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Author Topic: "On/Off" Switch allows researchers to turn HIV Dormant  (Read 2423 times)

0 Members and 1 Guest are viewing this topic.

Offline Magnus

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  • Posts: 63
"On/Off" Switch allows researchers to turn HIV Dormant
« on: March 16, 2008, 06:32:20 PM »
Researchers at the University of California, San Diego and Oak Ridge National Laboratory have discovered how a genetic circuit in HIV controls whether the virus turns on or stays dormant, and have succeeded in forcing the virus towards dormancy, a finding that shows promise as an avenue for HIV therapy.

They have increased the levels of the native cellular gene SirT1 (a gene implicated in aging) to reduce the lifespan of the HIV virus and force HIV-infected cells to go dormant.

"While latency is a ticking time bomb," said Simpson, "a possible therapeutic goal could be to stably maintain latency indefinitely."

http://www.sciencedaily.com/releases/2008/03/080317094858.htm
 
« Last Edit: March 17, 2008, 11:37:21 AM by Magnus »

Offline bimazek

  • Member
  • Posts: 781
Re: "On/Off" Switch allows researchers to turn HIV Dormant
« Reply #1 on: April 26, 2008, 08:06:59 PM »
http://scholar.google.com/scholar?num=50&hl=en&lr=&q=SirT1+hiv&as_ylo=2008&as_yhi=2008&btnG=Search
this seems very hot topic right now
already 30 papers in 2008 on this
and another 30 in 2007
i dont have time to read them all now
but worth a look

this one looks interesting. all talk about a feedback loop - negative one, where things get signaled, any that has always seemed to be the key to hiv, the cliff some people talk about

http://www.nature.com/ng/journal/v40/n4/abs/ng0408-382.html
Nature Genetics 40, 382 - 383 (2008)
doi:10.1038/ng0408-382
HIV-1 positive feedback and lytic fate
Iftach Nachman1 & Sharad Ramanathan1
   1. Sharad Ramanathan and Iftach Nachman are at the Faculty of Arts and Sciences Center for System Biology, Harvard University, Cambridge, Massachusetts 02138, USA.
Abstract
The HIV viral lifecycle includes infection of a host cell, followed by a critical decision between latency and lysis. A new study suggests that positive feedback in the HIV-1 promoter, involving Tat protein and gene expression, has a role in this critical choice of fate.

 


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