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PubMed2001

Genome of lumpy skin disease virus.

Lumpy skin disease virus (LSDV), a member of the capripoxvirus genus of the Poxviridae, is the etiologic agent of an important disease of cattle in Africa. Here we report the genomic sequence of LSDV. The 151-kbp LSDV genome consists of a central coding region bounded by identical 2.4 kbp-inverted terminal repeats and contains 156 putative genes. Comparison of LSDV with chordopoxviruses of other genera reveals 146 conserved genes which encode proteins involved in transcription and mRNA biogenesis, nucleotide metabolism, DNA replication, protein processing, virion structure and assembly, and viral virulence and host range. In the central genomic region, LSDV genes share a high degree of colinearity and amino acid identity (average of 65%) with genes of other known mammalian poxviruses, particularly suipoxvirus, yatapoxvirus, and leporipoxviruses. In the terminal regions, colinearity is disrupted and poxvirus homologues are either absent or share a lower percentage of amino acid identity (average of 43%). Most of these differences involve genes and gene families with likely functions involving viral virulence and host range. Although LSDV resembles leporipoxviruses in gene content and organization, it also contains homologues of interleukin-10 (IL-10), IL-1 binding proteins, G protein-coupled CC chemokine receptor, and epidermal growth factor-like protein which are found in other poxvirus genera. These data show that although LSDV is closely related to other members of the Chordopoxvirinae, it contains a unique complement of genes responsible for viral host range and virulence.

Animals↗

PubMed2026

Influence of Major Histocompatibility Complex (MHC) Diversity on Immune Modulation, Pathogenesis, and Control of Lumpy Skin Disease Virus.

INTRODUCTION: Lumpy Skin Disease Virus (LSDV), a member of the genus Capripoxvirus within the family Poxviridae, is an economically important transboundary viral pathogen affecting cattle and water buffalo. The disease causes severe production losses through decreased milk yield, infertility, hide damage, reduced growth performance, and occasional mortality. The rapid geographic spread of LSDV, together with its vectorborne transmission and emerging recombinant strains, has intensified the need for improved understanding of viral pathogenesis, host immune responses, and effective prevention strategies. In particular, the role of the bovine Major Histocompatibility Complex (BoLA/MHC) in regulating antiviral immunity, disease susceptibility, and vaccine responsiveness has gained increasing scientific attention. METHODS: This review summarises the published literature related to the epidemiology, transmission, structure, pathogenesis, diagnosis, prevention, and control of LSDV, with special emphasis on the immunological and molecular role of bovine MHC molecules. Relevant studies concerning BoLA-mediated antigen presentation, immunoinformaticsbased epitope prediction, vaccine development, antiviral drug repurposing, molecular docking, genomic surveillance, and diagnostic approaches, including PCR- and ELISAbased assays, were critically evaluated. Recent advances in computational biology, molecular virology, and host-pathogen interaction studies were also reviewed. RESULTS: The reviewed studies demonstrate that Lumpy Skin Disease Virus (LSDV) possesses a complex double-stranded DNA genome enabling immune modulation and efficient transmission through arthropod vectors such as mosquitoes, ticks, and biting flies. Disease progression involves systemic viral replication, vascular injury, dermal necrosis, and inflammatory skin lesions. Real-time PCR remains the most sensitive diagnostic method for early detection, while ELISA supports surveillance. Evidence highlights the central role of bovine Major Histocompatibility Complex (BoLA) molecules in antigen presentation and T-cell activation. Computational studies identified promising BoLA-binding epitopes and repurposed antiviral candidates, including ivermectin, theaflavin, canagliflozin, and tepotinib, for future therapeutic development. DISCUSSION: Current evidence indicates that effective LSDV control requires integration of molecular diagnostics, vector management, vaccination, and host immunogenetics. BoLAguided immunoinformatics provides promising opportunities for developing multi-epitope vaccines, although experimental validation remains essential. Similarly, repurposed antiviral candidates require comprehensive in vivo and pharmacological evaluation before clinical application. Future research should focus on elucidating viral immune-evasion mechanisms, validating predicted epitopes, and translating computational findings into practical vaccines and therapeutics for sustainable disease control. CONCLUSION: Lumpy Skin Disease continues to pose a major threat to global cattle health and livestock economies. Advances in molecular diagnostics, genomic surveillance, antiviral drug discovery, and BoLA-guided vaccine design provide promising opportunities for improved disease control. Understanding the interaction between LSDV and the bovine MHC system is essential for developing next-generation vaccines, immunotherapeutics, and precision disease-management strategies. Future research should prioritise experimental validation of predicted epitopes, large-scale vaccine trials, and mechanistic studies on host-virus immune interactions to establish effective and sustainable global control programs for LSDV.

