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Protein yang melindungi sel dari ancaman HIV ditemui?

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Post time 13-2-2012 03:29 PM | Show all posts |Read mode
Post Last Edit by dauswq at 13-2-2012 15:33

How a Protein Protects Cells from HIV Infection


                                                                                

ScienceDaily (Feb. 12, 2012) — A novel discovery by researchers at NYU Langone Medical Center and colleagues reveals a mechanism by which the immune system tries to halt the spread of HIV. Harnessing this mechanism may open up new paths for therapeutic research aimed at slowing the virus' progression to AIDS. The study was published online ahead of print on February 12 in Nature Immunology.

                                                               
                                
"A lot of research on viruses, especially HIV, is aimed at trying to understand what the body's mechanisms of resistance are and then to understand how the virus has gotten around these mechanisms," said co-lead investigator Nathaniel R. Landau, PhD, a professor of microbiology at the Joan and Joel Smilow Research Center at NYU School of Medicine.

The research focused on a protein called SAMHD1. Recent studies have found that immune cells, called dendritic cells, containing the protein are resistant to infection by HIV. Since the discovery, scientists have sought to understand how SAMHD1 works to protect these cells, with hopes that science might find a way to synthetically apply that protection to other cells.
Dr. Landau and his team are now able to provide an answer:

When a virus, like HIV, infects a cell, it hijacks the cell's molecular material to replicate. That molecular material is in the form of deoxynucleotide triphosphates (dNTPs), which are the building blocks for DNA. Once the virus replicates, the resulting DNA molecule contains all the genes of the virus and instructs the cell to make more virus.



Researchers wanted to understand how cells containing the SAMHD1 protein are protected from such hijacking. They found that SAMHD1 protects the cell from viruses by destroying the pool of dNTPs, leaving the virus without any building blocks to make its genetic information -- a process researchers call nucleotide pool depletion. "SAMHD1 essentially starves the virus," Dr. Landau said. "The virus enters the cell and then nothing happens. It has nothing to build and replicate with, so no DNA is made."

As a result, the most common form of HIV does not readily infect these cells. Instead, the virus has evolved to replicate mainly in a different kind of cell, called CD4 T-cells, which do not contain SAMHD1 and therefore have a healthy pool of dNTPs. Dr. Landau explained that the virus has evolved in such a way that it may deliberately avoid trying to infect immune cells with SAMHD1 to avoid alerting the greater immune system to activate a variety of antiviral mechanisms to attack the virus. Viruses that are related to HIV, like HIV-2 and SIV, have developed a protein called viral protein X (VPX) that directly attacks SAMHD1. This allows the virus to infect dendritic cells, an important type of immune cell.

"Viruses are remarkably clever about evading our immune defenses," Dr. Landau said. "They can evolve quickly and have developed ways to get around the systems we naturally have in place to protect us. It's a bit of evolutionary warfare and the viruses, unfortunately, usually win. We want to understand how the enemy fights so that we can outsmart it in the end."

Understanding the mechanism by which SAMHD1 provides protection to cells may provide a new idea about how to stop or slow the virus' ability to spread, Dr. Landau explained. Potential future research efforts, for example, might focus on finding a way to increase the amount of SAMHD1 in cells where it does not exist, or to reduce the amount of dNTPs in cells vulnerable to infection.
"Over the past few years, a number of these natural resistance mechanisms have been identified, specifically in HIV, but some have potential applications to other viruses, as well," he said. "This is a very exciting time in HIV research. Many of the virus' secrets are being revealed through molecular biology, and we're learning a tremendous amount about how our immune system works through the study of HIV."

Funded in part by the National Institutes of Health and the American Foundation for AIDS Research, the study was conducted in collaboration with researchers at several institutions, including the University of Rochester Medical Center and The Cochin Institute, in Paris.

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 Author| Post time 13-2-2012 03:31 PM | Show all posts
dr artikel di atas, difahamkan bahawa saintis telah menemui sejenis protein yg dpt melindungi sel dr diserang virus HIV tuk proses replikasi....

protein ni dpt melambatkan proses serangan virus HIV dlm sel badan
tp jgn salah fhm, ni bukan bermaksud dpt menghalang penyakit Aids...

analoginya spt "antibiotik"
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Post time 13-2-2012 03:52 PM | Show all posts
virus memang bijak nau...
HIV taknak kacau dendritic cell sebab takmo dendritic cell tu macam askar, pemberi maklumat kat sempadan yang akan call for backup anytime kena attack...
sebab tu bila masuk dendritic cell pun dia duk diam jeh...as if tengah cuba camouflage itself supaya takde orang perasan kehadiran dia...
kut...
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Post time 14-2-2012 12:29 AM | Show all posts
org pertame sembuh dr HIV

Timothy Ray Brown was already burdened with HIV and leukemia, when he received a stem cell bone marrow transplant in 2007.

The bone marrow donation came from a man immune to HIV, a condition enjoyed by only one percent of Caucasians in the world, according to a report by CBS.

Following the transplant, Brown's HIV was gone.

“I quit taking my HIV medication the day that I got the transplant and haven’t had to take any since,” said Brown.


saintis percaye yg transplant tu yg sebabkn die sembuh.. tp mustahil utk pesakit2 hiv yg lain..


Perhaps it's not so important who brought the mutation, but what it is they lacked. According to this story in Wired, those who can't get infected by HIV are lacking the so-called CCR5 receptor. If this cellular device isn't present, the AIDS virus has no way of breaking into the cell and taking over.

credit to business insider



jd ccr5 receptor ni la ye yg jd perantare utk hiv ni berjangkit?
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Post time 17-2-2012 11:32 AM | Show all posts
baguslah. harapan baru untuk smua..
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