Trojan Horse or Immunologic Catalyst? The Role of Cell-associated Virus in the Mucosal Transmission and Immunopathogenesis of FIV

摘要

In 2004, approximately 4.9 million people became newly infected with human immunodeficiency virus-1 (HIV-1) [1]. HIV-1 exposure across a mucosal surface is a major route of infection, either by sexual contact or through vertical transmission. In somepopulations, the rate of infection for women and girls has increased so rapidly that the majority of newly HIV-infected individuals are female. Lentiviruses readily and rapidly traverse the mucosa in HIV-1 explants, as well as simian immunodeficiency virus (SIV), simian-human immunodeficiency virus (SHIV), and feline immunodeficiency virus (FIV) animal models [2-10]. Thus, one might predict a high and efficient transmission rate for HIV-1 following sexual exposure. Yet the opposite is true where 1.1 infections are estimated to occur for every 1000 HIV-1 heterosexual exposures [11]. While genetic differences between species might explain the variations in transmission rates, this seems less likely as multiple studies have demonstrated marked similaritybetween the pathogen-esis of HIV, SHIV, SIV, and FIV, including cell and tissue targets, progressive immune dysfunction and lym-phodepletion, and susceptibility to secondary opportunistic infections and neoplasia.