HIV-1 entry into quiescent primary lymphocytes: molecular analysis reveals a labile, latent viral structure
JA Zack, SJ Arrigo, SR Weitsman, AS Go, A Haislip… - Cell, 1990 - cell.com
JA Zack, SJ Arrigo, SR Weitsman, AS Go, A Haislip, ISY Chen
Cell, 1990•cell.comProductive infection of human T lymphocytes by HIV-1 is dependent upon proliferation of the
infected cell. Nonproliferating quiescent T cells can be infected by HIV-1 and harbor the
virus in an inactive state until subsequent mitogenic stimulation. We use a modification of the
polymerase chain reaction method, which is both sensitive and quantitative, to demonstrate
that HIV-1 DNA synthesis is initiated in infected quiescent T cells at levels comparable with
those of activated T cells. However, unlike that of activated T cells, the viral genome is not …
infected cell. Nonproliferating quiescent T cells can be infected by HIV-1 and harbor the
virus in an inactive state until subsequent mitogenic stimulation. We use a modification of the
polymerase chain reaction method, which is both sensitive and quantitative, to demonstrate
that HIV-1 DNA synthesis is initiated in infected quiescent T cells at levels comparable with
those of activated T cells. However, unlike that of activated T cells, the viral genome is not …
Summary
Productive infection of human T lymphocytes by HIV-1 is dependent upon proliferation of the infected cell. Nonproliferating quiescent T cells can be infected by HIV-1 and harbor the virus in an inactive state until subsequent mitogenic stimulation. We use a modification of the polymerase chain reaction method, which is both sensitive and quantitative, to demonstrate that HIV-1 DNA synthesis is initiated in infected quiescent T cells at levels comparable with those of activated T cells. However, unlike that of activated T cells, the viral genome is not completely reverse transcribed in quiescent cells. Although this viral DNA structure can persist in quiescent cells as a latent form, it is labile. We discuss the lability of this HIV-1 DNA structure in relation to a “self-restricting persistent infection” by HIV-1 and propose that this may explain the low percentage of infected cells in the circulation of AIDS patients.
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