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How HIV-1 lost control

How HIV-1 lost control <h2>How HIV-1 lost control</h2> Less deadly ancestors of HIV-1 down-regulate CD3 so their host cells are spared. KIRCHHOFF/ELSEVIER Aminor change during evolution converted the relatively benign monkey SIV viruses into deadly HIV-1, according to Michael Schindler, Frank Kirchhoff (University of Ulm, Germany), and colleagues. They report that HIV-1, unlike most SIV strains, has lost the ability to protect its T cell hosts, and thus its human host, from death. The critical difference is in a virus protein called Nef, which increases virus infectivity and replication. But even more important than what HIV-1 Nef does may be what it does not do. The German group tested 30 different nef alleles in an HIV-1 vector. Most SIV Nef proteins down-regulated expression of the T cell receptor protein CD3 and thus blocked activation of infected T cells. Nef from HIV-1 and some closely related SIV relatives had neither of these effects. The T cell activation matters because of activation-induced cell death (AICD). A normal immune reaction starts with T cell proliferation. Once an invader is cleared, the reaction is self-limited by AICD—the suicide of most of the recently proliferating T cells. During HIV-1 infection, however, the virus is not cleared and http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Cell Biology Rockefeller University Press

How HIV-1 lost control

The Journal of Cell Biology , Volume 174 (2): 166 – Jul 17, 2006

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Publisher
Rockefeller University Press
Copyright
© 2006 Rockefeller University Press
ISSN
0021-9525
eISSN
1540-8140
DOI
10.1083/jcb.1742rr1
Publisher site
See Article on Publisher Site

Abstract

<h2>How HIV-1 lost control</h2> Less deadly ancestors of HIV-1 down-regulate CD3 so their host cells are spared. KIRCHHOFF/ELSEVIER Aminor change during evolution converted the relatively benign monkey SIV viruses into deadly HIV-1, according to Michael Schindler, Frank Kirchhoff (University of Ulm, Germany), and colleagues. They report that HIV-1, unlike most SIV strains, has lost the ability to protect its T cell hosts, and thus its human host, from death. The critical difference is in a virus protein called Nef, which increases virus infectivity and replication. But even more important than what HIV-1 Nef does may be what it does not do. The German group tested 30 different nef alleles in an HIV-1 vector. Most SIV Nef proteins down-regulated expression of the T cell receptor protein CD3 and thus blocked activation of infected T cells. Nef from HIV-1 and some closely related SIV relatives had neither of these effects. The T cell activation matters because of activation-induced cell death (AICD). A normal immune reaction starts with T cell proliferation. Once an invader is cleared, the reaction is self-limited by AICD—the suicide of most of the recently proliferating T cells. During HIV-1 infection, however, the virus is not cleared and

Journal

The Journal of Cell BiologyRockefeller University Press

Published: Jul 17, 2006

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