ANOTHER BREAKTHROUGH IN THE FIGHT AGAINST THE HIV



HealthDay - http://www.nlm.nih.gov/medlineplus/news/fullstory_72653.html

Wednesday, December 10, 2008


Researchers report that a treatment under development appears to stop the equivalent of the AIDS virus in monkeys.

Nine rhesus macaque monkeys infected with a virus known as SIV underwent treatment and remain alive eight months later. The treatment appears to work by preventing virus cells from fooling the immune system.

There's no guarantee that the treatment will work in people. But if it's effective in humans, the treatment could allow patients to avoid taking AIDS drugs for the rest of their lives, said study co-author Rama Rao Amara, an assistant professor at Emory University's Yerkes National Primate Research Center.

"If you wake up and realize you don't have to take a pill, it's a big step forward," he said. In addition, he said, current AIDS drugs are expensive and have serious side effects.

Existing AIDS drugs do have benefits: They're often effective and have allowed patients to live normal lives. However, they can't always keep up with the AIDS virus, which evolves quickly and can become immune to current treatments.

"The virus changes and then these drugs don't work after some time," Amara said.

In the new study, Amara and colleagues injected nine monkeys with an antibody that blocks a kind of "don't kill me" signal that cells infected with simian immunodeficiency virus (SIV) send to immune cells.

When the SIV-infected cells emit the signal, "the killer cell thinks, 'You are not my enemy. You're my friend,'" Amara said. But when the signal is blocked, the killer immune cells can do their job and wipe out the virus.

The researchers gave four injections of the antibody to the monkeys over 10 days and then watched to see what happened.

The study appears in the Dec. 10 online edition of Nature

The monkeys, infected with SIV for as long as 21 months, were able to beat back the virus. Levels of virus in the blood dropped and the animals remained alive.

By contrast, four out of five monkeys who received a "control" antibody died within four months.

"What is amazing to me how rapidly you can actually change these killer cells," Amara said. "Now they are good cells."

The work of the monkeys is done and they will be euthanized, Amara said. It is too expensive -- $7 a day each -- to pay for their care with available funding, he said.

In humans, the treatment could cost a couple thousand dollars per dose, Amara said, although patients might then avoid taking drugs for life.

Dr. Mark Connors, a specialist in AIDS research, said the research is "clearly valid and very interesting. I'm sure it's going to generate debate over the next year or so as to what it means."

Even skeptics may be convinced by evidence that the treatment directly affects survival and the level of the virus in the body, said Connors, chief of the HIV-Specific Immunity Section at the U.S. National Institute of Allergy & Infectious Diseases.

As for the future, Connors said he's "guardedly optimistic" that the treatment could be used in humans, perhaps in conjunction with other medications.

HealthDay

I think cure is entirely possible. We can't ignore past precedents on things like this. Other viruses have been beat. The key I think is understanding the small percentage of the population that is HIV immune for some reason (primarily people who's ancestors survived the black plague or as a previous poster pointed out, people with other odd immune responses that suppress the virus as opposed to being more resistant to it). What keeps them immune will be the knowledge that ultimately develops a proper vaccine and an immune therapy cure for those infected. This is not only hopeful, it's nearly certain.. but it's not the only way... attacking the virus with docking points like what we are computing here also holds nearly certain promise because there will be traits of the virus that can not mutate. Finding those shapes that don't change is also another key weakness that will provide a winning solution. This method is perhaps easier and quicker than understanding how to simulate or recreate the natural immunity that some people have. In the end, a combination of attacks from several angles may be what's needed to keep the squirmy bugger from mutating around any one barrier put up against it.

I know a guy in Palm Springs, CA who took an experimental set of injections to artificially "pump up" his immune system (which was healthy and HIV -) for science. They continue to pay his medical bills as this does have an adverse effect of some kinds of immune-reaction tissue destruction which causes him back trouble? In any case he's a very sexually active type and despite throwing caution to the wind, he remains free from any infections of any kind. It seems this approach worked for him to prevent infection although clearly it has a different kind of price to pay in terms of health.

