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Impact of Co-receptor Tropism on Human Immunodeficiency Virus Type 1 (HIV-1) Viral Output of Primary Cells

出版	University of California, San Francisco, 2006
ISBN	05428291349780542829130
URL	http://books.google.com.hk/books?id=xobri8y-97IC&hl=&source=gbs_api

註釋HIV-1 most often utilizes CD4 and one of two co-receptors, CCR5 and CXCR4, in order to enter host cells. Interestingly, many patients in early and in late disease maintain high circulating levels of CCR5 tropic (R5) viruses, even though the target population of CCR5+ cells appears to be small. Such viral loads may be sustained because, relative to CXCR4 tropic (X4) infection, RS infection of permissive CID4+ T-cells results in the production of significantly more infectious viral particles per cell. To investigate this possibility, the average amount of virus produced per infected cell by R5 and X4 HIV-1 in isolated CID4+ T-cell populations (PBMC) was determined, as well as the average amount of virus released per infected target CID4+ T-cell following isogenic R5 and X4 HIV-1 infections of dispersed human tonsil tissue. Prior stimulation using CD3 and CD28 antibodies was performed in the case of PBMC. Virus production was measured by flow cytometry and by p24 ELISA to quantitate both cell associated and cell released viral capsid protein, and infectious virus was quantitated via TCID50 assay. We provide evidence that R5 HIV-1 compensates for a small target cell population by producing to 100W-fold more infectious virus per CCR5+ target cell than X4 HIV-1. This phenomenon was observed in both of the infection models that were used, evidence that this mechanism of R5 HIV-1 predominance is not restricted to lymphoid tissue, but relevant to blood lymphocyte populations as well. This phenomenon may contribute to the predominance of R5 HIV-1 in early in vivo infection.