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(Health) HIV: Research Produces Images of AIDS Virus

 
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PostPosted: Mon May 29, 2006 9:45 am    Post subject: (Health) HIV: Research Produces Images of AIDS Virus Reply with quote






Source: Florida State University

Posted: May 28, 2006

Research Produces Images Of AIDS Virus That May Shape Vaccine

As the world marks the 25th year since the first diagnosed case of AIDS, groundbreaking research by scientists at Florida State University has produced remarkable three-dimensional images of the virus and the protein spikes on its surface that allow it to bind and fuse with human immune cells.


Envelope Spikes on Surface of HIV-1 virus. (Credit: Courtesy of Kenneth Roux)

Findings from this AIDS research could boost the development of vaccines that will thwart infection by targeting and crippling the sticky HIV-1 spike proteins. In fact, said principal investigator and FSU Professor Kenneth H. Roux, at least two laboratories already are crafting vaccine candidates based on preliminary results uncovered by his team of structural biologists.

Those results are described in the online edition of the journal Nature.

Never before generated in such intricate detail, the super-sized images of the virus and its viral spikes have given researchers their first good look at the pathogen's complex molecular surface architecture that facilitates the infection process.

"Until now, despite intensive study by many laboratories, the design details of the spikes and their distribution pattern on the surface of the virus membrane have been poorly understood, which has limited our understanding of how the virus infection actually occurs and frustrated efforts to create vaccines," Roux said.

To produce the images, research associate Ping Zhu, Roux, and their colleagues used a state-of-the art technique called cryoelectron microscopy tomography. It generates three-dimensional images similar to those from a CAT scan, but at the level of viruses and molecules rather than tissues and organs.

They imaged HIV samples as well as a mutant SIV (non-human primate) strain, genetically engineered for the study by collaborators at the National Cancer Institute to express about 74 spikes as opposed to the 14 found on the HIV virus –- more spikes make it easier to work with. The virus samples were suspended in a thin liquid film stretched across the holes of a small copper grid and then flash-frozen, creating a solid form of ice that is more like clear glass than the typical crystalline form in ice cubes.

Once inside the electron microscope, electrons bombarded the samples from myriad angles, magnifying it more than 43,000 times to reveal its surprising structure –- absent the degree of distortion caused by the more typical imaging methods involving drying and staining of specimens.

As a result, the researchers were able to hone in on the envelope –- the lipid membrane covering the virus itself. They imaged the spikes protruding from the envelope, which contain the only viral protein molecules on the HIV surface. The FSU scientists also were able to capture super-sized images of both the head of the spike and its supporting stalk. The spike head is responsible for binding the virus to the target cell. Its stalk is responsible for the fusion event in which HIV injects its genes into the human host cells for which the virus has a natural affinity –- T lymphocytes and macrophages.

"Antibodies that effectively bind to either of these spike parts will neutralize the virus to prevent infection," said Roux, a member of FSU's biological science faculty since 1978.

His biggest surprise: the stalk has legs.

"Researchers thought the spike stalk was comprised of a tight collection of three rods bound together with the head of the spike perched on top. But our images reveal that the stalk is split into three legs, spread more like a tripod, which increases their contact with the viral membrane," Roux said. "Seeing the tripod stalk suggests a novel mechanism by which HIV-1 is able to so effectively fuse with our cells. That essential knowledge should help us design better weapons to fight the virus."

FSU Arts and Sciences Dean Joseph Travis has declared the work "a beautiful example of what happens when strong, sound basic science is applied to a very difficult problem."

The National Institutes of Health funded the two-year study, conducted by members of the department of biological science and the Institute of Molecular Biophysics at FSU.

AIDS has produced one of the worst pandemics ever known. About 25 million people have died and 40 million are infected worldwide –- including 1 million in the United States.

*************************************************************

Questions to explore further this topic:

What are viruses?

http://www.paete.org/forums/viewtopic.php?t=816

What are retroviruses?

http://www.accessexcellence.or.....agram.html
http://www.accessexcellence.or.....virus.html
http://web.uct.ac.za/depts/mmi/jmoodie/hiv2.html
http://pathmicro.med.sc.edu/shockwave.htm

HIV/AIDS: A multimedia lesson

http://www.nlm.nih.gov/medline.....0_no_0.htm

What is HIV?

http://kidshealth.org/kid/heal.....n/hiv.html
http://www.avert.org/aids.htm

What is HIV (structure and life cycle)

http://www.sumanasinc.com/webc.....y/hiv.html
http://www.avert.org/virus.htm
http://www.hopkins-aids.edu/hi.....e_txt.html

HIV animations

http://www.hivinfosource.org/animation.html
http://www.pbs.org/wgbh/nova/aids/action.html
http://www.learner.org/channel.....mages.html

Does HIV cause AIDS?

http://www.avert.org/evidence.htm
http://www.niaid.nih.gov/factsheets/evidhiv.htm

How does HIV cause AIDS?

http://www.niaid.nih.gov/factsheets/howhiv.htm

What are the different types of HIV?

http://www.avert.org/hivtypes.htm

What is HIV infection?

http://www.niaid.nih.gov/factsheets/hivinf.htm
http://hivinsite.ucsf.edu/InSi.....b-02-01-04

What are the different stages in HIV infection?

http://www.avert.org/hivstages.htm

Where did HIV come from?

http://www.avert.org/origins.htm
http://news.bbc.co.uk/1/hi/health/5012268.stm
http://www.sciencemag.org/cgi/.....ct/1126531
http://app2.capitalreach.com/e.....&day=7

What is HIV (molecular level)?

http://www.cellsalive.com/hiv0.htm
http://hivinsite.ucsf.edu/InSi.....b-02-01-01

Molecular Biology of an HIV infection: an interactive animation

http://www.galaxygoo.org/hiv/hiv_lifecycle.html

Images of HIV

http://www.avert.org/photos.htm

What is the HIV genome?

http://hivinsite.ucsf.edu/InSi.....b-02-01-02

HIV and AIDS: Are You at Risk?

http://www.cdc.gov/hiv/pubs/brochure/atrisk.htm

Why is there stigma related to HIV and AIDS?

http://www.avert.org/aidsstigma.htm

Why do women have a greater chance of getting infected with HIV?

http://www.avert.org/women.htm

Children, HIV and AIDS

http://www.avert.org/children.htm

Older People and the risk of HIV infection

http://www.avert.org/older-people.htm

HIV and AIDS Statistics

http://www.avert.org/statindx.htm

How is HIV transmitted?

http://kidshealth.org/teen/sex...../AIDS.html
http://www.avert.org/faq1.htm
http://www.avert.org/howcan.htm


Concepts and Techniques of HIV Prevention

http://www.avert.org/prevent-hiv.htm



Clinical Overview of HIV Disease

http://hivinsite.ucsf.edu/InSite?page=kb-03-01-01

Are there vaccines against HIV?

http://www.avert.org/vaccines-microbicides.htm
http://www.aidsinfo.nih.gov/Co....._FS_en.pdf
http://www.aidsinfo.nih.gov/Co....._FS_en.pdf
http://www.aidsinfo.nih.gov/Va.....m=Vaccines
http://hivinsite.ucsf.edu/InSi.....b-02-01-06

How is AIDS treated?

http://www.nlm.nih.gov/medline.....cines.html

What are antiretroviral drugs?

http://hivinsite.ucsf.edu/InSite?page=ar-drugs

Who are getting AIDS drugs?

http://www.avert.org/aidsdrugs.htm

What are the tests for HIV infection?

http://www.hivtest.org/subindex.cfm?FuseAction=FAQ
http://www.labtestsonline.org/...../test.html
http://www.labtestsonline.org/...../test.html
http://www.avert.org/testing.htm
http://www.thebody.com/testing.html
http://hivinsite.ucsf.edu/InSi.....b-02-02-01
http://hivinsite.ucsf.edu/InSi.....2-02-02-01
http://hivinsite.ucsf.edu/InSi.....2-02-02-02
http://hivinsite.ucsf.edu/InSite?page=kb-02-02-03
http://hivinsite.ucsf.edu/InSite?page=kb-02-02-04

Epidemiology of HIV/AIDS in the United States

http://hivinsite.ucsf.edu/InSi.....c=kb-01-03

Cryptococcosis and HIV

http://hivinsite.ucsf.edu/InSite?page=kb-05-02-05

Cytomegalovirus and HIV

http://hivinsite.ucsf.edu/InSite?page=kb-05-03-03

What Are Healthy Living Strategies for People with HIV?

http://hivinsite.ucsf.edu/InSite?page=md-daily-00
http://hivinsite.ucsf.edu/InSite?page=kb-03-01-09

Clinical Guidelines for Treatment and Management of HIV

http://www.aidsinfo.nih.gov/Gu.....Guidelines
http://www.aidsinfo.nih.gov/Co.....FS_en.html

Symptom Management Guidelines of HIV

http://hivinsite.ucsf.edu/InSite?page=kb-03-01-06

When to Initiate Antiretroviral Therapy in Individuals with Established HIV Infection

http://hivinsite.ucsf.edu/InSite?page=kb-03-02-05

What are Metabolic Complications of HIV Therapy?

http://hivinsite.ucsf.edu/InSite?page=kb-03-02-10

Effects of HIV on other vaccinations

http://hivinsite.ucsf.edu/InSite?page=kb-03-01-08

Malaria and HIV

http://hivinsite.ucsf.edu/InSite?page=kb-05-04-04

HIV in the developing world

http://hivinsite.ucsf.edu/InSite?page=kbr-03-03-07

HIV in Asia

http://www.thebody.com/whatis/.....l#overview

HIV in the Philippines

http://www.thebody.com/whatis/.....philipines

GAMES

http://www.galaxy-h.gov.uk/new_mainmenu.html


Last edited by adedios on Sat Jan 27, 2007 4:45 pm; edited 2 times in total
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PostPosted: Mon Jul 31, 2006 3:39 pm    Post subject: HIV hiding from drugs in gut Reply with quote

University of California, Davis - Health System
29 July 2006

UC Davis study finds HIV hiding from drugs in gut, preventing immune recovery

Findings indicate need for reevaluation of treatment strategies
(Sacramento, Calif.) -- UC Davis researchers have discovered that the human immunodeficiency virus, the virus that causes AIDS, is able to survive efforts to destroy it by hiding out in the mucosal tissues of the intestine. They also found that HIV continues to replicate in the gut mucosa, suppressing immune function in patients being treated with antiretroviral therapy--even when blood samples from the same individuals indicated the treatment was working. Results of the three-year study appear in the August issue of the Journal of Virology (available online today at http://jvi.asm.org ).