There is a lot of research out there and a lot of approaches. It may not be any one approach that ends HIV, it may take several combined approaches to keep it in check, but like all good games, eventually the cleverest of opponents will be beat at their own game. The progress with protease-inhibiting drugs so far has been very very good. As things stand right now, almost nobody with early drug treatment stands to lose their life to HIV if they follow the doctor's orders.. It seems while we aren't ridding people of the virus, clearly we are stalling out the virus's attacks in most people's bodies, and that's a very good position to be in as long as we can keep coming up with more of these kinds of drugs to abate mutations whilst other novel approaches to kill it/mutate it/block it etc are in the queue to be worked out.

Stem cells trials are approved

http://www.medicalnewstoday.com/articles/136413.php

i hope soon we can use same technique to cure HIV/AIDS

http://www.amfar.org/lab/article.aspx?id=5796




Learning to Silence HIV

by jeffrey Laurence, M.D.

January 12, 2009—Individuals successfully treated with antiretroviral drugs have little to no detectable HIV in their blood. What they do have is a very small number of cells, a million or so, infected with latent virus. In these cells, HIV has entered a state of dormancy, existing below the radar of a person’s immune system and beyond the ability of standard anti-HIV drugs to attack it. This latent HIV infection persists for the lifetime of the patient.

Two amfAR-funded research fellows, Drs. Young Kyeung Kim and Kara Lassen, have opened a window into just how this viral silencing occurs and what might be done to alter it. Writing in the December 2008 issue of the Journal of Virology, Drs. Kim, Lassen, and colleagues, working at Case Western Reserve University, noted that HIV typically enters a latent state when the function of one of its key regulating genes, known as Tat, is disrupted.

The researchers introduced just such a disruption in Tat by using an experimental method that produced mutations in the Tat protein. Given the high rate of HIV growth and the huge frequency with which HIV suffers genetic errors during its growth, this mutation didn’t take long to expand; at least in the test tube, half of all viruses were "silenced" by the mutation within about two months. This left the Case Western group with an intriguing puzzle: How did errors in Tat’s regulation relate to this process, how are Tat levels normally controlled in the absence of such functional disruptions, and how could researchers take advantage of these mechanisms to design new anti-HIV therapies?

HIV typically enters a latent state when the function of one of its key regulating genes, known as Tat, is disrupted.
Prior to this work, most investigators believed that HIV latency arose as a passive process, a consequence of HIV being carried along inside a cell as it progressed along a normal pathway of growth and differentiation. But Drs. Kim and Lassen show that this process is much more active than previously believed: Chemical modifications of histones, normal cell proteins that bind to the DNA of genes and help regulate their function, are critical. These modifications—acetylation and methylation—change gene structures, and one consequence of these changes is that any HIV integrated into those genes can be activated or silenced.

Silent HIV carries high levels of histone proteins lacking in acetylation but abundantly methylated. Certain immune hormones known as cytokines can turn on HIV growth by reversing these chemical modifications. But how might researchers take advantage of these insights to develop new therapies?

One approach was pioneered by Dr. David Margolis. Working with amfAR funding, he showed that drugs known as histone deacetylase (HDAC) inhibitors could activate latent HIV in the test tube, rendering the virus susceptible to attack by standard anti-HIV drugs. Although pilot trials of one such drug in patients did not show clear results, development of better HDAC inhibitors or related drugs may hold promise in the future.

Dr. Laurence is amfAR’s senior scientific consultant.



http://www.amfar.org/lab/article.aspx?id=5338

Imagine There’s No HIV
Researchers Set Sights on HIV Eradication

By Rowena Johnston, Ph.D., and Jeffrey Laurence, M.D.

