HIV 101

Do you have a family member who was just diagnosed with HIV/AIDS? Are you looking for more information on HIV? Learn about our programs that serve those affected by HIV/AIDS such as thePositive Families Support Group and Community HIV 101

What is HIV/AIDS?

HIV is the human immunodeficiency virus. HIV can hide for long periods of time in the cells of your body and attack key parts of your immune system- your T cells or CD4 cells. Your body has to have these cells to fight infections and disease, but HIV invades them, uses them to make more copies of itself, and then destroys them. Over time, HIV can destroy so many of your CD4 cells that your body can’t fight infections and diseases anymore. When that happens HIV can lead to AIDS.

AIDS is the final stage of HIV infection. People at this stage of HIV disease have badly damaged immune systems, which put them at risk for opportunistic infections(OI's). You will be diagnosed with AIDS if you have one or more OI, certain cancers or a very low number of CD4 cells.

How do you get HIV?

HIV can be transmitted through any one of the following fluids:

• Blood
• Semen
• Pre-seminal fluid (pre-cum)
• Breast milk
• Vaginal fluids
• Rectal (anal) mucous

HIV is transmitted through body fluids in very specific ways:

• Sexual contact
• Pregnancy, childbirth, breastfeeding
• Injection drug use
• Occupational exposure i.e. health care workers coming in contact with infected body fluids
• Blood transfusions
• Organ transplants

How can I protect myself?

HIV can be spread by having unprotected sexual contact with an HIV-positive person. Some of the ways to reduce your risk of getting HIV through sexual contact include:

• Don’t have sex. Sex is the main way that HIV is transmitted. If you aren’t having sexual contact, you are 100% protected from getting HIV in that way.
• Be monogamous. Having only one sex partner reduces your risk of getting HIV.
• Get tested and know your partner's status. Talking about your HIV status can be difficult or uncomfortable - but it's important to start the discussion BEFORE you have sex.
• Use condoms consistently and correctly. Both male and female condoms will help protect you against HIV and other STIs.  

As reported by AIDS.gov

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Possibility of PrEP thats not made with Truvada

http://www.hivequal.org/hiv-equal-online/the-possibility-of-prep-that-s-not-truvada

Quote from E.T.

"It's bad enough people are dying of AIDS, but no one should die of ignorance"

First two rules of Reddit really should apply everywhere and always!

• Remember the human. When you communicate online, all you see is a computer screen. When talking to someone you might want to ask yourself "Would I say it to the person's face?" or "Would I get jumped if I said this to a buddy?"
• Adhere to the same standards of behavior online that you follow in real life.

“Game changer” in fight to protect women from HIV

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The Capsids of HIV-1 and HIV-2 Determine Immune Detection of the Viral cDNA by the Innate Sensor cGAS in Dendritic Cells #HIVTruth

Scientists find 'invisibility cloak' that shields HIV-1 from immune system

Findings, published in Immunity, open new avenues for the development of effective treatments against HIV-1

By Mary Beth O'Leary     Posted on 21 November 2013

Of the two major types of #HIV, only one, HIV-1, typically causes #AIDS in #PLWH who don't receive treatment. A study published by Cell Press today in the journal Immunity reveals how HIV-1 escapes detection by essentially becoming invisible to a patient's immune system, whereas HIV-2 triggers protective immune responses in patients. This understanding of how HIV-1's "invisibility cloak" works could lead to the development of effective vaccines against HIV-1.

"Our study shows for the first time exactly how immune cells sense the virus and how the virus uses one of its proteins to tune its stealthiness and infectivity," says senior study author Dr. Nicolas Manel of the Institut Curie in France. "We also show how to modify the virus so that it is properly recognized and leads to a beneficial immune response."