"This is the first longitudinal study to show that, while current HIV therapy is quite successful in reducing viral loads and increasing T-cells in peripheral blood, it is not so effective in gut mucosa," said Satya Dandekar, professor and chair of the Department of Medical Microbiology and Immunology at UC Davis Health System and senior author of the study.

"The real battle between the virus and exposed individuals is happening in the gut immediately after viral infection," she said. "We need to be focusing our efforts on improving treatment of gut mucosa, where massive destruction of immune cells is occurring. Gut-associated lymphoid tissue accounts for 70 percent of the body's immune system. Restoring its function is crucial to ridding the body of the virus."

Results of the study suggest that patients being treated with antiretroviral therapy should be monitored using gut biopsies and that the gut's immune function be restored through earlier antiretroviral treatment and the use of anti-inflammatory medications.

"We found a substantial delay in the time that it takes to restore the gut mucosal immune system in those with chronic infections," Dandekar said. "In these patients the gut is acting as a viral reservoir that keeps us from ridding patients of the virus."

Physicians treating HIV-infected patients have long relied on blood measurements of viral load and T-cell counts when choosing a course of treatment. Viral load is the number of viral particles in a milliliter sample of blood. T-cell counts reflect the number of CD4+ T-cells in the sample. These cells, also called T-helper cells, organize the immune system's attack on disease-causing invaders. They are, however, the targets of the virus and their numbers decrease as the amount of HIV increases, leaving the body vulnerable to a variety of infections.

Last year, Dandekar's team published a study of HIV-infected patients who, despite the lack of treatment, had survived over 10 years with healthy levels of T-cells and suppressed viral loads.

"We looked at their gut lymphoid tissue and did not see loss of T-cells there. This correlated with better clinical outcomes," Dandekar explained.

Those results prompted Dandekar and her team to undertake the current study in which they set out to evaluate the effect of highly active antiretroviral therapy, known as HAART, on viral suppression and immune restoration in gut-associated lymphoid tissue. They followed 10 patients being treated with HAART, taking blood and gut samples before and after three years of treatment. Three of the patients were treated during four to six weeks of first being infected with the virus. The other participants were known to be HIV positive for more than one year.

Hoping to figure out why HAART does not work as well in the gut, Dandekar and her colleagues further examined the post-treatment of gut-associated lymphoid tissue samples. They found evidence of inflammation, which disrupts tissue function, promotes cell death and upsets the normal balance of gut flora. They also found that the activity of genes that control and promote mucosal repair and regeneration were suppressed, while the genes responsible for the inflammatory response were more active than in normal tissue.

Dandekar said these results suggest anti-inflammatory drugs may improve antiretroviral treatment outcomes. She also pointed out that genes involved with the repair and regeneration of gut-associated lymphoid tissue would make excellent drug targets.

Researchers then compared HAART outcomes in those who chose to be treated within the weeks of exposure to those with chronic infection. They discovered that newly infected patients had fewer signs of inflammation at the beginning of the study and experienced greater recovery of the gut mucosal immune system function by the end of it.

Dandekar and her colleagues are currently following additional patients being treated with HAART. Unpublished data on these patients supports the current findings, said Thomas Prindiville, a gastroenterology professor at UC Davis and a co-author of the study.

"What we continue to see is that restoration of immune function is more likely when treatment is started early," said Prindiville. "Starting HAART before T-cell counts fall below 350 cells per cubic milliliter, would preserve immune function and hasten its full recovery."

The team of physicians and researchers plan to keep testing ways of improving the efficacy of antiretroviral therapy in gut-associated lymphoid tissue. These include treating gut inflammation, starting treatment earlier and using gut biopsies to monitor treatment success.

"If we are able to restore the gut's immune response, the patient will be more likely to clear the virus," Prindiville said. "You can't treat any infectious disease without the help of the immune system."


###
The research was supported with grants from the National Institutes of Health.
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PostPosted: Sun Aug 13, 2006 8:09 am    Post subject: HIV infection requires an accomplice: B cells Reply with quote

University of Pittsburgh Medical Center
12 August 2006

HIV infection requires an accomplice: B cells with special protein direct HIV to T cells

New pathway that may aid in treating, preventing HIV reported at AIDS 2006
Toronto, Aug. 12 -- HIV infection of T cells requires activation of a molecule on the surface of B cells, a finding that reveals yet another pathway the virus uses in its insidious attack on the immune system, University of Pittsburgh researchers will report at the XVI International AIDS Conference (AIDS 2006).

"The research supports a new role for B cells in the development and spread of HIV between cells, with important implications for future studies and drug development efforts that focus on reservoirs of HIV in cells other than T cells," said Charles R. Rinaldo, Jr., Ph.D., professor and chairman of the department of infectious diseases and microbiology at Pitt's Graduate School of Public Health (GSPH) and the study's senior author.

Nearly all approved HIV drug regimens and most of those being tested in clinical trials focus on T cells of the immune system, where HIV replicates and thrives. HIV hijacks T cells by binding to a cell membrane molecule called CD4 and to either or both of two other receptors, from which the two strains of HIV, X4 and C5, take their names. Once anchored on the membrane, it's able to slither inside and take command of the cell. But as the Pitt studies have found, there is an important first step in a new pathway involving B cells that express a protein called DC-SIGN. B cells are key players in an immune response.

While these cells themselves do not become infected, they play a pivotal role as an accomplice in HIV's takeover of T cells.

According to the research to be reported by Giovanna Rappocciolo, Ph.D., research assistant professor of infectious diseases and microbiology at GSPH, laboratory studies provide evidence of DC-SIGN in subsets of B cells from both healthy subjects and HIV infected individuals and indicate DC-SIGN is both a point of entry for HIV and necessary for T cell infection.

B cells were isolated from blood samples obtained in 33 healthy subjects and 20 adult patients with HIV from the Multicenter AIDS Cohort Study (MACS). Researchers found about 8 percent of these cells expressed DC-SIGN.

In one set of studies involving cells from the healthy subjects, the team activated DC-SIGN using two molecules that T cells typically engage in their communication with B cells. Once activated, the DC-SIGN B cells were placed in a culture with T cells and a small amount of virus. Within 24 hours, HIV had begun invading the T cells, yet the B cells were spared. Although they did not become infected, B cells nonetheless harbored virus that was transmissible to T cells for up to two days. HIV had little effect on the T cells when B cells were not present in the culture. Pretreating the B cells with a molecule that blocks DC-SIGN before culturing them with both T cells and HIV was a deterrent against T cell infection as well, further proof that to invade T cells, HIV requires DC-SIGN to be expressed on B cells.


###
In addition to Drs. Rinaldo and Rappacciolo, other authors include Paulo Piazza, Ph.D., Craig L. Fuller, Ph.D., Todd A. Reinhart, D.Sc., Simon C. Watkins, Ph.D., David T. Rowe, Ph.D., Mariel Jais, Aki Hoji, B.S., and Phalguni Gupta, Ph.D.

The research was supported by the National Institute of Allergy and Infectious Diseases and the National Cancer Institute, both of the National Institutes of Health.
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PostPosted: Sat Sep 09, 2006 11:03 pm    Post subject: Mayo researchers discover HIV dependence on a human protein Reply with quote

Mayo Clinic
7 September 2006

Mayo researchers discover HIV dependence on a human protein

Essential for infection, protein is potential therapy target
ROCHESTER, Minn. -- Mayo Clinic virologists have discovered that a specific human protein is essential for HIV to integrate into the human genome. Their findings show that when HIV inserts itself into a chromosome, a key step that enables it to establish a "safe haven," it requires a specific protein -- LEDGF/p75 (p75). This protein forms a molecular tether between chromosomes and HIV's integrating protein (integrase). If the connection can be disrupted in the future, it might lead to new therapy for HIV or safer methods of gene therapy. The details appear today in the journal Science.

"How an incoming virus co-opts the cell's assistance as it proceeds to establish its permanently integrated state is a fascinating question," says Eric Poeschla, M.D., the Mayo Clinic virologist who led the research. "It's critical to understand this better because permanently integrated viruses in long-lived cells prevent elimination of HIV. In the future, it will be of interest to examine whether HIV's dependence on p75 can be exploited therapeutically."

How They Did It

The researchers started by noticing that p75 "tethers" HIV integrase to human chromosomes like a molecular rope and also protects it from the cell's protein-degrading machinery. While these were provocative findings, what they meant for the whole virus was unclear.

The Mayo team then developed a highly effective version of a technique called "RNA interference" to strip all detectable p75 from human chromosomes. Without its p75 partner, HIV was highly impaired. An intriguing irony is their use of a crippled version of HIV itself, a virus with proven skill in accessing the human genome, to deliver the RNA interference. As a result, human T cells, HIV's main target, became resistant to HIV. Adding back p75 made them vulnerable again. And adding a "dominant-negative" piece of p75 to the mix, a sort of molecular spanner in the works, further impaired the virus (over 500-fold).