December 15, 2008—Recent news reports have publicized the case of an American HIV-positive patient in Berlin, Germany, who underwent a stem cell transplant in an attempt to cure his acute leukemia. The doctors performing the transplant surgery took a critical step by recruiting a stem cell donor who had a natural, harmless mutation that made his cells—and now those of the young man who received the stem cell transplant—resistant to HIV infection. It has been almost two years now and, off all anti-HIV drugs, this patient has a normal T cell count and his doctors have not been able to detect HIV anywhere in his body: blood, bone marrow, lymph node, intestine, or brain.

This case will require further in-depth study to understand just what happened in this patient, who, despite the success of the transplant, remains seriously ill. And while it has reignited hope in some quarters that a cure for HIV may be possible, there are many reasons this method cannot be employed in the millions who are HIV-infected today, not least the significant risk of mortality associated with the procedure as well as the price tag, which runs into the hundreds of thousands of dollars.

Thus it is vital that amfAR’s long-term efforts to improve the effectiveness of antiretroviral therapy (ART), and our pursuit of a practical cure for HIV, continue. amfAR recently convened two think tanks on these very topics—a small gathering in September to discuss the Berlin patient and a larger meeting in November to lay out a broad research strategy that could ultimately lead to the eradication of HIV from the bodies of infected people.

Around 40 top researchers and funders active in this second area—viral eradication—gathered in Washington, D.C., to discuss a broad and complex range of issues that future research into eradication must take into account. Think tank participants, including several amfAR grantees, addressed the ability of current antiretroviral regimens, as well as boosted regimens, to suppress HIV’s capacity to replicate, and they considered the challenges of rebuilding the immune system so that it can function properly after HIV infection inflicts damage. They also pondered the new technologies that will need to be developed in order to delve deeper into the mechanisms whereby HIV infection persists in the face of both an immune response and highly effective ART. And they discussed current as well as potential strategies to purge latent reservoirs of HIV so that emerging virus can be targeted by existing drugs.

Along with the two think tanks, amfAR has taken a leadership role by sponsoring two recent grant initiatives on urgent topics confronting HIV/AIDS research: “Exploring the potential for HIV eradication” and “Optimizing the treatment of HIV infection.” For the first of these initiatives, amfAR grantees were charged with investigating reservoirs of virus within the body and the mechanisms whereby virus within these reservoirs remains latent. They were also asked to explore the potential for using existing drugs to reduce the virus to levels approaching zero or as part of a regimen that might ultimately eradicate the virus; and to study what happens during the first few weeks of infection and how those events may determine disease course.

amfAR grantee Dr. Martin Markowitz has made seminal findings about the damage associated with HIV infection that occurs in the gut during the earliest stages of infection, and the extent to which this damage may be irreversible. To read more about his findings, click here. Meanwhile, Dr. Steven Deeks has been closely monitoring a very small group of patients known as elite controllers whose HIV disease remains at bay despite never being treated. You can read more on this here. Other grantees funded as part of this initiative are searching for the hidden locations where HIV resides beyond the reach of ART, and for agents that could purge the body of HIV.

The second grant initiative, on optimizing treatment, aimed to find ways to increase the number of people being tested for HIV; to identify those who are in the acute stages of infection; to facilitate access to HIV care and adherence to treatment; to explore the full potential of existing ART; and to better understand the persistence of HIV infection and how it can be eradicated. Along these lines, amfAR grantee Dr. Jennifer Sayles is exploring the extent to which women with HIV experience stigma and how it may affect their ability to access healthcare. She has already published three papers in prominent AIDS research journals describing her findings and pointing to potential ways to address the barriers women face in dealing with their infection. You can read more about her research here.

There are numerous angles from which a potential cure for HIV can and must be approached. amfAR continues to explore every possible avenue in its quest for that cure.

Dr. Laurence is amfAR’s senior scientific consultant and Dr. Johnston is amfAR’s vice president for research.



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Ideally, for all it would be nice to collect all the AIDS/HIV related news in the "interested news on..." threads each project science has. These are linked from the FAQ index for easy finding and allows for every visitor to find all without having the search through the forums.

Thus, plz put your news items in http://www.worldcommunitygrid.org/forums/wcg/viewthread?thread=5510 for this project.

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