Pathogenicity and virulence of lumpy skin disease virus: A comprehensive update

Abstract

Lumpy skin disease (LSD), which was confined to the Africa for many decades, has expanded its geographical distribution to numerous countries across Asia and Europe in recent years. The LSD virus (LSDV) is a relatively poorly studied virus. Its 151 Kb genome encodes 156 open reading frames (ORF); however, the exact number of the proteins encoded by the viral genome and their specific functions remain largely unknown. Arthropod vectors primarily transmit the LSDV mechanically, but the precise nature of these vectors in different regions and their role in transmission is not fully understood. Homologous live-attenuated vaccines prepared using LSDV have proven to be highly efficacious compared to heterologous vaccines based on sheep pox virus or goatpox virus, in protecting cattle against LSD. This review offers the latest insights into the molecular biology and transmission of LSDV and discusses the safety and efficacy of available vaccines, along with the challenges faced in controlling and eradicating the disease in endemic regions.

Keywords: DIVA; Lumpy skin disease; genome; transmission; vaccines.

Figure 1.

Global distribution of LSD.

Figure 2.

Genome organization. Capripoxvirus genome is organized into a central coding region which is relatively conserved and comprises of ORF024 to ORF123. It codes for viral genes related with DNA replication and nucleotide metabolism, RNA transcription and modification and virus structure and assembly. The central conserved region is flanked by variable inverted terminal repeats (ITRs) regions of about 2.4 kbp which are repeated in an inverted orientation at both ends of the genome. The terminal genomic region, comprises ORF001-ORF023 and OR124 to ORF156, respectively at 5’ ad 3’ end of the genome is highly variable and mostly code for virulence and host range genes.

Figure 3.

Pathogenesis of LSDV. LSDV infects the animal by vector bite or through direct contact (abrasions/cuts). The initial replication takes place in keratinocytes in the dermal/epidermal layer. Thereafter, the virus spread to regional lymph nodes via the lymphatics, where it infects various immune cell types. Via the lymphatics, the virus spreads from the regional lymph nodes to various organs and tissues. Viremia occurs when LSDV enters the bloodstream, either through direct infection of endothelial cells lining blood vessels or via the infected immune cells that migrate into the circulation. From the blood, the virus then spread into various organs such as skin, lungs, liver, intestine, spleen, kidneys which eventually results in the development of more severe clinical signs, generalized lymphadenopathy, fever, and widespread skin lesions.