Moreover, the Mayo team showed that each "knot" of the molecular tether was necessary, defining the mechanism in a way an artist would delineate the knots at each end of the rope that links a tetherball to a pole.

"It turns out that the virus needs surprisingly little p75 to integrate," says Dr. Poeschla. "Future studies will want to factor such potential potency into designs of screens for additional key cellular proteins that HIV either appropriates as partners, as in the case of p75, or schemes to evade. Quite a few more likely exist. The challenge is to use the right methods to find them."

How HIV Infects Humans -- Cannot Currently Be Eradicated

Each time HIV reproduces itself, it uses its integrase protein to insert a copy of its genome into a chromosome. That copy becomes a permanent archive of the virus's genetic program, like a tiny file burned onto a computer hard drive. While patients are kept healthy when those copies are "suppressed" with multiple daily antiviral medicines, they are never cured. Stopping the medicines even briefly lets HIV repopulate the body with many millions of copies, like a computer virus spreading around the world from a single infected computer.


###
The Mayo Clinic team also included Manuel Llano, M.D., Ph.D.; Dyana T. Saenz; Anne Meehan, M.D.; Phonphimon Wongthida; Mary Peretz; William H. Walker; and Wulin Teo. Dr. Poeschla's laboratory is supported by the National Institutes of Health and the John H. Tietze Foundation Research Trust.
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PostPosted: Fri Sep 29, 2006 6:09 pm    Post subject: Study defines effective microbicide design for HIV/AIDS prev Reply with quote

Duke University
29 September 2006

Study defines effective microbicide design for HIV/AIDS prevention

DURHAM, N.C. -- Duke University biomedical engineers have developed a computer tool they say could lead to improvements in topical microbicides being developed for women to use to prevent infection by the virus that causes AIDS.

Providing women with improved microbicides is a pressing challenge because women now account for a growing number of new infections worldwide, the researchers said.

By applying fundamentals of physics and chemistry, the researchers developed a computer model that can predict the effectiveness of various microbicidal recipes in destroying human immunodeficiency virus (HIV) before it reaches vulnerable body tissues.

Using the tool, the researchers have determined that a thin, long-lasting coating of microbicide delivered to susceptible tissues in a woman's vagina can significantly reduce the spread of HIV.

The researchers reported their findings in the September 2006 Biophysical Journal.

The findings emphasize a critical role for the "delivery vehicle," the various polymer gels or creams that carry the active antimicrobial ingredients, in determining the success or failure of microbicides, according to the researchers. Yet, they add, most scientists have concentrated on improving the antimicrobial compounds themselves, rather than their delivery.

"There is a huge push to produce microbicides that would have any effectiveness at all in reducing the spread of HIV, particularly in places like Africa and Southeast Asia where the disease is rampant," said David Katz, a professor of biomedical engineering at Duke's Pratt School of Engineering and one of the computer tool's developers. "We are developing methodologies to make the next round of microbicides even better."

"Existing microbicides are excellent in terms of their ability to inactivate HIV," added Anthony Geonnotti, the study's lead investigator, who is a Ph.D. candidate in Katz's laboratory. "Improvements to future generations of microbicides will largely depend on the delivery system and applicators." However, he added, advances made through continued research on new and better drugs should not be discounted.

In addition to their role in drug delivery, microbicide formulations can act as physical barriers or filters to slow HIV's passage from semen into body tissues, Geonnotti explained. That slowing would give the HIV-neutralizing ingredient in the microbicide layer, as well as the body's natural defenses against HIV, more time to work. If left untreated, HIV attacks a person's immune system and can progress to AIDS, acquired immune deficiency syndrome.

The HIV pandemic continues to overwhelm current preventative measures as an estimated 12,000 people contract the infection each day, the researchers said. Increasingly, a disproportionate number of women are becoming infected. In several African countries, for example, HIV infection rates among young women between the ages of 15 and 24 are more than three times higher than among their male counterparts.

Women are about twice as likely as men to contract HIV during vaginal intercourse, according to the federal Centers for Disease Control and Prevention. In developing countries particularly, cultural and socioeconomic inequities between the sexes also can leave women more susceptible.

"In many cases, women lack control over their abilities to protect themselves against the virus," Katz said. "Microbicide development is a response to the demonstrated need for new female-controlled methods for HIV prophylaxis."

In the current study, the researchers developed a mathematical model that simulates the biological interaction between HIV contained in semen and the protective coating that accumulates on the lining of a woman's vagina after she applies a topical microbicide. The model describes the diffusion of the virus and active ingredients into the tissues, as well as the chemical inactivation of virus by the microbicidal agent.

The model is easily adapted to studying different active ingredients and delivery vehicles simply by changing the data entered, the researchers said. For example, researchers might specify the thickness of the expected coating layer, the initial concentration of microbicide in that layer, and the microbicide's documented ability to bind to and disable the viral particles.

The researchers demonstrated their new tool by applying it to the promising microbicide Cyanovirin-N, a protein with anti-HIV activity that has been well documented by other scientists.

"Our results suggest HIV neutralization is achievable if coating thicknesses on the order of 100 microns remain in place after sex," Geonnotti said. One hundred microns is the approximate width of a human hair. "Increased microbicide concentration and potency hasten viral neutralization and diminish penetration of infectious virus through the coating layer, as do ingredients that restrict viral passage," he said.

"Our findings demonstrate the need to pair potent active ingredients with well-engineered delivery vehicles, and they highlight the importance of the dosage form -- especially its ability to restrict viral diffusion and remain in place -- in microbicide effectiveness," Katz added.

More than 20 microbicidal chemical compounds are now in development or testing and five of them have reached the final phase of clinical trials. The Duke group's new model provides a "rational guide" for design specifications that could further improve such microbicides' ability to cut the rate of HIV spread, the researchers said.

The researchers now are conducting studies to experimentally measure the diffusion of viral particles through various delivery vehicles. They also are collaborating with other researchers on developing high-performance polymer gels that might provide a more substantial physical barrier to HIV.
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PostPosted: Mon Oct 02, 2006 11:20 am    Post subject: 2 Americans win Nobel Prize in medicine Reply with quote

2 Americans win Nobel Prize in medicine

By MATT MOORE and KARL RITTER, Associated Press Writers
2 October 2006

STOCKHOLM, Sweden - Americans Andrew Z. Fire and Craig C. Mello won the Nobel Prize in medicine Monday for discovering a powerful way to turn off the effect of specific genes, opening a potential new avenue for fighting diseases as diverse as cancer and AIDS.

The process, called RNA interference, also is being studied for treating such conditions as hepatitis virus infection and heart disease. It is already widely used in basic science as a method to study the function of genes.

Fire, 47, of Stanford University, and Mello, 45, of the University of Massachusetts Medical School in Worcester, published their seminal work in a 1998 paper.


For the full article:

http://news.yahoo.com/s/ap/200.....l_medicine
or
http://www.livescience.com/hum.....nobel.html
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PostPosted: Mon Nov 27, 2006 3:41 pm    Post subject: World AIDS Day Reply with quote

There are just a few days to World AIDS Day!
(1 December 2006) The theme for this year is accountability.
World AIDS Campaign is promoting this under the broader slogan
Stop AIDS - Keep the Promise. Throughout our site you will find
important information about events, campaigns and materials for
World AIDS Day. What will you do?


http://www.worldaidscampaign.info/
http://www.unaids.org/en/
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PostPosted: Wed Dec 13, 2006 1:42 pm    Post subject: Male circumcision reduces HIV risk Reply with quote

University of Illinois at Chicago
13 December 2006

Male circumcision reduces HIV risk, study stopped early

A University of Illinois at Chicago study has been stopped early due to preliminary results indicating that medical circumcision of men reduces their risk of acquiring HIV during heterosexual intercourse by 53 percent.

The study's independent Data Safety and Monitoring Board met Dec. 12 to review the interim data. Based on the board's review, the National Institutes of Health halted the trial and recommended that all men enrolled in the study who remain uncircumcised be offered circumcision.

"Circumcision is now a proven, effective prevention strategy to reduce HIV infections in men," said Robert Bailey, professor of epidemiology in the UIC School of Public Health and principal investigator of the study.

The clinical trial, funded by the National Institute of Allergy and Infectious Diseases and the Canadian Institute of Health Research, enrolled 2,784 HIV negative, uncircumcised men between 18 and 24 years old in Kisumu, Kenya.

Half the men were randomly assigned to circumcision, half remained uncircumcised. All men enrolled in the study received free HIV testing and counseling, medical care, tests and treatment for sexually transmitted infections, condoms and behavioral risk counseling for 24 months.

Study results show that 22 of the 1,393 circumcised men in the study contracted HIV, compared to 47 of the 1,391 uncircumcised men. In other words, circumcised men had 53 percent fewer HIV infections than uncircumcised men.

Until now, public health organizations have not supported circumcision as a method of HIV prevention due to a lack of randomized controlled trials.

"With these findings, the evidence is now available for donor and normative agencies, like WHO and UNAIDS, to actively promote circumcision in a safe context and along with other HIV prevention strategies," Bailey said.

"Circumcision cannot be a stand-alone intervention. It has to be integrated with all the other things that we do to prevent new HIV infections, such as treating sexual transmitted diseases and providing condoms and behavioral counseling," Bailey said. "We can't expect to just cut off a foreskin and have the guy go on his merry way without additional tools to fight against getting infected."

Opponents of circumcision have speculated that circumcised men may feel they are not at risk of contracting HIV and may be more likely to engage in risky behavior. The Kenya study suggests that circumcision did not increase risky behavior among circumcised or uncircumcised men, according to Bailey.

