News Release

Variation in HIV's ability to disable host defenses contributes to rapid evolution

A preview of a new open-access journal published by the Public Library of Science – PLoS Pathogens

Peer-Reviewed Publication

PLOS

One of the reasons HIV is so difficult to contain and treat is its rapid evolution. Understanding how host defenses and viral countermeasures contribute to that evolution is vital.

Host cells produce two proteins that mutate HIV DNA and interfere with the virus's ability to replicate. But HIV produces a protein, called Vif, that can disable the two defensive proteins.

Vif is full of variation, both in sequence and in function, according to a new study in PLoS Pathogens, and this could in turn potentially accelerate the evolution of HIV.

Within a single patient, some versions of Vif don't work at all; others counteract only one of the host's defensive proteins. "It's a leaky system," according to Paul D. Bieniasz, senior author of the study and associate professor at The Rockefeller University's Aaron Diamond AIDS Research Center.

Some variations in Vif only partially inactivate the defensive proteins that cause HIV to mutate, and might even promote further variation in the virus within patients. "This work elucidates new pathways which shape the evolution of the virus," says Viviana Simon, lead author of the study.

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Citation: Simon V, Zennou V, Murray D, Huang Y, Ho DD, et al. (2005) Natural variation in Vif function can differentially impact APOBEC3G/3F neutralization: A potential role in HIV-1 diversification. PLoS Pathogens 1(1): e6.

CONTACT: Viviana Simon
Aaron Diamond AIDS Research Center
The Rockefeller University
455 First Avenue
New York, NY 10016
United States of America
212-448-5128
vsimon@adarc.org

Paul Bieniasz
Aaron Diamond AIDS Research Center
The Rockefeller University
455 First Avenue
New York, NY 10016
United States of America
212-448-5070
212-448-5159 (fax)
paul.bieniasz@adarc.org

The Public Library of Science (PLoS) is pleased to offer a preview of PLoS Pathogens (http://www.plospathogens.org), a new open-access, peer-reviewed journal that will premiere on September 30, 2005. The journal is led by Editor-in-Chief John A.T. Young, a professor in the Infectious Disease Laboratory at the Salk Institute for Biological Studies.

"Understanding pathogens and how they interact with their hosts is one of the most serious scientific challenges we face. New pathogens are emerging all the time, and others adapt to treatments efforts," Young says. The journal will publish rigorously peer-reviewed papers in the broad field of pathogens research, which includes bacteria, fungi, parasites, prions, and viruses.

Open access--free availability and unrestricted use­--to all articles published in the journal is central to the mission of PLoS Pathogens and the Public Library of Science. "Our open-access license means [the research published] is immediately available to scientists all over the world," the journal's editorial team explains.

PLEASE MENTION PLoS PATHOGENS (http://www.plospathogens.org/) AS THE SOURCE FOR THESE ARTICLES. THANK YOU.

All works published in PLoS Pathogens are open access. Everything is immediately available without cost to anyone, anywhere--to read, download, redistribute, include in databases, and otherwise use--subject only to the condition that the original authorship is properly attributed. Copyright is retained by the authors. The Public Library of Science uses the Creative Commons Attribution License.

CONTACT:
Rocky Choi
Publications Assistant
Public Library of Science
185 Berry Street, Suite 3100
San Francisco, CA USA 94107
U.S. :1-415-624-1210
U.K.: 44-1223-494493
rchoi@plos.org


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