BoLA↗

PubMed2026

Development and evaluation of a multiplex PCR-based dual-platform targeted sequencing framework for precise differentiation of lumpy skin disease virus.

BACKGROUND: Lumpy skin disease virus (LSDV) shares over 96% genomic identity with goatpox and sheeppox viruses, presenting severe diagnostic challenges due to cross-reactivity. METHODS: To address this bottleneck, we established a targeted sequencing framework integrating multiplex PCR with short-read and long-read platforms. By sequentially screening target pathogens, identifying low-homology genes, and designing short and gradient long-fragment primer pools, we evaluated these dual-platform panels using highly homologous poxvirus samples. RESULTS: The short-read panel stably detected target viruses at inputs as low as 5.26 ×101 copies/μL. Under strict alignment criteria, LSDV mapping rates reached 42.91%, suppressing non-target signals to 3.05%. The Nanopore-Targeted Sequencing (NTS) long-amplicon strategy successfully eliminated homologous interference. By applying length-dependent diagnostic thresholds (≥ 100 reads for short amplicons; ≥ 50 reads for long amplicons), precise species-level identification was achieved, maintaining near-zero cross-reads (0-5) in ultra-long regions. Crucially, the field-deployable NTS workflow enabled complete detection in approximately 4 h. CONCLUSION: This complementary strategy seamlessly meets both laboratory demands for high-sensitivity enrichment and frontline requirements for rapid typing, providing a reliable tool for LSDV surveillance, mutation tracking, and outbreak control.

Capripoxvirus differentiation↗

PubMed2001

Alternative cell lines for the propagation of lumpy skin disease virus.

In our Institute lumpy skin disease virus is grown on primary lamb testis cells for isolation, identification and vaccine production. However, the availability of lambs in Kenya has been seriously reduced over the past few years. This has led to an increase in the cost of using primary lamb testis cells. This study was undertaken to investigate other primary cell lines, which are easily available and provide an equivalent or better yield of lumpy skin disease virus. Foetal bovine muscle (FBM) cells were found to be an adequate alternative for lamb testis cells.

Animals↗

PubMed2003

Comparative sequence analysis of the South African vaccine strain and two virulent field isolates of Lumpy skin disease virus.

The genomic sequences of 3 strains of Lumpy skin disease virus (LSDV) (Neethling type) were compared to determine molecular differences, viz. the South African vaccine strain (LW), a virulent field-strain from a recent outbreak in South Africa (LD), and the virulent Kenyan 2490 strain (LK). A comparison between the virulent field isolates indicates that in 29 of the 156 putative genes, only 38 encoded amino acid differences were found, mostly in the variable terminal regions. When the attenuated vaccine strain (LW) was compared with field isolate LD, a total of 438 amino acid substitutions were observed. These were also mainly in the terminal regions, but with notably more frameshifts leading to truncated ORFs as well as deletions and insertions. These modified ORFs encode proteins involved in the regulation of host immune responses, gene expression, DNA repair, host-range specificity and proteins with unassigned functions. We suggest that these differences could lead to restricted immuno-evasive mechanisms and virulence factors present in attenuated LSDV strains. Further studies to determine the functions of the relevant encoded gene products will hopefully confirm this assumption. The molecular design of an improved LSDV vaccine is likely to be based on the strategic manipulation of such genes.

Animals↗

PubMed2003

Evaluation of lumpy skin disease virus, a capripoxvirus, as a replication-deficient vaccine vector.

