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