The image depicts an HIV-2 virus (left) getting in contact with a dendritic cell (right). When the virus enters the dendritic cell, the capsid shell (cone) containing a viral RNA (line) can get efficiently reverse-transcribed into DNA through activity of the Vpx protein (orange) that degrades SAMHD1 (not shown). The resulting cDNA (double line) has two different fates, which are determined by the sequence of the capsid and its interaction with Cyclophilin A proteins (red drops). In HIV-2 and capsid-mutated viruses described in the paper, the cDNA gets sensed by the cytosolic sensor cGAS (radar) leading to induction of antiviral and immune response gene expression. In HIV-1, the capsid allows the virus to escape sensing of its viral cDNA, leading to productive infection of the cell (integrated cDNA in the nucleus). Image by Dr. Nicolas Manel

Individuals who are living with both HIV-1 and HIV-2 do better than those living with HIV-1 alone, suggesting that the immune response against HIV-2 protects against the effects of HIV-1 infection. While searching for an explanation in previous studies, Dr. Manel and his collaborators found that HIV-2, but not HIV-1, naturally infects and activates dendritic cells, which play a major role in triggering protective immune responses. But until now, it was not known how HIV is detected in dendritic cells.

In the new study, Manel and his team focused on the capsid—the protein shell of a virus that encloses its genetic material. By mutating HIV-1 and HIV-2 capsids, they discovered that these viral proteins control the ability of dendritic cells to sense the viruses and activate immune responses.

The researchers found that the HIV-1 capsid allows the virus to escape detection by dendritic cells under normal conditions. But when they mutated the HIV-1 and HIV-2 capsids, the dendritic cells produced immune responses without getting infected by the viruses. These cells relied on a protein called cyclic GMP-AMP synthase (cGAS) to sense the viral DNA in the cytosol before the foreign DNA became integrated into the host genome.

These findings open new avenues for the development of effective treatments against HIV-1. "By modifying the capsid of a virus, we could engineer a virus that is both better recognized by the immune system and that has also lost its ability to infect cells," Dr. Manel said. "Beyond capsid-mutated viruses, our results suggest that activating the cGAS pathway in dendritic cells could induce immunity against HIV-1."
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For a full copy of this report available in PDF and links to other reports similar in context click here.
Immunity, Lahaye et al.: "The capsids of HIV-1 and HIV-2 determine immune detection of the viral cDNA by the innate sensor cGAS in dendritic cells."
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A study on the potential benefit of PLWH who participate in activism to fight #HIVStigma

HIV Insight: Stigma, Activism, and Well-Being among People Livi...: Evidence demonstrates that HIV stigma undermines the psychological and physical health of people living with HIV (PLWH). Yet, PLWH describe...

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An article published by: The Atlantic, HEATHER BOERNER OCT 12, 2014 on mixed status couples getting pregnant

Getting Pregnant When One Partner Has HIV

In "mixed-status" couples, the path to conception is often fraught with medical and legal obstacles.

The fact that Ted was HIV-positive didn’t come into play until the two started dating a year and a half later. But even that didn’t deter the dreams of pink-cheeked babies that had begun drifting through Hillsborough’s head. As a child in a Chicago suburb, she had turned spoons and forks into babies, tucking them in to the cutlery drawer with a prayer that they sleep soundly. She had always wanted to be a mother.

The fact that Ted was HIV-positive didn’t come into play until the two started dating a year and a half later. But even that didn’t deter the dreams of pink-cheeked babies that had begun drifting through Hillsborough’s head. As a child in a Chicago suburb, she had turned spoons and forks into babies, tucking them in to the cutlery drawer with a prayer that they sleep soundly. She had always wanted to be a mother.

If she dated Morgan, she wasn’t sure how that would happen. At the time, neither did science. Back then, condoms were the best and only option for HIV prevention between those with the virus and those without (called HIV mixed-status couples). So natural conception was out, without the aid of invasive and expensive procedures. Over the next 13 years, all that would change. In 2012, the Food and Drug Administration approved the drug Truvada for HIV prevention, an approach called pre-exposure prophylaxis, or PrEP. Nearly half of PrEP users (48 percent) in the first few years of approval have been women. Poppy is one of them.

