Does HIV cause depletion of CD4+ T cells in vivo by the induction of
apoptosis?

Jaworowski A, Crowe SM.

AIDS Pathogenesis Research Unit, Macfarlane Burnet Centre for Medical
Research, National Centre for HIV Virology Research, Fairfield, Victoria,
Australia. anthonyj@burnet.edu.au

The central pathogenic feature of AIDS is the dramatic loss of CD4+
lymphocytes. Despite more than a decade of intense research, the exact
mechanism by which HIV causes this is still not understood. A major model
for T cell depletion, proposed originally by Ameison and Capron in a
report published in 1991, is that HIV sensitizes CD4+ T cells for
activation-induced apoptosis. The apoptotic model of T cell depletion is
discussed, and experiments that address the questions of whether apoptosis
is restricted to infected cells or 'bystander' T cells, and whether T cell
apoptosis requires participation of separate HIV-infected haematopoietic
cell populations, are reviewed.

Publication Types:

* Review
* Review, Academic


PMID: 10101690 [PubMed - indexed for MEDLINE]

On Tue, 13 Apr 2004 02:53:05 -0400, "PaulKing"
<aimulti@aimultimedia.com> wrote:

Interesting abstract. I'll bet you have not a small clue what it
reflects. And I notice that you are too stupid to include the citation
which is: Immunol Cell Biol. 1999 Feb;77(1):90-8.

It is indeed a very important issue and more has been discovered about
this issue as it is now 2004.

George M. Carter

Yes here is a recent abstract on the subject;

AIDS Res Hum Retroviruses. 2004 Feb;20(2):175-82.

HIV type 1-infected dendritic cells induce apoptotic death in infected and

uninfected primary CD4 T lymphocytes.

Lichtner M, Maranon C, Vidalain PO, Azocar O, Hanau D, Lebon P, Burgard M,

Rouzioux C, Vullo V, Yagita H, Rabourdin-Combe C, Servet C, Hosmalin A.

Antigen Presentation by Dendritic Cell Group, Departement d'Immunologie,

Institut Cochin, INSERM U567, UMR CNRS 8104, IFR 116 Paris V University,

Paris, France.



In addition to their essential role in adaptive immunity, dendritic cells

(DCs) participate in innate immunity. In the context of measles virus (MV)

or cytomegalovirus infections, they develop cytotoxic functions that may

contribute in vivo to the elimination of virus-infected cells, but that also

kill infected and noninfected T lymphocytes. Because the human

immunodeficiency virus (HIV) induces T cell depletion through mechanisms

that are still obscure, we investigated its ability to trigger DC

cytotoxicity. When incubated with HIV, monocyte-derived DCs induced

apoptosis in MDA-231 cells, which are sensitive to MV-induced DC

cytotoxicity, and in uninfected as well as HIV-infected H9 CD4+ T cell

lines. This apoptosis was inhibited by a mixture of FasL, TRAIL, TNF-alpha,

and TWEAK inhibitors. Indeed, HIV infection induced or enhanced sensitivity

to TRAIL, TNF-alpha, and TWEAK in H9 cells. Moreover, dendritic cells

incubated with HIV-1 BAL or a wildtype HIV-1 isolate induced apoptosis in

autologous primary CD4+ T lymphocytes, infected or not with a wild-type

HIV-1 isolate. Therefore, induction of DC cytotoxicity by HIV may be

relevant to in vivo HIV infection. Induction of cytotoxicity in DCs by HIV

might contribute to HIV-associated T cell depletion through induction of

apoptosis, especially in the early stages of infection. It may also

contribute to elimination of infected cells in vivo, thereby enhancing

cross-presentation of HIV by DCs. Therefore this new cytotoxic function of

DCs may play an important role in innate and adaptive immunity during HIV

infection.



PMID: 15018705 [PubMed - in process]

"GMCarter" <fiar@verizon.net> wrote in message
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