"Both uncircumcised and circumcised men are reducing their sexual risk behavior," he said, "which indicates that our counseling is doing some good."

The study also evaluated the safety of circumcision in a community health clinic with specially trained practitioners. There were no severe or lasting complications from circumcision. However, 1.7 percent of surgeries resulted in mild complications, such as bleeding or infection.

Bailey said that promoting circumcision in Africa must be done in conjunction with proper technical training and medical tools, equipment and supplies necessary to perform large numbers of circumcisions safely.

"Already, there are large numbers of boys and young men who are seeking circumcision in areas of Africa where men are not traditionally circumcised," he said. "The danger is that unqualified practitioners will fill a niche by providing circumcision, but with much higher complication rates."

An estimated 30 million people in Africa are infected with HIV/AIDS and more than 90 percent of HIV infections in adults result from heterosexual intercourse. In Kisumu, the third-largest city in Kenya, an estimated 26 percent of uncircumcised men are HIV infected by age 25.

"This study will likely not have a large impact on the incidence of HIV/AIDS in the United States or Europe where heterosexual transmission of HIV is low compared with areas like sub-Saharan Africa and parts of Asia," Bailey said. "However, there are other proven health benefits of circumcision, including better hygiene, fewer urinary tract infections, and less risk of cervical cancer in the partners of circumcised men."

The armamentarium of HIV prevention strategies is very small, according to Bailey. The only other strategy proven effective is the use of antiretroviral drugs to reduce transmission from mother to child.

If a significant proportion of men in a population get circumcised, it will have an enormous impact on preventing HIV infection in men, as well as reducing infections in women, Bailey said.


###
Co-investigators of the study include Stephen Moses and Ian Maclean at the University of Manitoba, Jekoniah Ndinya-Achola at the University of Nairobi, Corette Parker at Research Triangle International, Kawango Agot at UNIM Project, John Krieger at University of Washington, and Richard Campbell at UIC.

During the past two decades, more than 40 observational epidemiological studies and one previous clinical trial have reported an association between male circumcision and a reduced risk of HIV infection.

On Dec. 12, the NIH stopped another clinical trial of male circumcision undertaken by investigators in Uganda and at Johns Hopkins University, after the study's Data Safety Monitoring Board reviewed the preliminary results and found a protective effect similar to that found in Bailey's study.

For more information about UIC, visit www.uic.edu.

[Editors Note: Extended interview as MP3 audio file available upon request. Photographs of Dr. Bailey are available at http://photo.lib.uic.edu/gallery/bailey]
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PostPosted: Fri Feb 23, 2007 9:09 am    Post subject: Circumcision: A proven strategy to prevent HIV Reply with quote

University of Illinois at Chicago
22 February 2007

Circumcision: A proven strategy to prevent HIV

Male circumcision significantly reduces the risk of acquiring HIV in young African men, according to a study led by University of Illinois at Chicago professor of epidemiology Robert Bailey.

The study is published in the Feb. 24 issue of The Lancet.

Researchers conducted a clinical trial enrolling 2,784 HIV negative, uncircumcised men between 18 and 24 years old in Kisumu, Kenya, where an estimated 26 percent of uncircumcised men are HIV infected by age 25. The majority of the men in the study were Luo, an ethnic group that does not traditionally practice circumcision.

Half the men were randomly assigned to circumcision and half the men remained uncircumcised for two years.

Participants received free HIV testing and counseling, medical care, tests and treatment for sexually transmitted infections, condoms and behavioral risk counseling during periodic assessments throughout the study.

The clinical trial found that 47 of the 1,391 uncircumcised men contracted HIV, compared to 22 of the 1,393 circumcised men.

"Our study shows that circumcised men had 53 percent fewer HIV infections than uncircumcised men," said Bailey. "We now have very concrete evidence that a relatively simple surgical procedure can have a very large impact on HIV."

The study also measured adverse events related to surgery. According to Bailey, in 1.7 percent of the surgeries there were minor complications -- usually bleeding or a mild infection. There were no severe adverse events.

Bailey cautions that circumcised men may feel they are protected from becoming HIV infected and may be more likely to engage in risky behavior.

"Circumcision is by no means a natural condom," said Bailey. "We do know that some circumcised men become infected with HIV. But we did find that the circumcised men in our study did not increase their risk behaviors after circumcision. In fact, all men in the trial increased their condom use and reduced their number of sexual partners."

The authors conclude that circumcision will be most effective if it is integrated with other prevention and reproductive health services.

"We have wonderful new drugs to at least maintain people for many years with the virus, but meanwhile more people are getting infected at a rate of approximately 5,000 persons per day," said Bailey. "We cannot treat our way out of this epidemic. Prevention of new infections is crucial."

Simulation models estimate that millions of new HIV infections, tens of thousands of deaths, and several million dollars could be saved if male circumcision became routine in sub-Saharan Africa.

"This is really the first good news we've had in quite a long time. If we can reduce the risk of infection by such a substantial amount then we can save a lot of lives."

In December the National Institutes of Health halted Bailey's trial of male circumcision after the study's independent data safety monitoring board reviewed the preliminary results and recommended that all men enrolled in the study who remain uncircumcised be offered circumcision due to the clearly protective effect.


###
The trial was funded by the National Institute of Allergy and Infectious Diseases and the Canadian Institute of Health Research.

Co-investigators of the study include Stephen Moses, Ian Maclean, and Kawango Agot at the University of Manitoba; Corette Parker at RTI International; John Krieger at University of Washington; Carolyn Williams at National Institute of Allergy and Infectious Diseases; Richard Campbell at UIC; and Jekoniah Ndinya-Achola at University of Nairobi.

For more information about UIC, visit www.uic.edu
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PostPosted: Tue Mar 06, 2007 7:19 am    Post subject: Risk of HIV transmission highest early in infection Reply with quote

Infectious Diseases Society of America
5 March 2007

Risk of HIV transmission highest early in infection

New evidence suggests that the risk of HIV transmission may be highest in the early stages of infection. According to a study published in the April 1 issue of The Journal of Infectious Diseases, now available online, early infection accounted for nearly half of all transmission occurrences in an HIV-infected population in the province of Quebec, Canada.

Bluma Brenner, PhD, and Mark Wainberg, PhD, of the McGill AIDS Centre in Montreal, and colleagues from several hospitals and health clinics in Canada studied HIV transmission through phylogenetic analysis—essentially, drawing the virus’s family tree. The technique follows the history of a virus as it spreads from one person to another by looking at the evolution of viral genetic material in infected individuals.

Drs. Brenner, Wainberg, and colleagues found that 49 percent of early infections formed phylogenetic clusters—very close branches on the family tree. This indicated that a large portion of HIV acquisition could be attributed to individuals transmitting the virus who were themselves in the early stages of infection, before the virus had had time to mutate much. Therefore, early infection—also known as primary infection—which represented “less than 10 percent of the total samples, disproportionately accounted for about half of subsequent transmission events.”

A high viral load associated with early HIV infection is what makes newly infected individuals so infectious, according to Drs. Brenner and Wainberg. In an editorial accompanying the article, authors Deenan Pillay, MD, of the Health Protection Agency and University College London, and Martin Fisher, MD, of the Brighton and Sussex University Hospitals, pointed out that diagnosis of HIV reduces the risk of transmission. But, they note, symptoms of primary HIV infection are non-specific. Only a small proportion of infected individuals are diagnosed in early infection, thus compounding the difficulties in preventing transmission at that stage of infection.

“The early infection stage can be entirely asymptomatic,” Dr. Wainberg added. “This is why people who are recently infected may not know it, and will probably often test negative by conventional antibody screening. Hence, we must do a much better job of identifying recently infected people if we are to be able to counsel them to modify high-risk sexual behavior and desist from transmitting the virus.”

He suggested the development of affordable tests such as polymerase chain reaction assays to directly monitor the presence of the virus, instead of relying on the current method of antibody screening.

In addition, Dr. Pillay and Fisher asserted that more innovative and effective prevention strategies are needed to stem HIV transmission during primary infection and block the spread of drug-resistant viruses.

###
Founded in 1904, The Journal of Infectious Diseases is the premier publication in the Western Hemisphere for original research on the pathogenesis, diagnosis, and treatment of infectious diseases; on the microbes that cause them; and on disorders of host immune mechanisms. Articles in JID include research results from microbiology, immunology, epidemiology, and related disciplines. It is published under the auspices of the Infectious Diseases Society of America (IDSA). Based in Alexandria, Va., IDSA is a professional society representing nearly 8,000 physicians and scientists who specialize in infectious diseases. Nested within the IDSA, the HIV Medicine Association (HIVMA) is the professional home for more than 2,600 physicians, scientists and other health care professionals dedicated to the field of HIV/AIDS. HIVMA promotes quality in HIV care and advocates policies that ensure a comprehensive and humane response to the AIDS pandemic informed by science and social justice.For more information, visit www.idsociety.org.
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PostPosted: Wed Apr 11, 2007 1:18 pm    Post subject: Rapid oral HIV test shows great promise according to MUHC-le Reply with quote

McGill University
11 April 2007

Rapid oral HIV test shows great promise according to MUHC-led research

A convenient, easy to use, and rapid alternative to blood-based HIV testing may become the new standard for field testing according to a new MUHC study. The study shows that the oral fluid-based OraQuick HIV1/2 test is 100 per cent accurate and patients’ preferred choice.

