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Author Topic: Finally an explanation ....  (Read 2553 times)

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Offline J.R.E.

  • Member
  • Posts: 7,093
  • Joined Dec-2003 Living positive, since 1985.
Finally an explanation ....
« on: November 28, 2010, 05:31:31 PM »

Finally, An Explanation For How HIV Infection Kills T Cells


http://www.medicalnewstoday.com/articles/209332.php

Main Category: HIV / AIDS
Article Date: 27 Nov 2010 - 0:00 PST


Researchers appear to have an explanation for a longstanding question in HIV biology: how it is that the virus kills so many CD4 T cells, despite the fact that most of them appear to be "bystander" cells that are themselves not productively infected. That loss of CD4 T cells marks the progression from HIV infection to full-blown AIDS, explain the researchers who report their findings in studies of human tonsils and spleens in the November 24th issue of Cell, a Cell Press publication.

"In [infected] primary human tonsils and spleens, there is a profound depletion of CD4 T cells," said Warner Greene of The Gladstone institute for Virology and Immunology in San Francisco. "In tonsils, only one to five percent of those cells are directly infected, yet 99 percent of them die."

Lymphoid tissues, including tonsils and spleen, contain the vast majority of the body's CD4 T cells and represent the major site where HIV reproduces itself. And it now appears that those dying T cells aren't bystanders exactly.

The HIV virus apparently does invade those T cells, but the cells somehow block virus replication. It is the byproducts of that aborted infection that trigger an immune response that is ultimately responsible for killing those cells.

More specifically, when the virus enters the CD4 T cells that will later die, it begins to copy its RNA into DNA, Greene and his colleague Gilad Doitsh explain. That process, called reverse transcription, is what normally allows a virus to hijack the machinery of its host cell and begin replicating itself. But in the majority of those cells, the new findings show that the process doesn't come to completion.

The cells sense partial DNA transcripts as they accumulate and, in a misguided attempt to protect the body, commit a form of suicide. Greene says that completed viral transcripts in cells that are productively infected probably don't provoke the same reaction because they are so rapidly shuttled into the nucleus and integrated into the host's own DNA.

The researchers narrowed down the precise "death window" of those so-called bystander cells by taking advantage of an array of HIV drugs that act at different points in the viral life cycle. Drugs that blocked viral entry or that prevented reverse transcription altogether stopped the CD4 T cell killing, they report. Those drugs that act later in the life cycle to prevent reverse transcription only after it has already begun did not save the cells from their death.

Those cells don't die quietly either, Greene says. The cells produce ingredients that are the hallmarks of inflammation and break open, spilling all of their contents. That may provide a missing link between HIV and the inflammation that tends to go with it.

"That inflammation will attract more cells leading to more infection," Greene said. "It's a vicious cycle."

The findings also show that the CD4 T cells' demise is a response designed to be protective of the host. All that goes awry in the case of HIV and "the CD4 T cells just get blown away," compromising the immune system.

Greene said that all the available varieties of anti-HIV drugs will still work to fight the infection by preventing the virus from spreading and reducing the viral load.

The findings may lead to some new treatment strategies, however. For instance, it may be possible to develop drugs that would act on the cell sensor that triggers the immune response, helping to prevent the loss of CD 4 T cells. His team plans to explore the identity of that sensor in further studies. They also are interested to find out if the virus has strategies in place to try and prevent the CD4 T cells' death.

"The cell death pathway is really not in the virus's best interest," Greene says. "It precludes the virus from replicating and the virus may have ways to repel it."
Current Meds ; Viramune, Epzicom, 40mg of simvastatin, 12.5mg of Hydrochlorothiazide.
Metoprolol tartrate 25mg



http://forums.poz.com/index.php?topic=40802.0

http://forums.poz.com/index.php?topic=45159.0

http://forums.poz.com/index.php?topic=39722.msg495621;topicseen#msg495621

http://forums.poz.com/index.php?topic=46806.0

http://forums.poz.com/index.php?topic=39414.msg491701#msg491701


 In October of 2003, My t-cell count was 16, Viral load was over 500,000, Percentage at that time was 5%. I started my first  HAART regimen  on October 24th,03.

 As of 6/4/14,  t-cells are at 423, Viral load <40

 Current % is at 13% 

  
 62 years young.

Offline tednlou2

  • Member
  • Posts: 4,758
Re: Finally an explanation ....
« Reply #1 on: November 29, 2010, 01:38:23 AM »
It seems like researchers are learning something new about HIV on a weekly basis.  All this discovery will eventually lead to a vaccine/cure/functional cure, I believe.

