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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↗
PubMed1982

Observations on the epidemiology of lumpy skin disease in Kenya.

Lumpy skin disease virus strains isolated in Kenya over a period of some 20 years have proved to be serologically identical. They were indistinguishable by indirect fluorescent antibody and serum neutralization test from the South African Neethling and West African serotypes. These two serological methods proved of value in studying the antibody responses to infection. While epizootic spread of LSD has occurred in Kenya, most cases are of a sporadic nature and are thought to be the result of accidental contacts with a maintenance cycle. There is evidence of antibody to LSD in the African buffalo (Syncerus caffer) in those areas where LSD is considered to be enzootic in Kenya, and also in small numbers of domestic cattle. No buffalo or bovine sera contained antibody to cowpox virus. An area enzootic for LSD is proposed and it is suggested that the maintenance cycle involves the buffalo. No antibody was found in the other wild ruminant species examined.

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

Lumpy skin disease in southern Africa: a review of the disease and aspects of control.

This article reviews some of the important aspects of lumpy skin disease (LSD) that may impact on its successful control. A resurgence of the disease in the last decade has highlighted some constraints of the Neethling strain vaccine, but there is no evidence of vaccine breakdowns owing to the presence of heterologous field strains. More research is needed on epidemiology and transmission of LSD in South Africa to formulate control measures.

Animals↗
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↗
PubMedDate not supplied

Lumpy skin disease, an African capripox virus disease of cattle.

Lumpy skin disease is an infectious viral disease of cattle, which often occurs in epizootic form. The disease is characterized by the eruption of nodules in the skin, which may cover the whole of the animal's body. Systemic effects include pyrexia, anorexia, dysgalactia and pneumonia; lesions are often found in the mouth and upper respiratory tract. The severity of the disease varies considerably between breeds and strains of cattle. Many cattle suffer severe emaciation and loss of production for several months. The skin lesions cause permanent damage to the hides. The mode of transmission of the disease has not been clearly established. Contact infections do not readily occur and the evidence from the epizootiology strongly suggests that insect vectors are involved. The disease has been confined to sub-Saharan Africa, until it recently appeared in epizootic form in Egypt and in Israel. Transmission occurs in a wide variety of biotypes, from semi-desert to temperate grasslands and irrigated land. It has the potential to extend its range further.

Africa↗
PubMed2003

Vaccines for lumpy skin disease, sheep pox and goat pox.

Sheep pox, goat pox and lumpy skin disease (Neethling) are diseases of sheep, goats and cattle respectively, caused by strains of poxvirus, within the genus Capripoxvirus. Strains affecting sheep and goats are not totally host-specific; some cause disease in both sheep and goats while others may cause disease in only one species. Those causing disease in cattle appear to be specific for cattle, and this is reflected in the different geographical distribution of lumpy skin disease (LSD) and sheep pox and goat pox (sheep and goat pox); LSD is confined to Africa, while sheep and goat pox are present in Africa north of the equator, and throughout West Asia and India, as far East as China and Bangladesh. Occasionally sheep and goat pox spreads from Turkey into Greece. All strains of capripoxvirus so far examined are antigenically indistinguishable, and recovery from infection with one strain provides immunity against all other strains. Because of this antigenic homology among all strains, there is the potential to use a single vaccine strain to protect cattle, sheep and goats.

Animals↗
PubMed1995

The clinical response of cattle experimentally infected with lumpy skin disease (Neethling) virus.

British cattle were inoculated with lumpy skin disease (Neethling) virus and their clinical signs observed over a three week period. Elevation of body temperature following infection was not found to be a consistent feature, and even in severe cases was limited to a peak temperature of 41 degrees C. Generalised lesions were seen 9-14 days post infection (p.i.), and the development of generalised infections did not appear to be dose related. Following intradermal inoculation lesions were detected from day 2 p.i. and first appearance and severity of local reaction appeared to be related to dose. Virus isolation was carried out on ocular, nasal and saliva swabs, and on buffy coat preparations. A transient viraemia was detected in two of eleven animals that did not show generalized signs; virus was not isolated from the secretions of seven animals without generalised signs. Virus was isolated from the peripheral secretions of an animal with generalised disease between 9 and 15 days p.i. and viraemia was detected in each of five animals with generalized signs. Delayed-type hypersensitivity reactions following intradermal inoculation of immune cattle with LSDV were found to be maximal at 24 h after 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↗
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↗
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↗
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↗
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↗
PubMed1993

Lumpy skin disease: observations on the recent outbreaks of the disease in the Sudan.

Outbreaks of lumpy skin disease in imported Friesian and indigenous cattle which occurred in the Khartoum State during the period of 1989-1991, are described. The disease was diagnosed from clinical findings, isolation and identification of the virus and from electron microscopy. Clinical findings included pyrexia, nasal discharge, appearance of multiple skin nodules of varying sizes, oedema of legs and brisket and abortion. The disease in purebred Friesian cattle was severe with a morbidity rate of 37.9% and a mortality rate of 4.2% while it was rather mild in indigenous cattle.

Animals↗
PubMed1995

Spread of lumpy skin disease in Israeli dairy herds.

Fourteen of the 17 dairy herds in Peduyim, an Israeli village, became infected with lumpy skin disease during a period of 37 days in August and September 1989. One cow in one neighbouring village and four cows in another neighbouring village also became infected, probably through being treated by a veterinarian who treated cows in Peduyim. Circumstantial evidence suggests that the original infection was brought to Peduyim and spread by stable flies (Stomoxys calcitrans) carried by the wind from foci of the disease at El Arish in northern Sinai, or at Ismailiya and the Nile delta in Egypt. All the cattle and the small flocks of sheep and goats in the village were slaughtered.

Animals↗