Senior and lead author Dr. Nitika Pai, a postdoctoral fellow at the McGill University Health Centre (MUHC), and her colleagues tested 450 individuals for HIV infection at the Mahatma Gandhi Institute of Medical Sciences in Sevagram India. Thirty two percent were found to be HIV positive. Researchers compared the diagnostic accuracy of the OraQuick test from two samples - one obtained from oral fluid (saliva) and the other from a blood-based finger stick - with traditional blood tests. They demonstrated that the oral fluid test had 100 per cent accuracy versus the finger-stick blood test, which showed one false positive (99.7 per cent specificity). There was little reported discomfort during sample collection for the oral test, but 66 per cent of the individuals reported discomfort with the finger testing.

Although the oral OraQuick test has been approved by the US Food and Drug Administration, some previous studies had indicated that it was not sufficiently precise. As a result, the Centre for Disease Control (CDC) called for more definitive studies leading to this study in rural India.

"Based on our findings, the oral test is the preferred choice for HIV field testing by rural Indians," says Dr. Pai, a physician epidemiologist supported by the Canadian HIV Trials Network. "The other advantages are that results are available within 40 minutes compared to the standard blood test, which takes up to two weeks. This test can also be performed by health workers with minimal training, eliminating the need for specialist laboratory technicians."

"Rapid point of care HIV testing is a very important component of HIV control initiatives and programs. In particular, non-invasive, simple, accurate oral fluid-based, rapid tests have the potential to make a big impact on HIV screening. They open the door to the possibility of home-based HIV testing," she says.

###
The study is published today in the international, peer-reviewed, online publication PLoS ONE, produced by the Public Library of Science (PLoS).

This research was funded through the National Institutes of Health Fogarty AIDS International Research and Training Grant.

The Research Institute of the McGill University Health Centre (RI MUHC) is a world-renowned biomedical and healthcare hospital research centre. Located in Montreal, Quebec, the Institute is the research arm of the MUHC, a university health centre affiliated with the Faculty of Medicine at McGill University. The Institute supports over 500 researchers, nearly 1,000 graduate and post-doctoral students and operates more than 300 laboratories devoted to a broad spectrum of fundamental and clinical research. The Research Institute operates at the forefront of knowledge, innovation and technology and is inextricably linked to the clinical programs of the MUHC, ensuring that patients benefit directly from the latest research-based knowledge. For further details visit: http://www.muhc.ca/research
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PostPosted: Tue Apr 24, 2007 9:11 am    Post subject: HIV infection appears to increases the risk of heart attack Reply with quote

Massachusetts General Hospital
24 April 2007

HIV infection appears to increases the risk of heart attack

More research needed to clarify underlying factors, how best to treat
Researchers from Massachusetts General Hospital (MGH) have found that infection with HIV, the virus that causes AIDS, is also associated with increased risk of myocardial infarction or heart attack. While rates of several cardiovascular risk factors were also increased in study participants infected with HIV, the increased incidence of heart attack was beyond what could be explained by risk factor differences. The report will be published in the Journal of Clinical Endocrinology and Metabolism and has been released online.

"Our study shows a higher incidence of myocardial infarction and major cardiovascular risk factors in HIV-infected patients, compared with noninfected patients," says Steven Grinspoon, MD, of the MGH Program in Nutritional Metabolism and Neuroendocrine Unit, the report's senior author. "Those findings indicate that those infected with HIV should be assessed for cardiovascular risk factors and that we urgently need to develop strategies to modify those risks."

It has been recognized that many HIV-infected individuals have metabolic abnormalities – including altered levels of blood lipids such as cholesterol, insulin resistance, type 2 diabetes, and changes in fat distribution in the body. Researchers have reported that patients taking antiretroviral medications may have increased risk of heart attacks, but few studies have directly examined whether HIV-infected patients in general have more heart attacks than non-infected individuals do.

The researchers took advantage of the Research Patient Data Registry, a database of demographic and diagnostic information on more than 1.7 million patients treated at MGH and Brigham and Women's Hospital since 1993. They compared information on almost 4,000 HIV-infected patients with data from more than one million patients without HIV. Study participants were aged 18 to 84 and were seen at least twice during the study period of almost eight years. Any patient whose initial visit was for a heart attack was excluded from the study group.

Across all age groups included, the risk of myocardial infarction occurring after the initial hospital visit was markedly higher for those infected with HIV. Although traditional cardiovascular risk factors – such as elevated lipid levels, diabetes and hypertension – also were more common among the HIV-infected patients and did account for some increased risk, the increased risk for heart attack associated with HIV remained significant even when adjusted for those risk factors. Overall, the risk of heart attack was almost doubled in all those with HIV and was almost tripled among women.

"Followup studies are needed to better determine why myocardial infarction rates are higher in HIV patients, which risk factors drive this risk most, and how smoking – which we weren't able to completely evaluate in this study – affects this risk," Grinspoon says. "We also need to analyze the relationship of antiretroviral medications to cardiovascular risk. HIV medications save lives, and patients should continue taking them as prescribed; but we want physicians to be aware of these increased heart attack rates, watch risk factors carefully and appropriately target their treatment." Grinspoon is an associate professor of Medicine at Harvard Medical School.


###
The study's lead author is Virginia Triant, MD, MPH, of the MGH Division of Infectious Diseases. Additional co-authors are Hang Lee, PhD, MGH Biostatistics, and Colleen Hadigan, MD, MPH, formerly of the MGH Neuroendocrine Unit and Program in Nutritional Metabolism and now at the National Institutes of Health (NIH). The study was supported by grants from the NIH and the Mary Fisher Clinical AIDS Research and Education Fund.

Massachusetts General Hospital, established in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of nearly $500 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, transplantation biology and photomedicine. MGH and Brigham and Women's Hospital are founding members of Partners HealthCare System, a Boston-based integrated health care delivery system.
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PostPosted: Fri May 11, 2007 6:38 am    Post subject: UCLA AIDS Institute researchers find a peptide that encourag Reply with quote

University of California - Los Angeles
11 May 2007

UCLA AIDS Institute researchers find a peptide that encourages HIV infection

New discovery could serve as a tool for gene therapy
UCLA AIDS Institute researchers have discovered that when a crucial portion of a peptide structure in monkeys that defends against viruses, bacteria and other foreign invaders is reversed, the peptide actually encourages infection with HIV.

The findings, published in the April issue of AIDS Research and Human Retroviruses, could pave the way for the use of such peptides in gene therapy using HIV-based vectors as the delivery method.

"Although it may seem counterintuitive to value or even study a peptide that increases the ability of HIV-1 to enter a broad range of human cells, retroviral vectors are currently being explored as vehicles for gene therapy," the authors wrote. "In this area, at least, agents that enhance retroviral uptake could contribute to an emerging field of medicine."

"So many people have tried to deliver genes into different kinds of cells," said study co-author Shen Pang, adjunct associate professor at the UCLA School of Dentistry and a member of the UCLA AIDS Institute. "If you know of some method that can enhance gene delivery, you would have a useful tool."

Retrocyclin-1 (RC-100) is a circular peptide that has been shown in previous studies to inhibit the infection of CD4 cells with HIV. RC-111 is also cyclic and has the same amino acid sequence as retrocyclin-1. In both peptides, the amino acids are strung like 18 beads along the molecule's backbone. The amino acids in RC-111, however, are in reverse order.

The researchers had initially wanted to quantify previous research by Dr. Robert I. Lehrer, distinguished professor of medicine in the division of infectious diseases at the David Geffen School of Medicine at UCLA and a co-author of the present study. Unexpectedly, the researchers discovered that while retrocyclin-1 inhibited infection of CD4 cells with HIV-1 by about 95 percent, the RC-111 variant enhanced viral infection five-fold.

There are three structural varieties of peptides, also known as defensins — alpha, beta and theta, Lehrer said. Humans have only alpha and beta; monkeys have all three.

"Here's a peptide whose normal structure allows it to protect against viruses, yet if you make the same peptide and place its amino acids in a reverse order, that lets the virus in," Lehrer said. "We would like to learn why it happens, but at the moment there's no explanation for this paradoxical result."

Still, the findings seem to show promise in gene therapy.


###
In addition to Pang and Lehrer, study researchers were Rose Q. Wang, Wei Wang, Junying Zheng, Sina Tabibian, Yimin Xie, Jun song, Alan J. Waring, Robert Chiu, Otto O. Yang and Irvin S.Y. Chen.

Grants from the National Institutes of Health and the U.S. Department of Defense funded the study.

Established in 1992, the UCLA AIDS Institute is a multidisciplinary think-tank drawing on the skills of top-flight researchers in the worldwide fight against HIV/AIDS, the first cases of which were reported in 1981 by UCLA physicians. Institute members include researchers in virology and immunology, genetics, cancer, neurology, ophthalmology, epidemiology, social science, public health, nursing, and disease prevention. Their findings have led to advances in treating HIV, as well as other diseases, such as hepatitis B and C, influenza, and cancer.
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PostPosted: Tue May 29, 2007 8:59 am    Post subject: HIV and malaria combine to adversely affect pregnant women a Reply with quote

University of Toronto
28 May 2007

HIV and malaria combine to adversely affect pregnant women and their infants

Toronto, On -- University of Toronto researchers have uncovered the basis by which pregnant women protect themselves against malaria and have also discovered how the HIV virus works to counteract this defence. The research could lead to improved vaccines for pregnant women in malaria-ravished regions.

Malaria is a parasitic disease spread by mosquitoes that kills more than one million people every year. While the disease affects mostly children, malaria also severely affects pregnant women, especially during their first pregnancy, accounting for an estimated 400,000 cases of severe anaemia and 200,000 infant deaths each year. With the recent realization that HIV further aggravates pregnancy-associated malaria (PAM) there is an urgent need to understand these diseases during pregnancy and turn this knowledge into effective therapies.

