Lumpy skin disease, sheeppox, and goatpox are notifiable diseases of cattle, sheep, and goats, respectively, caused by viruses of the Capripoxvirus genus. They are responsible for both direct and indirect financial losses. These losses arise through animal mortality, morbidity cost of vaccinations, and constraints to animals and animal products’ trade. Control and eradication of capripoxviruses depend on early detection of outbreaks, vector control, strict animal movement, and vaccination which remains the most effective means of control. To date, live attenuated vaccines are widely used; however, conferred protection remains controversial. Many vaccines have been associated with adverse reactions and incomplete protection in sheep, goats, and cattle. Many combination- and recombinant-based vaccines have also been developed. Here, we review capripoxvirus infections and the immunity conferred against capripoxviruses by their respective vaccines for each ruminant species. We also review their related cross protection to heterologous infections.
Poxvirus vectors represent promising human immunodeficiency virus (HIV) vaccine candidates and were a component of the only successful HIV vaccine efficacy trial to date. We tested the immunogenicity of a novel recombinant capripoxvirus vector, lumpy skin disease virus (LSDV), in combination with modified vaccinia Ankara (MVA), both expressing genes from HIV-1. Here, we demonstrated that the combination regimen was immunogenic in rhesus macaques, inducing high-magnitude, broad and balanced CD4 + and CD8 + T-cell responses, and transient activation of the immune response. These studies support further development of LSDV as a vaccine vector.
Lumpy skin disease is an important economic disease of cattle that is controlled by vaccination. This paper presents an investigation into the role of the lumpy skin disease virus (LSDV) superoxide dismutase (SOD) homologue on growth and histopathology of the virus both in vitro and in vivo. SOD homologue knock-out and knock-in recombinants (nLSDV∆SOD-UCT and nLSDVSODis-UCT, respectively) were constructed and compared to the Neethling vaccine (nLSDV) for growth in a permissive bovine cell line as well as on fertilized chick chorioallantoic membranes (CAMs). The infected CAMs were scored for histological changes. Deletion of the SOD homologue from LSDV reduced virus growth both in Madin-Darby bovine kidney (MDBK) cells as well as on CAMs. Furthermore, the knockout virus showed reduced inflammation in CAMs and more ballooning degeneration. A pilot experiment was performed in cattle to compare the lesions produced by the different LSDV constructs in the same animal. One animal developed a larger lesion to nLSDV∆SOD-UCT compared to both nLSDVSODis-UCT and nLSDV. Histological analysis of biopsies of these lesions shows less inflammation and necrosis associated with nLSDVSODis-UCT compared to nLSDV and nLSDV∆SOD-UCT. None of the vaccinated animals showed disseminated LSDV disease, indicating that the candidate vaccines are safe for further testing. Our results suggest that the SOD homologue may improve immunogenicity and reduce virulence.
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