A new finding from scientists at the National Institutes of Health could help efforts to design vaccines and other prevention tools to block HIV in the early stages of sexual transmission, before infection takes hold. Researchers at the NIH National Institute of Allergy and Infectious Diseases have helped explain genetic differences that can distinguish some early-transmitting HIVs--viruses found in an infected individual within the first month after infection--from forms of HIV isolated later in infection. These genetic features help HIV bind tightly to a molecule called integrin α4β7. According to the scientists, the capacity to bind tightly to α4β7 likely enhances the ability of certain HIV viruses to complete the many steps of sexual transmission and become the "founder" virus that establishes infection in an individual.
The study also sheds light on CD4+ T cells, the primary immune cell targeted by HIV. The authors previously reported that gp120, an HIV surface protein, can bind to integrin α4β7 via a receptor that may be present on the surface of the CD4+ T-cell. α4β7 helps direct HIV-infected CD4+ T cells into the gut, where the virus can then begin to replicate quickly. Given the new finding that certain early-transmitting isolates of HIV can have an affinity for α4β7, the scientists believe it is likely that CD4+ T cells with the α4β7 receptor play an important role in the sexual transmission of HIV.
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ARTICLE: F Nawaz et al. The genotype of early-transmitting HIV gp120s promotes α4β7 reactivity, revealing α4β7+/CD4+ T cells as key targets in mucosal transmission. PloS Pathogens. DOI: ppat1001301 (2011).
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