Until now the mechanisms by which pregnant women defend themselves against malaria and how HIV impairs this defence have been unknown, but a paper published in PLoS Medicine (Public Library of Science) pinpoints how the virus targets the immune response in pregnant women. "PAM can be a deadly condition that leaves mothers and their children particularly vulnerable," says Professor Kevin Kain, an infectious disease specialist and lead author of the study. "We set out to understand how women acquire protection against malaria during pregnancy and how HIV infection impairs that protection. By understanding how they lost protection in the face of HIV we learned how they acquired protection against malaria in the first place."

PAM occurs when red blood cells infected with malaria parasites gather in the placenta resulting in damage to both mother and developing infant. First-time mothers are particularly susceptible to PAM whereas women in subsequent pregnancies become protected against PAM. Having HIV results in this loss of protection and makes them as susceptible as first-time mothers.

To uncover how HIV affects PAM, Kain and his team collected samples from women in the first pregnancy as well as from women in their subsequent ones living in the Kenyan region where malaria is common. The researchers demonstrated that protection to PAM is mediated by a special type of antibody that allows women to preferentially clear the parasites in their placentas. They found that HIV-infected women lose these antibodies and again become susceptible to the ravages of PAM.

The findings, according to Kain, may help in the development of PAM vaccines. "This is only the first step in creating therapeutics to treat this devastating disease," he stresses. "We hope to help translate this knowledge into more effective vaccines designed to generate these types of protective antibodies."

###
The study was funded by Canadian Institutes of Health Research (CIHR) Team grant in Malaria, Genome Canada through the Ontario Genome Institute, and the McLaughlin-Rotman Centre/MCMM.
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PostPosted: Wed Jun 20, 2007 8:49 am    Post subject: Male circumcision overstated as prevention tool against AIDS Reply with quote

Public Library of Science
20 June 2007

Male circumcision overstated as prevention tool against AIDS

New study finds the key to understanding the global spread of AIDS is the size of the infected prostitute community around the world
In new academic research published today in the online, open-access, peer-reviewed scientific journal PLoS ONE, male circumcision is found to be much less important as a deterrent to the global AIDS pandemic than previously thought. The author, John R. Talbott, has conducted statistical empirical research across 77 countries of the world and has uncovered some surprising results.

The new study finds that the number of infected prostitutes in a country is the key to explaining the degree to which AIDS has infected the general population. Prostitute communities are typically very highly infected with the virus themselves, and because of the large number of sex partners they have each year, can act as an engine driving infection rates to unusually high levels in the general population. The new study is entitled “Size Matters: The Number of Prostitutes and the Global HIV/AIDS Pandemic” and is freely available online at the PLoS ONE publication website at http://plosone.org/doi/pone.0000543

The study has a number of important findings that should impact policy decisions in the future. First, male circumcision, which in previous studies had been found to be important in controlling AIDS, becomes statistically irrelevant once the study controls for the number of prostitutes in a country. The study finds that the more Muslim countries of North Africa do indeed suffer much less AIDS than southern and western Africa, but this lower prevalence is not due to higher numbers of circumscribed males in these Muslim communities, but rather results from the fact that there are significantly fewer prostitutes in northern Africa on a per capita basis. It appears that religious families in the north, specifically concerned fathers and brothers, do a much better job protecting their daughters from predatory males than do those in the south. A history of polygamy in these Muslim communities does not appear to contribute to hi gher AIDS prevalence as previously speculated. In a frequently cited academic paper, Daniel Halperin, an H.I.V. specialist at the Harvard Center for Population and Development and one of the world’s leading advocates for male circumcision, weighted results from individual countries by their population. When this artificial weighting was removed Talbott found that circumcision was no longer statistically significant in explaining the variance in AIDS infection rates across the countries of the World.

Second, to date, there has not been an adequate explanation as to why Africa as a continent is experiencing an AIDS epidemic far in excess of any other region of the world with some African countries’ prevalence rates exceeding 25% of the adult population and tens of millions dying from the disease on the continent. Talbott’s new study suggests that the reason is that Africa as a whole has four times as many prostitutes as the rest of the word and they are more than four times as infected. Some southern Africa countries have as many as 7% of their adult females infected and working as prostitutes while in the developed world typically this percentage of infected prostitutes is less than .1%. If these 7% of infected prostitutes in Africa sleep with five men in a week that means they are subjecting 35% of the country’s male population to the virus weekly. The virus is not easy to transmit heterosexually, b ut over time with multiple exposures, infection is inevitable. These men then act as a conduit to bring the virus home to their villages, their other casual sex partners and to their wives.

The study has important policy implications. Several international AIDS organizations have begun to provide funding for male circumcisions as a deterrent to AIDS. While male circumcision may indeed reduce the risk of transmission by some 50% to 60% in each sexual encounter, reducing single encounter transmission rates alone cannot control the epidemic. The reason is that individuals in highly infected countries have multiple contacts with the infected so reducing transmission rates only defers the inevitable.

The real question is what can be done with the prostitute community. Outlawing the world’s oldest profession would most likely prove to be ineffective. If the profession can be legalized and treatment and care provided to the practitioners, there would be much more reason to be hopeful. But, and this is the key, programs of action can not just be voluntary. Too many innocent people are dying and there is too much disregard for human life among infected prostitutes to leave treatment decisions solely up to them. A program of testing and treatment for prostitutes must be mandatory and those that refuse treatment must be held liable.

Many international aid organizations are against such mandatory treatment programs for prostitutes as they find them to be discriminatory, violate the individual’s human rights and are perceived as an attack on female prostitutes who are viewed as victims of gender and income inequality. Such organizations do not properly weigh the loss of human rights and life itself that this virus, unleashed on a community, is causing. This virus, itself, is a violation of human rights and we must do everything in our power to stop it. To argue we should do nothing about infected prostitutes during an AIDS epidemic because of a fear of creating a stigma against the infected would be like an animal rights activist claiming that a rabid dog must be allowed to run free in a neighborhood regardless of how many men women and children he infected and killed.

It is not surprising that computer models rarely show the virus reaching epidemic proportions; it is very hard to transmit this illness heterosexually. Only when model building researchers introduce a highly sexually active infected subset of “prostitutes” to their mathematical models does the infection spread exponentially to the general population.

###
Disclaimer

The following press release refers to an upcoming article in PLoS ONE. The release has been provided by the article authors and/or their institutions. Any opinions expressed in this are the personal views of the contributors, and do not necessarily represent the views or policies of PLoS. PLoS expressly disclaims any and all warranties and liability in connection with the information found in the release and article and your use of such information.

Contact:
John Talbott (corresponding author)
Email: johntalbs@hotmail.com Tel: +1 646 202 0903

Citation: Talbott JR (2007) Size Matters: The Number of Prostitutes and the Global HIV/AIDS Pandemic. PLoS ONE 2(6): e543. doi:10.1371/journal.pone.0000543

PLEASE ADD THE LINK TO THE PUBLISHED ARTICLE IN ONLINE VERSIONS OF YOUR REPORT: http://www.plosone.org/doi/pone.0000543
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PostPosted: Mon Jul 16, 2007 11:49 am    Post subject: Clues to future evolution of HIV come from African green mon Reply with quote

University of Arizona

Clues to future evolution of HIV come from African green monkeys

16 July 2007

Monkey viruses related to HIV may have swept across Africa more recently than previously thought, according to new research from The University of Arizona in Tucson.

A new family tree for African green monkeys shows that an HIV-like virus, simian immunodeficiency virus, or SIV, first infected those monkeys after the lineage split into four species. The new research reveals the split happened about 3 million years ago.

Previously, scientists thought SIV infected an ancestor of green monkeys before the lineage split, much longer ago.

"Studying SIV helps us learn more about HIV," said the paper's first author Joel Wertheim, a doctoral candidate in the UA department of ecology and evolutionary biology. "This finding sheds light on the future direction of HIV evolution."

All SIVs and HIVs have a common ancestor, added senior author Michael Worobey, a UA assistant professor of ecology and evolutionary biology.

The new work suggests African green monkeys' SIVs, or SIVagm, may have lost their virulence more recently than the millions of years previously thought. Green monkeys almost never get sick from SIVagm. If SIVagm was once a monkey killer, the change in its virulence may shed light on the future course and timing of the evolution of HIV.

The new research also challenges the idea that one ancient SIV was transmitted vertically, down through time, and evolved into many SIVs as its original host diverged into many different species.


Wertheim and Worobey suggest various SIVs arose because SIVs were transmitted horizontally, between primate species, and evolved into a new host-specific form only after transmission.

HIV arose from chimpanzee SIV that was transmitted to humans, probably when people had contact with chimpanzee blood from hunting and butchering the animals, Worobey said.

The team's research article, "A Challenge to the Ancient Origin of SIVagm Based on African Green Monkey Mitochondrial Genomes," is in the July issue of PLoS Pathogens and can be found at http://www.plospathogens.org. The National Science Foundation and National Institutes of Health funded the research.

Previous research had sketched out the family trees, or phylogenies, of the four species of African green monkeys and their accompanying SIVagm, but Wertheim wanted to know more.

"I wasn't convinced by the evidence out there that these monkeys were infected before they speciated," Wertheim said. "So I set out to perform a rigorous test of that hypothesis."

He extensively sequenced the mitochondrial DNA genes of the four species of African green monkeys. Mitochondrial DNA is passed from mother to child.

The four green monkeys he studied are the sabaeus monkey, Chlorocebus sabaeus, which lives in western Africa; the tantalus monkey, Chlorocebus tantalus, which is found in central Africa; the vervet monkey, Chlorocebus pygerythrus, which lives in eastern and southern Africa; and the grivet monkey, Chlorocebus aethiops, which lives in northeast Africa.