Lumpy skin disease virus (LSDV), a capripoxvirus with a host range limited to ruminants, was evaluated as a replication-deficient vaccine vector for use in non-ruminant hosts. By using the rabies virus glycoprotein (RG) as a model antigen, it was demonstrated that recombinant LSDV encoding the rabies glycoprotein (rLSDV-RG) was able to express RG in both permissive (ruminant) and non-permissive (non-ruminant) cells. The recombinant LSDV, however, replicated to maturity only in permissive but not in non-permissive cells. Recombinant LSDV-RG was assessed for its ability to generate immunity against RG in non-ruminant hosts (rabbits and mice). Rabbits inoculated with rLSDV-RG produced rabies virus (RV) neutralizing antibodies at levels twofold higher than those reported by the WHO to be protective. BALB/c mice immunized with rLSDV-RG elicited levels of RV-specific cellular immunity (T-cell proliferation) comparable with those of mice immunized with a commercial inactivated rabies vaccine (Verorab; Pasteur Merieux). Most importantly, mice immunized with rLSDV-RG were protected from an aggressive intracranial rabies virus challenge.

Animals↗

PubMed1990

The isolation of lumpy skin disease virus and bovine herpesvirus-4 from cattle in Egypt.

Lumpy skin disease (LSD) virus (LSDV) was isolated for the first time from cattle in Egypt in 2 disease outbreaks. Bovine herpesvirus-4 (BHV-4) and LSDV were detected in a pooled sample from the first outbreak (Suez). Only LSDV was isolated from the second outbreak (Ismalia). The capripoxviruses were identified as LSDV by neutralization with specific antiserum and by their ability to produce generalized LSD in experimentally inoculated cattle.

Animals↗

PubMed1999

Identification and characterisation of an early/late bi-directional promoter of the capripoxvirus, lumpy skin disease virus.

Identification and characterisation of an early/late bi-directional promoter element of lumpy skin disease virus (LSDV) is described. The 56 bp element shows substantial structural similarities with other poxvirus promoters, providing further evidence that transcriptional elements are conserved within the Poxviridae. The relative strengths of the LSDV early and late promoters were compared to the vaccinia virus (VV) P7.5K and P11K promoters in transient expression assays. These transient assays also verified the temporally regulated nature of the promoter. Favourable expression levels suggest that the identified LSDV promoters could be used for expressing foreign genes in a recombinant LSDV system.

Amino Acid Sequence↗

PubMed1995

An investigation of possible routes of transmission of lumpy skin disease virus (Neethling).

British cattle were infected with the South African (Neethling) strain of lumpy skin disease virus (LSDV) and their clinical signs monitored over a 3-week period. Different routes of infection were assessed for effect on the clinical characteristics of the disease by using a clinical scoring system. Neither of 2 animals inoculated onto the conjunctival sac showed clinical signs of seroconverted. The intradermal route produced local lesions in 21 of 25 animals, and generalized infection in 4. In contrast the intravenous route produced generalized lesions in 8 of 11 animals. Seven uninfected animals were housed in contact with infected animals for 1 month. None developed clinical signs or produced detectable serum neutralizing antibodies. Six of seven of these animals were then challenged and were fully susceptible to infection. The results suggest that the transmission of LSDV between animals by contagion is extremely inefficient, and that parenteral inoculation of virus is required to establish infection. The high proportion of animals with generalized disease following intravenous inoculation implies that naturally occurring cases of generalized LSD may follow spread by intravenously feeding arthropods.

Animals↗

PubMed2005

Immune responses to recombinants of the South African vaccine strain of lumpy skin disease virus generated by using thymidine kinase gene insertion.

The South African vaccine strain of lumpy skin disease virus (type SA-Neethling) is currently being developed as a vector for recombinant vaccines of economically important livestock diseases throughout Africa. In this study, the feasibility of using the viral thymidine kinase gene as the site of insertion was investigated and recombinant viruses were evaluated in animal trials. Two separate recombinants were generated and selected for homogeneity expressing either the structural glycoprotein gene of bovine ephemeral fever virus (BEFV) or the two structural glycoprotein genes of Rift Valley fever virus (RVFV). Both recombinants incorporate the enhanced green fluorescent protein (EGFP) as a visual marker and the Escherichia coli guanine phosphoribosyl transferase (gpt) gene for dominant positive selection. The LSDV-RVFV recombinant construct (rLSDV-RVFV) protected mice against virulent RVFV challenge. In a small-scale BEFV-challenge cattle trial the rLSDV-BEFV construct failed to fully protect the cattle against virulent challenge, although both a humoral and cellular BEFV-specific immune response was elicited.

Animals↗

PubMed2005

Excretion of lumpy skin disease virus in bull semen.

