Bcl-2 upregulation by HIV-1 Tat during infection of primary human macrophages in culture.
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.
Zhang
Mingjie
M
Division of Emerging and Transfusion Transmitted Diseases, Office of Blood Research and Review, Center for Biologics Evaluation and Research, Rockville, MD 20852-1448, USA.
Li
Xingxiang
X
Pang
Xiaowu
X
Ding
Lina
L
Wood
Owen
O
Clouse
Kathleen A
KA
Hewlett
Indira
I
Dayton
Andrew I
AI
D017209:Apoptosis / Q000187:drug effects; D018929:Cell Culture Techniques; D015696:Gene Products, tat / Q000494:pharmacology / Q000502:physiology*; D015658:HIV Infections / Q000473:pathology; D015497:HIV-1 / Q000472:pathogenicity*; D006801:Humans; D008264:Macrophages / Q000378:metabolism / Q000821:virology*; D010446:Peptide Fragments / Q000494:pharmacology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000187:drug effects / Q000378:metabolism; D054322:tat Gene Products, Human Immunodeficiency Virus
D015696:Gene Products, tat; D010446:Peptide Fragments; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D054322:tat Gene Products, Human Immunodeficiency Virus