Narayan O
Johns Hopkins University School of Medicine, Division of Comparative Medicine, Baltimore, Maryland.
Curr Opin Immunol. 1989;2(3):399-402. doi: 10.1016/0952-7915(89)90149-0.
The immunopathogenesis of lentiviral lesions in sheep and goats requires continuous replication of the virus in tissues of the animal. This entails escape from various defense mechanisms of the host. Viral expression occurs mainly in tissue-specific macrophage populations and viral proteins produced by the cells induce and combine with antibodies to form immune complexes. These may be pathogenic locally. Infected macrophages also present lentiviral antigens to T lymphocytes and this results in a cascade of cellular responses including proliferation and accumulation of CD8 cells. Cytokines including interferon(s) are produced by lymphocytes and these enhance the antigen-presenting capacity of the macrophages. These lymphoproliferative cellular responses vary from those in human immunodeficiency virus- and simian immunodeficiency virus-infected hosts, mainly because CD4 cells of sheep and goats are not killed by the viruses. These cells, therefore, respond immunologically to viral antigens and this leads to active-chronic inflammation.