At the University of North Carolina at Chapel Hill, Dr. Myron “Mike” Cohen has four different titles in immunology, global health, and infectious diseases. His early career included research on diseases of the reproductive tract and immune system, but by the mid 1990s, he was publishing on HIV and AIDS in earnest. His work was increasingly focused on figuring out the mechanics of HIV in the blood and genital fluids, and how other sexually transmitted infections (STIs) can make people more likely to pass on the virus or to become infected.
California banned the donation of sperm from HIV-positive men in 1989—even if that donation was made for a couple to use in artificial insemination.Cohen was tackling a complex problem. The HIV virus is tricky: It targets and hijacks precisely the cells of the immune system that are designed to tell the immune system how to get rid of invading cells, hobbling the body’s ability to mount an immune response. What’s more, HIV seems to use molecules within those immune cells to hide from the rest of the immune system—what some have called an “invisibility cloak.” And even when the virus is well-controlled, it’s still present, ready to re-emerge when treatment ends.
The chance of someone passing on HIV is one in 1,000 for unprotected penile-vaginal sex and about five in 1,000 for unprotected anal sex. But people with HIV are more infectious at certain times, depending on the amount of virus in their blood and other fluids. The virus can also show up at one level in the blood (this statistic is called the "viral load") but at another level in seminal fluid and vaginal secretions. That makes it hard to track how infectious someone is.
A group of new highly-effective HIV medications—highly active antiretroviral treatment (HAART)—came out in 1995. The cocktail of drugs could slow or stop the replication of HIV in the cell, and the virus couldn’t mutate quickly enough to develop resistance to all three of the cocktail’s components at once. Here, it seemed, was a treatment that could outpace HIV, knocking the virus down before it could undermine the immune system. Scientists wondered: If new treatments can maintain lower levels of virus in the blood and the semen, does that mean that the person is less infectious? Could treatment stop the spread of the virus? Cohen wasn’t willing to make any bets without research.

Cohen began to assemble what has so far been the largest study of its kind. He found collaborators in Africa, South America, Asia, and the U.S., who recruited HIV-affected couples in stable relationships willing to submit to questions about their HIV status, STIs, and other factors. The idea was to separate these couples into two groups. In one, the HIV-positive partner would receive HAART immediately. The HIV-positive partners in the other group would get it later—when their immune function dropped, but before infection or immune system failure. The study would also try to remove variables that can increase infectiousness—by screening for and treating gonorrhea or chlamydia, for example. Couples in both groups were offered condoms and urged to use them—which, Cohen said, “they don’t, even when you ask them to.” The goal was to test the limits of HAART’s power—to see, really, if treatment could prevent transmission.
As the year 2000 wound down, Cohen and his team settled in for a long period of preparation, well aware that the National Institutes of Health, which was funding the study, could pull the plug on it at any time if it discovered that the study’s HIV-negative partners were contracting the virus at high rates.
“It was,” Cohen told me, “not at all clear to me what the results would be.”

* * * Back in San Francisco, Hillsborough made an appointment with Morgan’s primary-care doctor, who had diagnosed him with the virus. Hillsborough wanted to know if she and Morgan could ever safely have a baby.
The virus can also show up at one level in the blood and another level in semen, making it hard to track how infectious someone is.Morgan’s doctor sent her to the Bay Area Perinatal AIDS Center (BAPAC), a clinic within the University of California, San Francisco’s Division of HIV/AIDS, which provides counseling and care to pregnant women and their families affected by HIV. There, she received a consultation from nurse practitioner Cynthia Feakins on her options. Many, like adoption or using donor sperm, meant her boyfriend could not be the biological father of their child.
But Hillsborough was attached to the idea of having a child who shared both her and Morgan’s DNA.