This got me to thinking about something.  What happens with people who no longer have their tonsils or spleen and have HIV?  I know people just like this--well, they don't have HIV that I know.  They have had their tonsils and spleens removed.

Offline Hellraiser

  • Member
  • Posts: 4,136
  • Semi-misanthropic
Re: Finally an explanation ....
« Reply #2 on: November 29, 2010, 01:40:14 AM »
It seems like researchers are learning something new about HIV on a weekly basis.  All this discovery will eventually lead to a vaccine/cure/functional cure, I believe.

This got me to thinking about something.  What happens with people who no longer have their tonsils or spleen and have HIV?  I know people just like this--well, they don't have HIV that I know.  They have had their tonsils and spleens removed.

I'm not sure exactly what you're asking here.  When they say lymphoid tissues they were saying that the tonsils and spleens are examples of them.  You have lymph nodes and glands all over your body.

Offline Inchlingblue

  • Member
  • Posts: 3,119
  • Chad Ochocinco PETA Ad
Re: Finally an explanation ....
« Reply #3 on: December 01, 2010, 02:17:38 PM »
The article below explains the process very well and there are a couple of pics of the doctor, Gilad Doitsh, who looks like a hottie.

LINK:

http://www.kqed.org/quest/blog/2010/12/01/aids-researchers-unlock-cell-death-mystery/

Offline J.R.E.

  • Member
  • Posts: 7,093
  • Joined Dec-2003 Living positive, since 1985.
Re: Finally an explanation ....
« Reply #4 on: December 18, 2010, 05:16:28 AM »

Making It Harder For HIV To Hide From Drugs



http://www.medicalnewstoday.com/articles/211775.php


Just passing on some more info :

Making It Harder For HIV To Hide From Drugs
Main Category: HIV / AIDS
Article Date: 17 Dec 2010 - 4:00 PST


The virus that causes AIDS is chameleon-like in its replication. As HIV copies itself in humans, it constantly mutates into forms that can evade even the best cocktail of current therapies. Understanding exactly how HIV cells change as they reproduce is key to developing better tests and treatments for patients.

In the Journal of Biological Chemistry and Nature Structural & Molecular Biology, MU microbiologist and biochemist Stefan Sarafianos, PhD, reveals new findings that shed light on how HIV eludes treatment by mutating. His discoveries provide clues into HIV's mechanisms for resisting two main families of drugs.

"These findings are important because identifying a new mutation that affects HIV drug resistance allows physicians to make better decisions and prescribe the proper drugs," Sarafianos said. "Without that knowledge, therapy can be suboptimal and lead to early failure."

Patients with HIV are routinely tested to track the levels of the virus and immune cells in their body. Results of the tests help physicians gauge the health of their patients and prescribe the right mix of antiviral drugs. The drugs help prevent the spread of HIV in patients by inhibiting the virus' ability to replicate.


Sarafianos' lab determined the biochemical properties that allow strains of HIV with a specific mutation - the N348I mutation - to escape inhibition despite treatment with Nevirapine. The drug is commonly used in combination with other antiviral medications to decrease the amount of HIV in the blood. As a result of Sarafianos' discovery, at least one major company that manufactures HIV mutation-testing kits has modified its test to detect the N348I mutation.



Sarafianos' recent findings resulted from research supported by five National Institutes of Health grants. He recently received another $417,000 award from the NIH to assist him in developing modified antibodies for HIV therapy.

"Our latest efforts to design broadly neutralizing antibodies against HIV will hopefully expand our toolbox against the virus, which remains a constantly moving target," Sarafianos said.



« Last Edit: December 18, 2010, 06:07:34 AM by J.R.E. »
Current Meds ; Viramune, Epzicom, 40mg of simvastatin, 12.5mg of Hydrochlorothiazide.
Metoprolol tartrate 25mg



http://forums.poz.com/index.php?topic=40802.0

http://forums.poz.com/index.php?topic=45159.0

http://forums.poz.com/index.php?topic=39722.msg495621;topicseen#msg495621

http://forums.poz.com/index.php?topic=46806.0

http://forums.poz.com/index.php?topic=39414.msg491701#msg491701


 In October of 2003, My t-cell count was 16, Viral load was over 500,000, Percentage at that time was 5%. I started my first  HAART regimen  on October 24th,03.

 As of 6/4/14,  t-cells are at 423, Viral load <40

 Current % is at 13% 

  
 62 years young.

Offline sensual1973

  • Member
  • Posts: 195
Re: Finally an explanation ....
« Reply #5 on: December 18, 2010, 12:09:39 PM »
so many findings,not so much solutions.
God grant me the serenity to accept the things i can not change.

 


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