Abstract
Upon transmission, human immunodeficiency virus type 1 (HIV-1) establishes infection of the lymphatic reservoir, leading to profound depletion of the memory CD4(+) T cell population, despite the induction of the adaptive immune response. The rapid evolution and association of viral variants having distinct characteristics with different stages of infection, the level of viral burden, and rate of disease progression suggest a role for viral variants in this process. Here, we review the literature on HIV-1 variants and disease and discuss the importance of viral fitness for transmission and disease.
Highlights
Upon transmission, human immunodeficiency virus type 1 (HIV-1) establishes infection of the lymphatic reservoir, leading to profound depletion of the memory CD4+ T cell population despite the induction of the adaptive immune response
While most basic and clinical studies seem to agree that variants isolated early during infection appear to be less pathogenic and have lower replicative capacity compared to late stage isolates, mathematical modeling of within-host virus evolution suggests that over the course of host infection viral variants move toward reduced replicative fitness (Wodarz and Levy, 2007; Ball et al 2007)
While infection of these cell types remain important throughout the course of disease progression in regard to latently infected cell populations (Aquino-de Jesus et al 2000), a shift in cell tropism occurs early and rapidly as virus is trafficked from the site of infection to lymphatic tissues where robust replication can take place in CD4+ T cells
Summary
Transmission of HIV-1 can occur via sexual, parenteral, or vertical routes of infection (Lamers et al 1993; Mulder-Kampinga et al 1993; Pang et al 1992; Scarlatti et al 1993; Wolfs et al 1992; Wolinsky et al 1992; Zhang et al 1993; Zhu et al 1993) Each of these represents a distinct environment and a distinct set of factors affecting selection of viral variants.
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