journal PLoS pathogens

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http://www.plos.org/news/announce_pathogenspreview.html

A preview of a new open access journal from the Public Library of Science—PLoS

Pathogens

San Francisco, July 22, 2005 - 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 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.

The first article in this preview reports how a common bacterium in the human

nose overcomes a competing species. The second describes the functional

variation of an HIV-1 protein that helps the virus disable host defenses and

explains that this variation might contribute to the virus's rapid evolution.

The full text of both articles is freely available at

http://www.plospathogens.org/.

Bacteria use hosts' immune response to their competitive advantage

Millions of bacteria live within the recesses of our noses and upper respiratory

tracts, waiting for a chance to infiltrate and infect. But long before these

bacteria break through our immune defenses, they must first compete against

other bacterial species to colonize the mucus-lined surfaces of our noses.

Competition between two common nose bacteria involves some interesting trickery,

according to a new study in PLoS Pathogens. " We're looking at how bacteria use

their host, and we've found that the presence of one species leads to the

elimination of another, " says Weiser, coauthor of the study and

professor of pediatrics and microbiology at the University of Pennsylvania

School of Medicine.

In a mouse model, Haemophilus influenzae—a common bacterium that infects

children—stimulates the immune system to send out specialized white blood cells

that attack its competitor, Streptococcus pneumoniae—a leading cause of

pneumonia. " It is striking that the host's response can so completely eliminate

the competitor, " says Weiser.

The findings also demonstrate how antibiotics and vaccines that target one

microbe might inadvertently alter the competitive interactions among other

species present.

Read the full research article at http://www.plospathogens.org/.

Citation: Lysenko ES, Ratner AJ, AL, Weiser JN (2005) The role of innate

immune responses in the outcome of interspecies competition for colonization of

mucosal surfaces. PLoS Pathogens 1(1): e1.

Contact:

N. Weiser M.D.

University of Pennsylvania School of Medicine

402A Pavilion

3610 Hamilton Walk

Philadelphia, PA 19104-6076

215-573-3511; FAX 215-573-4856

weiser@...

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

evolution

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 D. Bieniasz, senior author of the study and associate

professor at The Rockefeller University's 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.

Read the full research article at http://www.plospathogens.org/.

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): e17.

Contact:

Viviana Simon

Diamond AIDS Research Center

The Rockefeller University

455 First Avenue

New York, NY 10016

United States of America

212 448 5128

vsimon@...

Bieniasz

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@...

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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 author and source are credited. Copyright is retained by the authors.

The Public Library of Science uses the Creative Commons Attribution License

(http://creativecommons.org/licenses/by/2.5/).

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@...