This work was done to establish the incidence and duration of excretion of lumpy skin disease virus (LSDV) in semen of experimentally infected susceptible bulls. Six serologically negative bulls 11-20 months of age were experimentally infected with a virulent field isolate (strain V248/93) of LSDV. Animals were observed for the development of clinical signs, blood was collected until day 90 after infection, and semen was collected every second day until day 18, then twice a week till day 63 and twice a month until three consecutive samples were negative when tested for LSDV by polymerase chain reaction (PCR). An aliquot of each sample which tested positive using PCR was inoculated onto cell monolayers for the recovery of virus. Two bulls developed severe lumpy skin disease (LSD), two bulls showed mild signs and two bulls showed a transient fever only. Multiple samples were positive on PCR from both of the severely affected bulls and one of the mildly affected bulls; between days 10 and 159, days 8 and 132, and days 10 and 21 respectively. Only one sample from each of the other three bulls was positive on PCR. Virus was only isolated from two samples from one of the severely affected bulls and from five semen samples from the other. This study confirmed the excretion of LSDV in bovine semen for prolonged periods, even when obvious clinical signs of the disease were no longer apparent.

Animals↗

PubMed2001

Mechanical transmission of lumpy skin disease virus by Aedes aegypti (Diptera: Culicidae).

Aedes aegypti female mosquitoes are capable of the mechanical transmission of lumpy skin disease virus (LSDV) from infected to susceptible cattle. Mosquitoes that had fed upon lesions of LSDV-infected cattle were able to transmit virus to susceptible cattle over a period of 2-6 days post-infective feeding. Virus was isolated from the recipient animals in 5 out of 7 cases. The clinical disease recorded in the animals exposed to infected mosquitoes was generally of a mild nature, with only one case being moderate. LSDV has long been suspected to be insect transmitted, but these findings are the first to demonstrate this unequivocally, and they suggest that mosquito species are competent vectors.

Animals↗

PubMed1994

Early and late transcriptional phases in the replication of lumpy-skin-disease virus.

Approximately 71 of the estimated 145 kilobase pairs of the genome of the South African isolate of lumpy-skin-disease virus, Neethling strain, was cloned into the plasmid vector pBluescribe. Selected clones were used in Northern blot analysis to investigate the replication cycle of the virus. The synthesis of early mRNA was initiated immediately after infection, and continued for approximately 9 h. The transition to late-gene transcription occurred approximately 10 h post-infection and required DNA replication. Transcription of endogenous late genes cannot occur when viral DNA replication is prevented, while it is activated after DNA replication has occurred. The cloned fragments of the genome are expected to help in the identification of important promoter elements.

Animals↗

PubMed2005

The detection of lumpy skin disease virus in samples of experimentally infected cattle using different diagnostic techniques.

Lumpy skin disease (LSD) is a disease of cattle, primarily in Africa and Madagascar and rarely in the Middle East. It is caused by a capripoxvirus that belongs to the family Poxviridae. The disease is of economic importance in endemic areas. Effective control of LSD requires accurate and rapid laboratory techniques to confirm a tentative clinical diagnosis. Comparative studies on different diagnostic tests used at different stages of the disease have not been done. The aim of this study was to compare several of these tests. Six seronegative bulls, between 11 and 20 months of age, were infected intravenously and kept in an insect-free facility. The course of the infection was monitored. During a 3-month period blood samples and skin biopsies were collected for virus isolation and polymerase chain reaction (PCR). Skin biopsies were also examined using transmission electron microscopy (TEM). The incubation period in infected animals varied from 4-5 days. The length of the viraemic period did not correlate with the severity of clinical disease. Viraemia was detected from 1-12 days using virus isolation and from 4-11 days using the PCR, which is longer than has previously been reported. Virus was isolated from skin biopsies until Day 39 post infection (p.i.) and PCR could demonstrate viral DNA until Day 92 p.i. Transmission electron microscopy of negatively stained skin biopsies detected LSD virus only in one of the four bulls that developed skin lesions until Day 33 p.i. The PCR was a fast and sensitive method to demonstrate viral DNA in blood and skin samples. It could detect viral nucleic acid in skin lesions 53 days longer than virus isolation. Virus isolation from blood and skin samples was sensitive and reliable, but as a single test it may be too time-consuming to use although this depends on how rapidly the diagnosis must be confirmed. In conclusion, this study showed the PCR to be superior in detecting LSD virus from blood and skin samples. However, virus isolation is still required when the infectivity of the LSD virus is to be determined.

