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HIV Can Hide in Bone Marrow

Discussion in 'Other Health News and Research' started by Summer, Mar 7, 2010.

  1. Summer

    Summer Senior Member

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    Researchers: AIDS virus can hide in bone marrow

    WASHINGTON The virus that causes AIDS can hide in the bone marrow, avoiding drugs and later awakening to cause illness, according to new research that could point the way toward better treatments for the disease.

    Finding that hide-out is a first step, but years of research lie ahead.

    Dr. Kathleen Collins of the University of Michigan and her colleagues report in this week's edition of the journal Nature Medicine that the HIV virus can infect long-lived bone marrow cells that eventually convert into blood cells.

    The virus is dormant in the bone marrow cells, she said, but when those progenitor cells develop into blood cells, it can be reactivated and cause renewed infection. The virus kills the new blood cells and then moves on to infect other cells, said.

    "If we're ever going to be able to find a way to get rid of the cells, the first step is to understand" where a latent infection can continue, Collins said.

    In recent years, drugs have reduced AIDS deaths sharply, but patients need to keep taking the medicines for life or the infection comes back, she said. That's an indication that while the drugs battle the active virus, some of the disease remains hidden away to flare up once the therapy is stopped.

    One hide-out was found earlier in blood cells called macrophages. Another pool was discovered in memory T-cells, and research began on attacking those.

    But those couldn't account for all the HIV virus still circulating, Collins said, showing there were more locations to check out and leading her to study the blood cell progenitors.

    Finding these sources of infection is important because eliminating them would allow AIDS patients to stop taking drugs after their infection was over. That's critical in countries where the treatment is hard to afford and deliver.

    "I don't know how many people realize that although the drugs have reduced mortality we still have a long way to go," Collins said in a telephone interview. "That is mainly because we can't stop the drugs, people have to take it for a lifetime."

    The research was funded by the National Institutes of Health, Burroughs Wellcome Foundation, University of Michigan, Rackham Predoctoral Fellowship, National Science Foundation and a Bernard Maas Fellowship.
     
  2. Robin

    Robin Guest

    Wow, thanks for posting. That's really exciting!!

    Have to love that joint funding! :)
     
  3. starryeyes

    starryeyes Senior Member

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    Summer, thanks for posting this. This is important for us to know.
     
  4. cfs since 1998

    cfs since 1998 *****

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    There is a passage on the Wikipedia article for HIV that an HIV+ man received a bone marrow transplant and seems to have been "cured" of HIV. Of course, bone marrow transplant carries a 30% or so chance of death. The same thing has been reported with Epstein-Barr. I wonder if all "incurable" viruses will be discovered to be hiding in bone marrow? You'd think they'd already know things like this from animal studies. I wonder if this is also why bone pain is a symptom of CFS, especially for people on antivirals.
     
  5. Summer

    Summer Senior Member

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    A Doctor, a Mutation and a Potential Cure for AIDS

    A Bone Marrow Transplant to Treat a Leukemia Patient Also Gives Him Virus-Resistant Cells

     
  6. creekfeet

    creekfeet Sockfeet

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    Where's the XMRV party metaphor? + Source link for orig research pub.

    Thanks for posting this. My bro just emailed me an article on this HIV-in-bone-marrow story, remarking how "sneaky" the HIV virus is, and asking me if there were any progress in ME/CFS research. I wanted to tell him the party metaphor about XMRV---you know, where if the science of locating viruses were a party HIV would be dancing on a table in the living room and XMRV would be, what, crouched behind the toilet or something? I can't remember quite how it went. Can anyone tell me where that metaphor came from or better still link me to it?

    This is great news, by the way, and I tracked down the original article that various news reporters are citing, in Nature Medicine:
    http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.2109.html

    Unfortunately the entire article is not available to read for free, but if someone has a subscription or wants to pay to read, they can get the full science. It seems the "news" isn't so much the fact of bone marrow infection, but something about the mechanisms of infection.
     
  7. Gerwyn

    Gerwyn Guest

    afraid it was me
     
  8. creekfeet

    creekfeet Sockfeet

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    Thanks, Gerwyn! May I quote you, or at least paraphrase?
     