The scientists used the genetic sequences to sort out the ancestral relationships among the different species of monkeys. Other researchers had already constructed phylogenies for the four different SIVagm that showed their relationships.

"We put together, for the first time, a really solid phylogeny for African green monkeys, which we didn't have before," Worobey said.

If the monkeys' ancestor had been infected with an ancient SIV, the SIV family tree should match that of the four monkey species.

The trees didn't match.

"The monkey tree was significantly different from the virus tree," Wertheim said.

The researchers then looked at the geographic distribution of the four African green monkey species. The relative ages and information on which pairs of SIVagm were most closely related revealed the probable transmission route of SIV.

The researchers hypothesize that the infection started in the westernmost species, sabaeus monkeys, moved east into neighboring tantalus monkeys, and then took one of two paths: southeast into vervets and then north into grivets or northeast into grivets and then south into vervets.

Wertheim said, "I was surprised that the geography could explain the virus phylogenetic tree, how well it fit. You just look and -- there it is!"

The UA researchers suggest that in the border zones where two African green monkey species' ranges come in contact, transmission probably happened during interspecies sexual encounters or fights. Wertheim pointed out that hybrid monkeys have been seen in the wild in the border zones.

Worobey said, "Some of the trends we see give new evidence on how quickly or slowly these changes take place."

Citing some laboratory research that suggests HIVs from the late 1980s are more virulent than HIVs from the 2000s, Worobey added, "For HIV, the really cool thing is that these changes can take place on a more rapid timeline that previously thought."

Wertheim adds, "Understanding how emerging infectious diseases evolve in their natural host organism helps us understand the disease's possible trajectory."

The team's next steps are figuring out exactly when SIV infected African green monkeys and studying SIVs in other species of monkeys.


###


Related websites:

Michael Worobey
http://eebweb.arizona.edu/Facu.....robey.html

UA Department of Ecology and Evolutionary Biology
http://eebweb.arizona.edu/index.htm
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PostPosted: Sat Jul 21, 2007 10:20 am    Post subject: AIDS Abated: Genome scans illuminate immune control of HIV Reply with quote

Week of July 21, 2007; Vol. 172, No. 3 , p. 35

AIDS Abated: Genome scans illuminate immune control of HIV
Brian Vastag

Some people who contract HIV, the virus that causes AIDS, maintain low amounts of the virus in their bodies for years. These long-term nonprogressors—so called because a decade or more can pass before they develop full-blown AIDS—have attracted great attention from researchers.

For the full article:

http://sciencenews.org/articles/20070721/fob1.asp
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PostPosted: Wed Jul 25, 2007 1:37 pm    Post subject: Carnegie Mellon scientists find key HIV protein makes cell m Reply with quote

Carnegie Mellon University
25 July 2007

Carnegie Mellon scientists find key HIV protein makes cell membranes bend more easily

Discovery should improve modeling to understand, thwart infection and design therapies
PITTSBURGH -- Carnegie Mellon University scientists have made an important discovery that aids the understanding of why HIV enters immune cells with ease. The researchers found that after HIV docks onto a host cell, it dramatically lowers the energy required for a cell membrane to bend, making it easier for the virus to infect immune cells. The finding, in press in Biophysical Journal, will provide vital data to conduct future computer simulations of HIV dynamics to help further drug discovery and prevent deadly infections.

“We found that HIV fusion peptide dramatically decreases the amount of energy needed to bend a cell-like membrane,” said Stephanie Tristram-Nagle, associate research professor of biological physics at Carnegie Mellon. “This helps membranes to curve, a necessary step for HIV to fuse with an immune cell as it infects it.”

The Carnegie Mellon scientists used X-rays to study how HIV fusion peptide (part of a larger protein) affected the energy of manufactured lipid bilayers made to mimic normal cell membranes. Lipid bilayers provide a protective barrier for the cell against intruders, yet also contain molecules to recognize and communicate with other cells or get nutrients. Cells also communicate with one another via small, membrane-bound vesicles that contain proteins or other molecular cargo. When delivering their goods, vesicles from one cell fuse with the outermost membrane of another cell to form a series of hybrid structures called fusion intermediates.

Through evolution, viruses have also become skilled at fusing with cells to unload their genetic contents, which turn host cells into virus-producing factories. In the case of HIV, a molecule called gp120 initially helps the virus lock onto its host T cell, a cell critical for maintaining immunity. Another protein — gp41 — then enables HIV to penetrate a T-cell membrane. Fusion takes place specifically through a short stretch of gp41 called fusion peptide 23, or FP-23 for short. Prior studies have shown that FP-23 fuses with, and can even break apart, blood cells and other man-made, cell-like structures called liposomes.

FP-23 likely plays several roles in viral fusion, according to the researchers. One role already suspected is that FP-23 attaches to its T cell victim to facilitate a change in the shape of gp41, which in turn drives uptake of HIV RNA and proteins by the T cell. But the Carnegie Mellon work suggests that FP-23 plays another, equally important function — reducing the free energy of curved fusion intermediates. These fleeting shapes arise and disappear as HIV enters a T cell.

Normally, a cell membrane resists bending. Scientists can quantify the energy needed to overcome this resistance. The Carnegie Mellon team found that FP-23 reduces the energy required to penetrate an artificial cell membrane by up to 13 fold, depending on the thickness of that membrane.

“Reducing this energy should help explain in part how HIV infection occurs so readily,” said Tristram-Nagle. “Our findings definitely will change how theoreticians think about virus-cell interactions. This same phenomenon could provide a general way that viruses use to infect cells, so it will be exciting to look at other viral systems with our experimental method,” she said.

Many different viruses could enter cells by efficiently lowering the energy required to penetrate a cell’s outer membrane, according to Tristram-Nagle and her collaborator, John Nagle, professor of physics and biological sciences at Carnegie Mellon.

The Carnegie Mellon scientists used X-rays to detect the effect of FP-23 on lipid bilayers that mimic cell membranes. Lipid bilayers form different phases that change with temperature, but the “fluid” phase is the most biologically relevant. Using X-ray diffuse scattering, the team quantified structural properties of different lipid bilayers seeded with FP-23 peptides. The lipid bilayers varied in their thicknesses, which affects the stiffness of cell membranes.

The research was conducted at Cornell University’s CHESS synchrotron, which provides a high-intensity source of X-rays for various studies. In their next trip to this facility, the team plans to study FP-23 together with cholesterol, a molecule known to modulate the stiffness of cell membranes.

###
The work was supported by the National Institute of General Medicine. The Cornell High Energy Synchrotron Source is funded by the National Science Foundation. To view the Biophysical Journal article, visit
www.biophysj.org/cgi/rapidpdf/.....7.109181v1

For more on this research, see
www.cmu.edu/mcs/about-mcs/news/030328-nagles.html
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PostPosted: Fri Sep 07, 2007 2:38 pm    Post subject: Scripps Research scientists shed new light on how antibodies Reply with quote

Scripps Research Institute
6 September 2007

Scripps Research scientists shed new light on how antibodies fight HIV

New findings may further efforts to create AIDS vaccine
By furthering scientists’ understanding of the molecular mechanisms that separate the minority of successful HIV antibodies from the majority of ineffective antibodies, the work may have implications for future attempts to design an HIV vaccine.

The study was published on September 6, 2007, in the journal Nature.

“This study is part of the effort to understand how protection against HIV occurs,” says Dennis Burton, a professor at The Scripps Research Institute. “If we really understand this, then we can design tailor-made vaccines in a way that has never been done before.”

Although vaccines have long been used with great success to prevent diseases, scientists are still learning about the exact mechanisms of how vaccines work and how the antibodies that vaccines prompt the body to create can neutralize a pathogen. The spread of HIV, which is resistant to most antibodies the body produces against it, has made fully understanding this method of action more urgent.

With this in mind, Burton and colleagues sought to tease apart the action of the b12 antibody-one of the rare antibodies that protects against the HIV virus. The antibody, first identified by Burton, Scripps Research Professor Carlos Barbas III, and colleagues in 1992, originally came from the bone marrow of a 31-year-old male who had been HIV positive without symptoms for six years.

In the current study, researchers created mutated versions of b12 to see what effect various changes would have on the antibody’s effectiveness.

“Hopefully, we can work backwards towards a vaccine, using b12 and the very few other really great, broadly neutralizing antibodies against HIV that have been found,” says Scripps Research Senior Research Associate Ann Hessell, who was first author of the Nature paper jointly with Lars Hangartner, a Scripps Research postdoctoral fellow.

Results from the new study suggest the importance of antibody activity against both infected cells and free virus for effective protection. As well as simply binding to HIV, protection was dependent upon the ability of antibodies to interact with immune cell Fc receptors.

Fc receptors are found on the surface of immune cells, such as natural killer cells. The Fc receptor binds to the Fc region of an antibody after an antibody binds to a pathogen, targeting the pathogen for attack by the immune system. Although Fc receptor function was known to be important for the function of antibodies against other diseases, a role in protecting against HIV had never before been demonstrated.

Burton’s team examined the ability of two antibodies mutated from b12, dubbed KA and LALA, to prevent infection using the SHIV/macaque model, in which macaques are challenged with a hybrid human-simian virus that infects the model but is recognized by human antibodies. The KA antibody contained a mutation that prevented it from interacting with the complement cascade, a major component of the immune system responsible for destroying invading pathogens. The LALA antibody contained a mutation that rendered it unable to interact with either the complement pathway or the Fc receptor.

In both mutants, the site where the antibody binds to free-floating virus was unaltered, allowing the researchers specifically to investigate the importance of the complement cascade and Fc receptor system for preventing infection.

