Abstract
Small ruminant lentiviruses (SRLV) are members of the Retrovirus family comprising the closely related Visna/Maedi Virus (VMV) and the Caprine Arthritis-Encephalitis Virus (CAEV), which infect sheep and goats. Both infect cells of the monocyte/macrophage lineage and cause lifelong infections. Infection by VMV and CAEV can lead to Visna/Maedi (VM) and Caprine Arthritis-Encephalitis (CAE) respectively, slow progressive inflammatory diseases primarily affecting the lungs, nervous system, joints and mammary glands. VM and CAE are distributed worldwide and develop over a period of months or years, always leading to the death of the host, with the consequent economic and welfare implications. Currently, the control of VM and CAE relies on the control of transmission and culling of infected animals. However, there is evidence that host genetics play an important role in determining Susceptibility/Resistance to SRLV infection and disease progression, but little work has been performed in small ruminants. More research is necessary to understand the host-SRLV interaction.
Highlights
Small ruminant lentiviruses (SRLV) Innfection andd DiseaseAlthoughh SRLVs caan infect a variety of cells, their target cellss are of thee monocyte/macrophagge liineage wherre viral exppression is closely depeendent on th he monocytee to macropphage maturration [4,5,6,7]
Small ruminant lentiviruses (SRLV) are members of the Retrovirus family comprising the closely related Visna/Maedi Virus (VMV) and the Caprine ArthritisEncephalitis Virus (CAEV), which infect sheep and goats
There is evidence that host genetics play an important role in determining susceptibility/resistance to SRLV infection and pathogenesis, but little work has been performed in small ruminants [64]
Summary
Althoughh SRLVs caan infect a variety of cells, their target cellss are of thee monocyte/macrophagge liineage wherre viral exppression is closely depeendent on th he monocytee to macropphage maturration [4,5,6,7]. In both casess, symptom ms take sevveral monthhs to yearss to develoop (see Figure 1 for diseaase timelinee). M animalss remain asyymptomaticc, but a certaain percentaage of the animals a develoop the cliniccal disease inn one or sevveral target organs. Subbclinical inffection and disease d progreession may range from m months to years. H geneticc factors, inffecting virall strain and management m influence thhe occurrennce, length and a spectrum m of affecteed target org gans
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