  9. Summer

    Summer Senior Member

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    Transcription of Judy Mikovits Prohealth Lecture

    Part V Transcribed by Garcia

     
  10. Summer

    Summer Senior Member

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    U-M scientists identify reservoirs where HIV-infected cells can lie in wait

    Targeting these reservoirs of latent cells may open door to new treatments

    University of Michigan scientists have identified a new reservoir for hidden HIV-infected cells that can serve as a factory for new infections. The findings, which appear online today in Nature Medicine, indicate a new target for curing the disease so those infected with the virus may someday no longer rely on AIDS drugs for a lifetime.

    “Antiviral drugs have been effective at keeping the virus at bay. However once the drug therapy is stopped, the virus comes back,” says senior author of the study Kathleen L. Collins, M.D., Ph.D., associate professor of both internal medicine and microbiology and immunology at the U-M Medical School.

    In people infected with HIV (human immunodeficiency virus), the virus that causes AIDS, there’s an unsolved problem with current anti-viral drugs. Though life-saving, they cannot root the virus out of the body. Infected cells are able to live on, undetected by the immune system, and provide the machinery for the virus to reproduce and spread.

    This has led researchers to believe HIV-infected cells may lay-in-wait somewhere in the body. Important new research by U-M has discovered that bone marrow, previously thought to be resistant to the virus, can contain latent forms of the infection.

    “This finding is important because it helps explain why it’s hard to cure the disease,” Collins says. “Ultimately to cure this disease, we’re going to have to develop specific strategies aimed at targeting these latently infected cells.”

    “Currently people have to take anti-viral drugs for their entire life to control the infection,” she says. “It would be easier to treat this disease in countries that don’t have the same resources as we do with a course of therapy for a few months, or even years. But based on what we know now people have to stay on drugs for their entire life.”

    Using tissue samples, U-M researchers detected HIV genomes in bone marrow isolated from people effectively treated with antiviral drugs for more than six months.

    While further studies are needed to demonstrate that stem cells can harbor the HIV virus, the study results confirm that HIV targets some long-lived progenitor cells, young cells that have not fully developed but mature into cells with special immune functions. When active infection occurs the toxic effects of the virus kill the cell even as the newly made viral particles spread the infection to new target cells.

    “Our finding that HIV infects these cells has clear ramifications for HIV disease because some of these cells may be long-lived and could carry latent HIV for extended periods of time,” she says. “These HIV cell reservoirs can be induced to generate new infections.”

    The new research gives a broader view of how HIV overwhelms the body’s immune system and devastates its ability to regenerate itself.

    Globally more than 30 million people are infected with HIV, including millions of children. Improvements have been made since the 1990s in the way the disease is treated that has led to an 85 percent to 90 percent reduction in mortality.

    “Drugs now available are effective at treating the virus, making HIV more of a chronic disease than a death sentence,” Collins says. “This has made a huge impact in quality of life, however only 40 percent of people worldwide are receiving anti-viral drugs and unfortunately that means that not everybody is benefiting.”
     
  11. Summer

    Summer Senior Member

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    Stem cells: home of HIV?

    Stem cells: home of HIV?

    Human immunodeficiency virus (HIV) can infect bone marrow cells -- including, possibly, hematopoietic stem cells, according to a study published online today (March 7) in Nature.

    The findings suggest the virus can hide in an inactive state for long periods of time, evading treatment, even in individuals without detectable viral loads.

    "It's a little bit surprising to see that [HIV infects] progenitor cells, and [possibly] stem cells as well," said virologist Michael Bukrinsky of The George Washington University in Washington, DC, who was not involved in the research. It's a "novel and important" discovery that "will have big implications for pathogenesis of the disease and potential treatment of these patients."

    Even patients who respond to highly active antiretroviral therapy (HAART) can harbor undetectably low viral loads, which can be reactivated later in life to cause a resurgence of the disease. Resting T cells can conceal such latent infections, and are the only well established and characterized HIV reservoirs. But a recent study found circulating viral genomes that differ from those found in T cells, suggesting that additional reservoirs may also exist.

