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Lumpy skin disease virus (LSDV) causes lumpy skin disease (LSD) in cattle and buffalo. Other wild ruminants have been reported to be susceptible to LSDV, such as springbok, impala, giraffe, camel, Indian gazelle, and yak. The exact mechanisms of LSDV transmission between animals and herds are not fully understood. Strong evidence suggests that the virus is spread by biting insects such as flies. While direct transmission between animals is believed to occur, its significance compared to vector transmission remains unclear. Lumpy skin disease (LSD) was originally found in southern Africa but has spread northwards over the past decade. The disease is endemic in most African countries. The emergence of recombinant lumpy skin disease virus (LSDV) antigen has completely changed serum diagnosis, achieving highly accurate detection and monitoring.
Figure 1. The prediction diagram of LSDV structure mode. (Liang, Zhengji,et al, 2022)
The pathogenic process of LSDV begins with virus adsorption mediated by P32 protein. After entering the cell, the virus immediately begins to express early genes, including a series of immune escape proteins.
These viral proteins can efficiently "hijack" or "mimic" the host's immune signaling pathway. For example, IL-10 analogs encoded by its virus can inhibit macrophage activation and the production of pro-inflammatory cytokines, creating an immunosuppressive microenvironment conducive to virus replication. Meanwhile, proteins like F13L ensure that newly assembled virus particles can obtain an outer envelope, thereby more effectively infecting neighboring cells and promoting systemic spread, leading to skin nodules and multiple systemic symptoms.
Transmission of LSD virus (LSDV) is thought to be predominantly by arthropods (wide range of blood-feeding insects, such as certain species of flies and mosquitoes, or ticks). Direct contact with an infected animal is considered to play a minor role in the transmission of the virus. The possibility of transmission via fomites, such as through ingestion of feed and water contaminated with infected saliva, has not been confirmed. However, the emergence of new strains indicates that multiple transmission routes cannot be excluded. Infected bulls have been shown to shed the virus in their semen, and transmission of LSD via infected semen has been experimentally demonstrated. Additionally, there is a single report suggesting the possibility of placental transmission of LSD. It is also known that LSDV can be shed in milk, by which the virus can be transmitted to suckling calves.
Figure 2. Diagram of the transmission modes of lumpy skin disease. (Liang, Zhengji,et al, 2022)
| Virology | Details |
| Virion | LSDV virion displays a typical poxvirus morphology: brick-shaped virions (220-450 long × 140-260 wide × 140-260 nm thick). Virions consist of a lipoprotein surface membrane enclosing a biconcave core that contains the DNA genome. Two lateral bodies are present in the concave regions between the core and the membrane. |
| Genome | The LSDV genome is a linear molecule of dsDNA,151,000 base pairs (bp) in length, with covalently-closed ends. The viral genome encodes 156 putative genes and is organized in a central region flanked by identical inverted terminal repeats of ~2,400 bp each. |
| Lifecycle | Virus entry is mediated by fusion between viral and cellular membranes at the plasma membrane or following endocytosis. The early phase of replication includes expression of proteins needed for replication of viral DNA and modulation of the host cellular functions and antiviral defences. DNA replication and gene expression occur in the cytoplasm in 'virus factories' and is mediated by virus-encoded proteins. The late phase of replication includes the expression of structural proteins involved in the multistage assembly of new virions. Virions are released by exocytosis or after cell lysis. |
Infection with lumpy skin disease (LSD) virus is an infectious viral disease of bovine animals caused by a Capripoxvirus of the Poxviridae family. It is mainly transmitted by biting insects and is characterised by fever, painful nodules on the skin, mucous membranes and internal organs, enlarged lymph nodes, oedema of the skin, and sometimes death. LSD can cause significant economic losses for farmers due to temporary reduction in milk production, weight loss, damage to hides and reproductive impairment. LSD does not affect humans. LSD virus is a stable virus, survives well in the environment but is sensitive to most disinfectants.
| Harmful Symptoms | Details |
| General symptoms | Sick cows have fever, difficulty breathing, salivation, purulent nasal fluid, swollen lymph nodes on the surface, edema in the lower chest, breasts, and limbs. Pregnant cows often experience miscarriage, temporary decrease in milk production, and temporary or permanent infertility in bulls. |
| Characteristic symptoms | There are many nodules (lumps) on the skin, which are hard and protruding with clear boundaries. The diameter is generally 2-3 centimeters, ranging from 1-2 to over a hundred. Nodules often appear in the head, neck, chest, back, and other areas, sometimes affecting the whole body. Nodules may be completely necrotic or ulcerated, but hard skin lesions may persist for several months or even years |
The prevention and control of bovine nodular skin disease are very important. Based on prevention experience, successful control and eradication of bovine nodular skin disease rely on early detection of individual cases and rapid and widespread vaccination measures. The effect of culling all clinically infected cattle and cattle in the same group in the cattle farm is similar to that of culling only clinically infected cattle, depending on the mode of infection and disease - vector insects. Because the probability of direct contact transmission is very low, this indirectly reflects the importance of early detection and culling of individual cases. In addition, it is also important to receive vaccination before the virus invades, and early vaccination of healthy cattle is crucial.
Lumpy Skin Disease Virus poses a significant threat to the global cattle industry. The pathogenesis depends on specific viral proteins that interact with the basic components of host cells, such as attachment protein P32 and transmission enhancer protein F13L. In addition, the large genome and genetic modification capabilities of the virus are being used to develop advanced recombinant vector vaccines. Continuing to study its molecular biology and host interactions is crucial for improving diagnostic tools, developing next-generation vaccines, and implementing effective control measures to mitigate the impact of this economically devastating disease.
Reference
| Target | Cat. No. | Product Name | Host | |
| LSDV | DAG-WT5800 | Recombinant Lumpy skin disease virus (LSDV) antigen [His] | E. coli | Inquiry |
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