National Institutes of Health, National Institute for Allergy and Infectious Disease - September 1995
Table 1. Lentiviruses
| Virus | Host | Primary cell type infected | Clinical disorder |
|---|---|---|---|
| Equine infectious anemia virus (EIAV) | Horse | Macrophages | Cyclical infection in the first year: hemolytic anemia and sometimes encephalopathy |
| Visna virus | Sheep | Macrophages | Encephalopathy |
| Caprine arthritis-encephalitis virus (CAEV) | Goat | Macrophages | Immune deficiency, encephalopathy |
| Bovine immune deficiency virus (BIV) | Cow | Macrophages | Lymphadenopathy, lymphocytosis, CNS disease (?) |
| Feline immunodeficiency virus (FIV) | Cat | T lymphocytes | Immune deficiency |
| Simian immunodeficiency (SIV) | Primate | T lymphocytes | Immune deficiency, encephalopathy |
| Human immunodeficiency virus (HIV) | Human | T lymphocytes | Immune deficiency, encephalopathy |
Lentiviruses often cause immunodeficiency in their hosts in addition to slow, progressive wasting disorders, neurodegeneration and death (Haase, 1986, 1990). SIV, for example, infects several subspecies of macaque monkeys, causing diarrhea, wasting, CD4+ T cell depletion, opportunistic infections and death (Desrosiers, 1990; Fultz, 1993). HIV is closely related to SIV, as evidenced by viral protein cross-reactivity and genetic sequence similarities (Franchini et al., 1987; Hirsch et al., 1989; Desrosiers, 1990; Myers, 1992).
One feature that distinguishes lentiviruses from other retroviruses is the remarkable complexity of their viral genomes. Most retroviruses that are capable of replication contain only three genes--env, gag and pol (Varmus, 1988). HIV contains not only these essential genes but also the complex regulatory genes tat, rev, nef, and auxiliary genes vif, vpr and vpu (Greene, 1991). The actions of these additional genes probably contribute to the profound pathogenicity that differentiates HIV from many other retroviruses.
CD4+ T cells, the cells depleted in AIDS patients, are primary targets of HIV because of the affinity of the gp120 glycoprotein component of the viral envelope for the CD4 molecule (Dalgleish et al., 1984; Klatzmann et al., 1984b; McDougal et al., 1985a, 1986). These so-called T-helper cells coordinate a number of critical immunologic functions. The loss of these cells results in the progressive impairment of the immune system and is associated with a deteriorating clinical course (Pantaleo et al., 1993a). In advanced HIV disease, abnormalities of virtually every component of the immune system are evident (Fauci, 1993a; Pantaleo et al., 1993a).
DT 950901
DOCN: NIAID95_FACT_SHEET_HIVAIDS_8