    When virologist Kathleen Collins of the University of Michigan in Ann Arbor and her colleagues exposed hematopoietic progenitor cells (HPCs) from bone marrow to HIV, some of the cells were quickly infected and killed by the virus. The team then pushed the progenitors to differentiate -- mostly into an antigen-presenting type of white blood cell -- and saw "a dramatic increase in viral gene expression," Collins said. These results suggested that HPCs likely harbored a latent form of the virus that could be activated by cellular differentiation. In short, HPCs represented another HIV reservoir.

    "To my knowledge, we are the first to find another real reservoir beyond the resting T cell," Collins said.

    "It reveals another obstacle" for viral eradication, said virologist Mario Stevenson of the University of Massachusetts Medical School, who did not participate in the study. "It shows us another area that we have to target in order to achieve a cure."

    The researchers further confirmed the ability of HPCs to carry a latent infection by identifying HIV in the bone marrow in about 40 percent of patients who had undetectable viral loads for at least 6 months.

    In order for cells to be able to maintain the latent virus for long periods of time, Collins said, they must live long enough to survive years of HAART. The discovery of latent infection in HPCs is "suggestive" that the new reservoir may be hematopoietic stem cells, which "we carry for our entire lives," she said. Furthermore, as stem cells have the capacity to self renew, the virus could spread through cell division, Collins added.

    However, because of the type of HIV that persisted in HPCs, "I have my doubts of the functionality of these cells as reservoirs," Bukrinsky said. The HPCs infected by HIV predominately expressed chemokine receptor CXCR4, meaning they could only be infected by viruses that bind specifically to that receptor. These forms of the virus generally appear much later in infection than the major CCR5-binding viruses, which are primarily involved in transmission from one person to another, meaning the HPC reservoirs would not likely contribute to the spread of the virus through the population.

    On the other hand, he added, because "CXCR4 viruses are more pathogenic than CCR5 [viruses], and HPCs are rapidly killed by the [activated] virus, patients will have some problems, even on HAART treatment, generating new T cells and macrophages."

    "It all depends on the numbers," Bukrinsky said -- specifically, "the real percentage of these cells" that maintain a latent infection. With only nine patients in this study, it is unclear how frequently these cells harbor the infection. "This needs to be expanded to a bigger population to generate information about the importance of these reservoirs."

    Furthermore, there may be additional reservoirs not yet identified, Stevenson said. "I think this study is going to generate a lot of interest," he said. "Whether it's the end of the story, I very much doubt it."
     
  12. Carrigon

    Carrigon Senior Member

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    Still makes me wonder how many CFIDS/ME cases might actually be HIV Negative AIDS. Particularly the ones that get every infection in the world all the time.
     
  13. Summer

    Summer Senior Member

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    History of ME / CFS
     
  14. Carrigon

    Carrigon Senior Member

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    Yes, and miraculously, it was all managed to be covered up by the media and everyone else involved. All of a sudden, we never heard of HIV Negative AIDS again. And I've met several CFIDS/ME patients over the years who certainly qualify.
     
  15. Rosemary

    Rosemary Senior Member

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    Zinc-ing differently about HIV

    -- California academics and Sangamo BioSciences Inc. have devised a gene therapy strategy for blocking HIV infection by deleting the gene for an HIV co-receptor in hematopoietic stem cells and enriching the population via HSC transplantation. The group is planning a clinical trial sponsored by the California Institute for Regenerative Medicine.

    For more information
    Click on link below for free access to the article: Full Text or PDF

    Zinc-ing differently about HIV

    An industry-academic collaboration in California has yielded a practical gene therapy strategy for blocking HIV infection. With financial support from the California Institute for Regenerative Medicine, the team now is planning a clinical trial in AIDS patients with lymphoma who are prime candidates for the hematopoietic stem cell transplantation, which is a key part of the technique.

    The method uses a zinc finger nuclease from Sangamo BioSciences Inc. to create hematopoietic stem cells (HSCs) missing both copies of the CC chemokine receptor 5 (CCR5; CD195) gene. Most HIV strains cannot colonize cells without CCR5, so the genetic modification deprives the virus of a place to bind and breed.

    http://www.nature.com/scibx/journal/v3/n27/full/scibx.2010.814.html

    http://www.nature.com/scibx/journal/v3/n27/pdf/scibx.2010.814.pdf
     

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