Lentiviruses are widespread pathogens of primates, ungulates and felids. While the ungulate lentiviruses induce a disease state typical of a chronic inflammatory condition, the felid and primate lentiviruses induce an immunodeficiency characterised by a progressive depletion of CD4+ T helper cells. FIV infection of the domestic cat may lead to a spectrum of diseases, ranging from a rapid, acute-onset immunodeficiency to a chronic wasting disease with concomitant neuropathology and persistent recurring opportunistic infections. Here, we examine the host and viral determinants of FIV cell tropism and pathogenicity. The virus targets activated CD4+ T cells selectively by interactions with its primary receptor, CD134 and co-receptor, CXCR4.
from Lentiviruses and Macrophages: Molecular and Cellular InteractionsFurther reading:Labels: CD134, CD4 T helper cells, CXCR4, FIV
Simian-human immunodeficiency virus (SHIV) was generated as a model for acquired immunodeficiency syndrome (AIDS) in order to overcome the narrow host range of human immunodeficiency virus (HIV-1). The first-generation SHIVs were nonpathogenic but evolved to become highly pathogenic viruses. Highly pathogenic SHIVs induce a distinct disease phenotype: a massive, systemic, and irreversible depletion of CD4+ T cells occurs within weeks of infection, followed by AIDS-like clinical manifestations. During the acute phase of infection, the virus predominantly infects and destroys CD4+ T cells. As a result, macrophages become the major virus-producing cell type.
Virus isolated during the macrophage phase of infection exhibits macrophage tropism, a property not possessed by the inoculum SHIV. The V1/V2 region of the env gene was found to be responsible for the expanded cell tropism observed in the macrophage-tropic virus. The viral entry coreceptor, CXCR4, was maintained during the evolution of the virus.
from Lentiviruses and Macrophages: Molecular and Cellular InteractionsFurther reading:Labels: aids, CXCR4, HIV-1, Macrophage tropism, SHIV