vacuities and lymphangitis in affected areas [ 2 ]. After cattle recover from infection, they acquire antibodies for about 6 months [ 6 ]. Lumpy skin disease is an economically impact disease in an outbreak because the severity in cows peaks during lactation and causes a decreased milk harvest during the high fever caused by the viral infection and bacterial mastitis. Clinical signs after the incubation period can be classified into 4 phases.

Phase 1 (acute phase) after the incubation period, animals have fever as high as 41°C for about 7 days sometimes prolonged to 10 days with anoxia, depression, lacrimation, increased nasal discharge, saliva secretions, lack of milk, found multinodular lesions around skin, and mucous membrane. Some cases are non–febrile.

Phase 2 subscapular and precrural lymph nodes develop noticeable enlargement 3–5 times of their normal, and there are increased multi nodules, mostly on the head, neck, limbs, genitalia, udder, mucous membrane, nasal and oral cavities, or plaques at the site of inoculation. The diameter of the nodule lesion is 0.5–5 cm, apparent in varying numbers and sizes, from only a few to multiple lesions covering the entire animal ( Figure-2a ). After 1–2 days, nodules rupture, also shedding virus depending on the concentration of virus. Sometimes found edema of limbs is caused by lymphangitis and vasculitis.

The clinical sign of lumpy skin disease in cattle in Thailand. (a) The lymph nodes develop noticeably enlarged 3–5 times of its normal; (b) the nodule lesions’ transformation into ulceration and necrosis.

Phase 3, after 2–3 weeks, nodules lesions into ulceration and become necrotic. Also, beaded serum exudes, especially from limbs and causes lameness, pain, and lack of movement. In severe cases, an ulcerative lesion appears in the mucous membranes at various points, such as the eye and nasal cavities; there is excessive salivation, lachrymation, and nasal discharge. The secretions from animals may contain LSDV [ 19 ].

Phase 4, after at least 1 month, there is complete healing of ulcerations and also thickening of the skin and hyperpigmentation of the lesion ( Figure-2b ).

Bacterial and virus infections can occur in lesions, and these pathogens are able to be inhaled by the host, causing a sequence of complications. These complications include keratitis, mastitis, pneumonia, and myiasis and can increase mortality. Other clinical signs of complications are abortion, decreased lactation, anestrus, infertility, and subclinical sign may be present. Post-mortal LSDV infected cattle have been found with nodule formation and ulceration in the trachea, lung, and gallbladder [ 6 , 19 , 24 ]. Differential diagnosis include pseudo LSD/bovine Herpes mammillitis by bovine Herpes virus type 2, pseudocowpox and bovine papular stomatitis by Parapoxvirus , insect biting, urticaria, and demodicosis [ 4 ]. In outbreaks of the disease, the morbidity rate varies widely depending on the immune status of the hosts and the abundance of mechanical arthropod vectors.

Lumpy skin disease virus affects large ruminants, especially cattle and domestic water buffalo; however, this virus has also been reported in wildlife due to these animals belonging to the suborder Ruminantia, as well as cattle and buffaloes. Clinical signs of LSDV infection in wildlife are difficult to monitor and may range from asymptomatic to severe clinical signs [ 24 ]. Although reports of disease in wildlife are low incidence, it is still a concern whether the disease spreads from pets to wildlife [ 25 ]. It is difficult to prevent and control the disease due to the inability to control livestock and make preventive vaccines for wildlife as well as livestock. There are also many species of ruminant wildlife that are not known how to transmit disease, which can affect their natural population.

Humoral and Cellular Immunity

In cases of natural infection, the immunity caused by infection can be detected approximately 2 weeks after infection. From experimental infection, antibodies are detectable from 6 to 8 day post-infection. The highest immunity can be detected during 3–4 weeks after infection and remain detectable for up to 5 months [ 26 ]. Although antibodies are able to limit the spread of extracellular organisms, most LSDV are predominantly intracellular. Humoral immunity cannot be enough to eliminate the proliferation of viruses inside cells. Therefore, cell-mediated immunity is essential for the effective control of infection in animals. Once an animal has been vaccinated, the humoral immune response can last longer than 7 months which is capable of preventing disease [ 27 ]. However, animals in endemic regions are recommended to receive an annual vaccination booster due to the duration of humoral and cellular immunity is still unknown.

