Bcl-2 upregulation by HIV-1 Tat during infection of primary human macrophages in culture.

Abstract:

:The ability of cells of the human monocyte/macrophage lineage to host HIV-1 replication while resisting cell death is believed to significantly contribute to their ability to serve as a reservoir for viral replication in the host. Although macrophages are generally resistant to apoptosis, interruption of anti-apoptotic pathways can render them susceptible to apoptosis. Here we report that HIV-1(BAL )infection of primary human monocyte-derived macrophages (MDM) upregulates the mRNA and protein levels of the anti-apoptic gene, Bcl-2. Furthermore, this upregulation can be quantitatively mimicked by treating MDM with soluble HIV-1 Tat-86 protein. These results suggest that in infecting cells of the monocyte/macrophage lineage, HIV-1 may be benefiting from additional protection against apoptosis caused by specific upregulation of cellular anti-apoptotic genes.

journal_name

J Biomed Sci

authors

Zhang M,Li X,Pang X,Ding L,Wood O,Clouse KA,Hewlett I,Dayton AI

doi

10.1007/BF02256024

keywords:

subject

Has Abstract

pub_date

2002-03-01 00:00:00

pages

133-9

issue

2

eissn

1021-7770

issn

1423-0127

pii

48209

journal_volume

9

pub_type

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