“We saw that the KA antibody, which could still bind to the Fc receptors on the immune cells but not to the complement cascade, protected the animals from becoming infected just as the wild type b12 antibody,” says Hessell. “In contrast, the LALA group became infected much like the controls.”

The results provide the first evidence that the Fc receptor, but not the complement cascade, is important to the function of the b12 antibody in preventing HIV infection.

Additional in vitro experiments revealed that the wild type and KA antibodies, but not the LALA antibody, blocked infection more efficiently in the presence of other effector cells of the immune system.

“Our results are fully consistent with the antibody doing two jobs,” says Burton, “job one, stick to the virus; job two, recruit immune cells to come and kill infected cells.”


###
In addition to Burton, Hessell, and Hangartner, authors of the study, “Fc Receptor But Not Complement Binding Is Important in Antibody Protection Against HIV,” are Meredith Hunter and Preston A. Marx of Tulane University; Carin E.G. Havenith, Frank J. Beurskens, Joost M. Bakker, and Paul W.H.I. Parren of Genmab (Utrecht, The Netherlands); Gary Landucci and Donald N. Forthal of University of California, Irvine, School of Medicine; and Caroline Lanigan of The Scripps Research Institute.

Support for this work was provided by grants from the National Institutes of Health and the Neutralizing Antibody Consortium of the International AIDS Vaccine Initiative, and by a fellowship from the Swiss National Foundation.
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PostPosted: Sat Nov 03, 2007 7:03 am    Post subject: Earlier Diagnosis Would Allow Life-Saving Treatments That Reply with quote

Earlier Diagnosis Would Allow Life-Saving Treatments That
Delay Progression From HIV Infection to AIDS


Albert Einstein College of Medicine

November 2, 2007 – (BRONX, NY) – Despite the availability of life-saving antiretroviral treatment, people infected with HIV (human immunodeficiency virus) continue to die and suffer from complications of AIDS, mainly due to delayed diagnosis and initiation of treatment. A researcher at the Albert Einstein College of Medicine of Yeshiva University and colleagues at Yale University have shed light on why this problem persists. They report their findings in the November issue of the journal Medical Care.

Led by Dr. Neel Gandhi, assistant professor of medicine and of epidemiology and population health at Einstein, the researchers examined 4,368 patients presenting for AIDS treatment to Veteran’s Administration (VA) Medical Centers nationwide for the first time between 1998 and 2002. Their aim was to determine whether patients who had received medical care in the VA healthcare system were diagnosed with the HIV infection that causes AIDS earlier than patients outside the VA or those who were accessing the VA system for the first time.

Half of all the patients in the study had AIDS at the time of presentation—a high rate that nevertheless was similar to studies conducted outside the VA healthcare system. “What was particularly astounding to us was the fact that 40 percent of these patients with AIDS had previously received medical care at the VA for other illnesses, but had not been diagnosed with HIV infections and treated earlier,” explains Dr. Gandhi. “This occurred even though they had an average of six physician visits over three-and-a-half years. Even more concerning was that those patients who already interacted with the healthcare system for several years suffered the end-stage complications of AIDS at the same rate as those who were new to the VA healthcare system.”

One explanation for why this may occur is that patients with HIV infection remain asymptomatic until very late in the disease, providing few clues to doctors of the patient’s underlying HIV infection. “In our study, we found that only 12% of patients with AIDS at the time of presentation for treatment had previously suffered from an illness indicative of unrecognized HIV infection,” notes Dr Gandhi. “The vast majority of these patients with AIDS had no signs or symptoms of HIV infection until they suffered end stage complications from AIDS. Most of these AIDS complications could have been prevented if these HIV-infected people had been routinely screened when they were first seen by a doctor and had begun antiretroviral treatment earlier.”

He adds, “A previously published study has shown routine screening for HIV infection is a cost-effective addition to the screening done for other life-threatening diseases, such as heart disease and several types of cancer. Assuming that patients give their permission to be screened for HIV, the potential savings from diagnosing an infection earlier would be quite significant.”

The findings of the study support a recommendation by the US Centers for Disease Control and Prevention (CDC) to screen all patients in all healthcare settings for HIV-infection.

Dr. Gandhi conducted much of this study as a member of the Robert Wood Johnson Clinical Scholars Program of Yale University, with colleagues from Veterans Aging Cohort Study of the West Haven Veteran’s Administration Hospital. The research received funding from the Robert Wood Johnson Clinical Scholars Program, The National Institute of Alcoholism and Alcohol, and the Veterans Affairs Office of Research and Development. Dr. Gandhi joined the faculty of the Albert Einstein College of Medicine in August 2006.
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PostPosted: Tue Nov 27, 2007 2:10 pm    Post subject: Studies Suggest HIV Subtype More Deadly Than Others Reply with quote

November 27, 2007
Johns Hopkins Bloomberg School of Public Health

Studies Suggest HIV Subtype More Deadly Than Others

HIV Survival Rate Significantly Shorter in Thailand Compared to Other Regions

Two studies led by researchers at the Johns Hopkins Bloomberg School of Public Health found that people infected with HIV in Thailand die from the disease significantly sooner than those with HIV living in other parts of the world. According to the researchers, the shorter survival time measured in the studies suggests that HIV subtype E, which is the most common HIV subtype in Thailand, may be more virulent than other subtypes of the virus. Both studies are published in a special issue of the journal AIDS, the offical journal of the International AIDS Society.

The first study followed 228 men over a 14-year period starting in 1991. All of the men were serving in the Thai military and were HIV-negative when they enrolled in the study. The researchers tested for HIV every six months to determine approximately when they acquired HIV. The men were also diagnosed at a time before combination antiretroviral drug therapy was available.

The researchers compared the group of Thai men to a group of similar HIV-positive men living in North America and Europe who were included in another study. The median time from HIV infection to death for the Thai men was 7.8 years compared to 11 years for HIV-positive men living in North America and Europe. The survival rate for the Thai men was also lower than studies of similar populations living in low- and middle-income countries in sub-Saharan Africa where subtypes A, C, D and G circulate. However, the shorter survival after HIV infection among persons in Africa infected with subtype D was similar to the survival among the Thai men.

“We were surprised to learn that the young military recruits from Thailand appeared to develop AIDS more quickly and have shorter survival after their HIV infection than persons in Africa who were carefully followed,” said lead author Ram Rangsin, assistant professor of Community and Military Medicine at Phramongkutklao College of Medicine in Bangkok. Rangsin conducted the research while studying at the Bloomberg School of Public Health. “Fortunately, the men who have survived after their infection are now receiving treatment with effective antiviral drugs and doing very well.”

For the second study, researchers followed a small group of male blood donors and their wives from 1992 to 2007. All of the men and women were determined to have acquired HIV fewer than two years prior to enrolling in the study. The median survival rate from infection to death was 7.8 years for the men and 9.6 years for the women. Again, the survival rate was lower than the 11 years reported for HIV-positive men in developed countries.

“The fact that both young military conscripts and blood donors and their wives in Thailand had similarly shortened survival compared to persons in the U.S. and Africa–except those infected with subtype D viruses—suggests that viral subtypes D and E may be more virulent than many other viral subtypes,” said Kenrad E. Nelson, MD, a senior author of both studies and professor in the departments of Epidemiology and International Health at the Bloomberg School. “If we could understand better the virulence characteristics of these viruses, we might learn something more about why those with HIV infection progress to AIDS, usually many years after they are infected.”

“The natural history of HIV-1 subtype E infection in young men in Thailand with up to 14 years of follow-up” was written by Ram Rangsin, Phunlerd Piyaraj, Thira Sirisanthana, Narongrid Sirisopana, Onsri Short and Kenrad E. Nelson.

The research was supported by the Office of AIDS Research at the National Institutes of Health and Thailand Research Fund. Funding was also provided by the Fogarty International Center of the National Institutes of Health.

“Survival of blood donors and their spouses with HIV-1 subtype E infection in northern Thailand 1992-2007” was written by Kenrad E. Nelson, Caroline Costello, Vinai Suriyanon, Supaluk Sennun and Ann Duerr.

The research was supported by the Center for Disease Control and Prevention through the CONRAD program at East Virginia Medical School.
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PostPosted: Mon Sep 01, 2008 9:31 am    Post subject: Vaginal proteins in HIV-resistant prostitutes suggest new pr Reply with quote

Vaginal proteins in HIV-resistant prostitutes suggest new prevention measures
1 September 2008
Journal of Proteome Research

Researchers in Canada report discovery of unusual proteins in a small group of Kenyan sex workers that appear to be associated with resistance to infection with HIV, the virus that causes AIDS. The discovery could lead to the improved design of vaccines and drugs to fight the deadly virus, which infects an estimated 40 million people worldwide, the scientists say in a report scheduled for the Sept. 3 issue of ACS' Journal of Proteome Research, a monthly publication.

In the new study, Adam Burgener and colleagues note that 140 of more than 2000 sex workers studied in Nairobi, Kenya, appear resistant to HIV infection. Although evidence suggests that certain biological factors in their vaginal fluid may play a role in resistance, the exact identity of these substances was unclear.

The scientists used a high-tech analytical method to compare differences among proteins in vaginal fluids from HIV-resistant women and those infected with the virus or susceptible to it. HIV-resistant women had proteins significantly different from other women. Vaginal fluids of the HIV-resistant women had higher levels of proteins with anti-viral and anti-inflammatory actions. These proteins could be used as the basis for new medications to prevent infection, the scientists suggest.

ARTICLE # 4
"Identification of Differentially Expressed Proteins in the Cervical Mucosa of HIV-1-Resistant Sex Workers"

DOWNLOAD FULL TEXT ARTICLE
http://dx.doi.org/10.1021/pr800406r
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