Diagnosis of LSDV is based on characteristic clinical signs combined with various laboratory approaches. Virus isolation and electron microscopy can be done but are rather expensive, labor and time–consuming, and cannot differentiate between poxvirus virions. The immunological–based techniques such as enzyme-linked immunosorbent assay have been developed to detect antibodies for LSDV infection; however, false detection caused by non-specific binding can occur between Parapoxvirus and Capripoxvirus [ 28 ]. In the laboratory, DNA–based detection methods by polymerase chain reaction (PCR) or real-time-PCR (RT-PCR) is used to detect viral DNA in specimens, including nodules, secretion, semen, and blood of suspected animals [ 29 ]. Target genes for PCR or RT-PCR detection are often used for the gene–specific viral attachment proteins such as P32, RPO30, and GPCR [ 30 , 31 ]. For diagnosis, LSDV, sheep and goat poxviruses can be distinguished by real-time PCR technique [ 32 ]. The differentiation among natural genotypic targets of either vaccine or field strain genomes was developed by using a universal TaqMan probe to cover the field, vaccine, and recombinant strains of LSD [ 33 ]. The virulent LSDV from the vaccine strain was established by the restriction fragment length polymorphism [ 34 ].

Necropsy and Histopathological Finding

Infection with LSDV classically causes an acute disease with fever, depression, and appearance of nodules and lesions in the skin. The clinical signs of LSD are lymph nodes to form a skin blister about 2–5 cm in diameter on the skin, such as head, neck, legs, breast, and genitals. The necrotic nodules were ulcerated and formed deep scabs [ 35 ]. Larger vesicles may become necrotic and scarred for several months, while smaller vesicles heal faster. Blisters or ruptures of the cyst can be found. The mucus in the mouth, gastrointestinal tract, trachea, and lungs may be seen with edema. For asymptomatic infection, lesions are found in the subcutaneous or muscular layer. After the postmortem, lesions are often found in the respiratory organs, gastrointestinal tract, breast, lungs, bladder, kidneys, uterus, or testicles [ 36 ]. Histopathological examination of nodular skin biopsies showed edema, hyperemia, acanthosis, hydropic degeneration, and hyperkeratosis in epidermis [ 37 ].

Epidemiology (Susceptibility Hosts, Prevalence in Other Countries)

Lumpy skin disease virus was first investigated in Zambia in 1929 and was endemic in Africa during 1988–1989. However, the disease had been transmitted to middle Asian countries, including Saudi Arabia, Iran, Israel, and Iraq, by 1990 [ 6 ]. The incidence of LSD worldwide in 2016–2020 included African and Asian countries, and the epidemiology dynamically changed between the years. The prevalence and incidence of LSD detected by RT-PCR were reviewed during 2016–2020 ( Figure-3 ). In 2016, the prevalence of LSD in the countries was 4.66% in Iraq [ 38 ], 4.77% in Uganda [ 39 ], 5.00% in Nigeria [ 40 ], 6.00% in Saudi Arabia [ 23 ], 7.22%–18.0% in Ethiopia [ 41 , 42 ], and 12.9%–22.00% in Kazakhstan [ 43 , 44 ]. In 2017, the prevalence of LSD in countries was 24.00% in Egypt [ 45 ] and 5.67% in Ethiopia [ 46 ]. In 2018, the prevalence of LSD was 29.00% in Russia [ 47 ] and 31.20%–88.80% in Egypt [ 48 – 50 ]. In 2019, the prevalence of LSD was 10.00% in Bangladesh [ 51 ], 19.50% in China [ 52 ], 22.28%–27.50% in Egypt [ 36 , 53 ], and 37.66% in India [ 54 ]. In 2020, the prevalence of LSD was 3.00%–6.00% in Myanmar [ 55 ], 4.85% and 53.20% in Nepal [ 56 , 57 ], 13.93% in India [ 58 ], and 78.00% in Bangladesh [ 59 ]. In 2021–2022, the prevalence of LSD was 70% in Egypt [ 60 ], 4.17% in Thailand [ 61 ], 5.9% in Mongolia [ 62 ], and 36.2% in Ethiopia [ 63 ].

Prevalence of lumpy skin disease positively detected by polymerase chain reaction assay during 2016–2022. [Source: base map from the public Geo-Informatics and Space Technology Development Agency (GISTDA) using ArcGIS software (ESRI Inc., Redlands, CA, USA)].

Prevalence of LSD in Southeast Asia

Lumpy skin disease was shown to be distributed to South Asia through Southeast Asia (SEA) in 2019–2020 [ 1 ]. The first detection was found in the upper part of Vietnam in 2020 by the World Organization for Animal Health or Office International des Epizooties; OIE. The virus was isolated, identified, and investigated. The virus was similar to that endemic in Russia in 2017 and in China in 2019, indicating the disease was introduced from China–Vietnam border, and became distributed through 27 provinces in the country [ 64 , 65 ]. Thereafter, LSD was transmitted to other countries in SEA, such as Laos, Cambodia, Thailand, and Myanmar [ 55 , 66 , 67 ]. In Malaysia, the disease has been reported but some cases have not been confirmed as LSD [ 68 ]. In Indonesia and the Philippines, LSD has not been found and critical notification in the prevention and control of LSD were concerned [ 69 , 70 ]. In Thailand, at least 65 of 76 Provinces had reported infected animals to OIE by April, 2021. The Thai government produced strategies for prevention and controls, such as non–transfer of the animals from endemic areas, and vaccination in cattle and buffalo [ 71 ], which resulted in a sharp drop in morbidity rate in cattle in Thailand in 2022. Our experiences are agreeable with the encounter of LSD in Turkey in 2013 where uncontrolled animal movement is an important risk factor for spreading LSD to the neighboring countries, including Balkan, Caucasus, Iran, and Asia. Therefore, when any case occurs, isolation, quarantine, and vector control are necessary and have to be applied immediately [ 72 ].