Animals↗

PubMed2002

Importance of thymidine kinase activity for normal growth of lumpy skin disease virus (SA-Neethling).

In order to study the importance of an intact thymidine kinase (TK) gene for the vaccine strain of a southern African capripoxvirus, namely, lumpy skin disease virus (LSDV) (type SA-Neethling), a TK disruption recombinant was generated expressing the Escherichia coli beta-galactosidase (lacZ) reporter gene. A comparative growth study of the recombinant and wild-type (wt) LSDV in TK-positive primary and secondary cells and TK-negative secondary cells was performed. It was found that although recombinant and wt virus both grew in TK-positive cells without selection, the recombinant was unable to grow in TK-negative cells (with or without selection), indicating that TK activity is important, if not essential, for normal growth of LSDV.

Animals↗

PubMed2003

Attempted mechanical transmission of lumpy skin disease virus by biting insects.

The mosquitoes Anopheles stephensi Liston and Culex quinquefasciatus Say (Diptera: Culicidae), the stable fly Stomoxys calcitrans Linnaeus (Diptera: Muscidae) and the biting midge Culicoides nubeculosus Meigen (Diptera: Ceratopogonidae) were allowed to feed on either lumpy skin disease (LSD) infected animals or through a membrane on a bloodmeal containing lumpy skin disease virus (LSDV). These arthropods were then allowed to refeed on susceptible cattle at various intervals after the infective feed. Virus was detected in the insects by polymerase chain reaction immediately after feeding and at sufficiently high titre to enable transmission to occur. However, no transmission of virus from infected to susceptible animals by An. stephensi, S. calcitrans, C. nubeculosus and Cx. quinquefasciatus was observed.

Animals↗

PubMed1994

Recombinant capripoxvirus expressing the hemagglutinin protein gene of rinderpest virus: protection of cattle against rinderpest and lumpy skin disease viruses.

A cDNA clone containing the complete coding sequence of the hemagglutinin (H) protein gene of the RBOK vaccine strain of rinderpest virus, under the control of the vaccinia late promoter p11, was inserted by homologous recombination into the thymidine kinase gene of the KS-1 strain of capripoxvirus. The recombinant virus produced authentic H protein as judged by its electrophoretic mobility, transport to the cell surface of infected lamb testis cells, and reactivity with monoclonal antibodies specific for the H protein of rinderpest virus. The recombinant virus induced significant levels of rinderpest virus neutralizing antibodies in vaccinated cattle and protected them from clinical rinderpest after challenge with a lethal dose of a highly virulent heterologous strain of the virus. Protection was achieved using vaccine doses lower than those used with a similar recombinant expressing the fusion protein gene of rinderpest. The parental KS-1 virus is widely used as a vaccine against capripox viruses and so the rinderpest recombinant acts as a dual vaccine to protect cattle against both rinderpest and lumpy skin disease.

Animals↗

PubMed2002

Immunogenicity of a recombinant lumpy skin disease virus (neethling vaccine strain) expressing the rabies virus glycoprotein in cattle.

Rabies virus (RV) readily infects cattle and causes a fatal neurological disease. A stable vaccine, which does not require the maintenance of a cold chain and that is administered once to elicit lifelong immunity to rabies would be advantageous. The present study describes the construction of a live recombinant lumpy skin disease virus (LSDV) vaccine, expressing the glycoprotein of rabies virus (RG) and assessment of its ability to generate a humoral and cellular immune response against rabies virus in cattle. Cattle inoculated with the recombinant virus (rLSDV-RG) developed humoral immunity that was demonstrated in ELISA and neutralisation assays to RV. High titres of up to 1513IU/ml of RV neutralising antibodies were induced. In addition, peripheral blood mononuclear cells from rLSDV-RG-immunised animals demonstrated the ability to proliferate in response to stimulation with inactivated RV, whereas the animal vaccinated with wild type LSDV did not. This recombinant vaccine candidate thus has the potential to be used in ruminants as a cost-effective vaccine against both lumpy skin disease (LSD) and rabies.

Animals↗