Prevention Control and Eradication (Risk Factors, Regulations, Actions, and Vaccinations)

The stability of viruses in ambient conditions for a long period has certainly been established. It can persist in desiccated lesions on skin for 25–50 days and persist for many months in the dark environment in animal sheds. Veterinary education is needed for livestock workers to enable the performance of timely diagnoses of the disease to diminish the spread of the disease. Effective treatment against LSD has not been recognized. Symptomatic treatment for anti–inflammatory symptoms and antibiotics for preventing secondary microbial infection was used. Supportive therapy such as the Vitamin B–complex, Vitamin AD3E to retain the feeding capacity, and reproductive maintenance was frequently used ( Table-3 ) [ 73 – 75 ].

Therapeutic agents for LSD treatment.

LSD=Lumpy skin disease

Disease spreading can occur by infected animals or contaminated equipment or vectors. Early outbreaks can be controlled if the animal population is quarantined, sanitation on equipment or locality and biosafety. Controlling the movement or quarantine of newly imported animals for at least 3–4 weeks before being imported to the farm is one of the practices during the epidemic period [ 26 ]. Blood–sucking insects are the main vectors that cause the rapid spread of the disease; therefore, destroying breeding grounds, removing manure and cleaning with pesticides to disinfect and eliminate vectors regularly are recommended. Moreover, vaccination is an important preventive measure to reduce the spread and severity of the disease.

To prevent and control strategies, including the assortment of risks and affected animals, movement restrictions, and compulsory and consistent vaccination are recommended, including the following:

Restriction of animal movement

The movement of animals infected with LSDV and/or effects of LSD must be exactingly prohibited to prevent the distribution of the disease to other areas and crossover to non-infected farms. The prevention of transboundary movements and the restriction of animal movement should be strict. Animals with skin lesions should be investigated and should be isolated for assessment.

Control the distribution of vectors

The distribution of arthropod vectors’ movement and spread is risk factors for LSD transmission. Insecticides and traps are frequently used in livestock to prevent the disease.

Vaccination

The immunization of LSD by live attenuated vaccines has been effectively used in endemic areas. Antigenic homology of Carpipoxvirus , including SPPV, GTPV, and LSDV, cross-protection of immune response was beneficial [ 1 , 4 , 24 , 76 ]. A live attenuated vaccine is commercially available for LSD eradication. Sheep pox vaccine from SPPV and GTPV is used for control in countries with high LSD outbreaks. Types of LSD vaccines are as follows: (1) Attenuated LSDV vaccines (Neethling vaccines) are the currently effective vaccine to prevent LSD in cattle. The effective control success possibility is 80% in the livestock, (2) Attenuated SPPV vaccines are suitable for the areas that SPPV and LSDV outbreak and (3) Attenuated Gorgan GTPV vaccine is suitable for the areas where outbreaks are a combination of SPPV and LSDV [ 1 ]. The live attenuated LSDV vaccine (Neethling vaccines), which is used in livestock worldwide, is the only ubiquitous LSDV vaccine. After vaccination, the immunity is raised within 10–30 days. This vaccine is recommended at any age unless contemporaries showing signs of infection have already occurred.

Lumpy skin disease is an infectious disease in large ruminants, cattle, and domestic water buffalo. This disease regularly occurs in Africa, Europe, and some regions of Asia and spread to Southeast Asia in 2020. The clinical signs range from subclinical to high fever, lymph node enlargement, and apparent nodules over the entire body, followed by developing necrotic tissue and scarring. Although LSD has a low mortality rate, the development of lesions can cause complications and has no specific treatment. Successful prevention of LSD is vaccination together with vector control, controlling animals, especially from endemic regions, and monitoring the situations of LSD outbreaks continuously by disease surveillance.

Authors’ Contributions

KR: Performed literature search and drafted the manuscript. SukP: Reviewed and edited the manuscript. SP: Conceived the study, reviewed and edited the manuscript, and performed final manuscript revision. All authors have read and approved the final manuscript.

Acknowledgments

The authors are thankful to the One Health Research Unit and the Veterinary Infectious Disease Research Unit, Mahasarakham University, Thailand, for supporting the study. The authors did not receive any funds for this study.

Competing Interests

The authors declare that they have no competing interests.

Publisher’s Note

Veterinary World remains neutral with regard to jurisdictional claims in published map and institutional affiliation.

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