She discovered that the options that allowed this were high-tech and expensive. In vitro fertilization (IVF) or intrauterine insemination (IUI) cost anywhere from $865 to $8,158 for one round, not including fertility drugs, which can run up to $5,000 per IVF cycle, according to the National Infertility Association. Then there’s ICSI, which stands for intracytoplasmic sperm injection, a process that takes IVF one step further. A scientist injects one sperm into one egg and allows it to grow before placing it in a woman’s uterus. That procedure costs about $1,500 more per cycle than IVF. All three options are available to HIV-mixed status couples only after they’ve also paid $200 or more for a process called sperm washing, which separates sperm from the seminal fluid via chemicals and centrifuge. That sperm, now “washed” of potentially infectious seminal fluid, can then be used to fertilize an egg.
There remains some debate on the safety and effectiveness of sperm washing. A woman contracted HIV in 1990 from her husband while the couple was doing sperm washing, leading everyone from the American Society for Reproductive Medicine to the Centers for Disease Control to recommend against doctors helping HIV-affected couples with insemination using the sperm of HIV-positive men. ASRM reversed its policy in 2002 . The CDC guidelines are in place to this day. It’s unclear how many clinics are willing to provide HIV-affected couples with sperm washing, but some fertility clinics claim it may be as few as 25 .
On top of that, the California legislature banned the donation of sperm from HIV-positive men in 1989—even if that donation was made specifically so a couple could “wash” it and use it for artificial insemination. So Hillsborough and Morgan couldn’t get reproductive help in the state, even if a doctor was willing to go against the CDC and ASRM’s recommendations.
Hillsborough went back to planning her life with Morgan, who would become her husband two years later. Her parents weren’t invited to the elopement in 2002, and, when they found out that their daughter had married an HIV-positive man, they boycotted the couple’s first anniversary party. Hillsborough, now Morgan, did not talk to her parents for the next five years.

* * * Poppy Morgan was in a staff meeting in 2007 when her phone rang. She answered without looking at it; on the other end of the line was Shannon Weber, a social worker who ran UCSF’s National Perinatal HIV Hotline and Clinicians’ Network. Technically, Weber’s job was to help OB-GYNs and other physicians navigate the federal perinatal HIV guidelines and provide the highest quality of care to their HIV-positive patients. But very quickly, she had started fielding calls from HIV-affected couples and their doctors.

"The virus can also show up at one level in the blood and another level in semen, making it hard to track how infectious someone is."

“Sperm washing’s not legal yet,” Poppy remembered Weber saying, “but it’s about to be.” At this point, Poppy had talked several times with Weber, who was a source of moral support as she called clinics in Colorado, Chicago, and New York and researched services in Switzerland and Italy online.
For Poppy, then, this latest phone call was thrilling news, and not just because it could make her longed-for baby a reality; it was also good news for the couple’s bank account. The Morgans had determined that the cost of airfare, lodging, and leave from work to do sperm washing in another state would have been prohibitive—up to $5,000 per trip, plus any medications Poppy might need to increase her egg production and chances of conception. When Poppy hung up the phone, her heart was racing. “Oh my gosh,” she remembered thinking. “I’m going to have a baby tomorrow!”

* * * In 2008, Pietro Vernazza, chief of the Division of Infectious Diseases at the Cantonal Hospital in St. Gallen, Switzerland, had been offering PrEP for conception to mixed-status HIV couples in which the male was HIV-positive for five years.
The treatment he offered was specific and targeted: The HIV-positive partners would have their viral load measured and both people in the couple would be tested regularly for STIs. The women would be given urine tests to monitor for spikes in a hormone that indicates ovulation. Then, when the time was right, the woman would take one pill 36 hours before unprotected sex and another the morning before sex. After, they’d come in for tests to check for HIV transmission and pregnancy. Conception rates among his patients had jumped from 40 percent for sperm washing and IUI to 75 percent for timed intercourse or timed intercourse with PrEP.

So in January 2008, Vernazza made this recommendation to Swiss doctors: HIV-positive patients with undetectable viral loads, no other STIs, in monogamous relationships, and with excellent adherence to their medications were not infectious and need not use condoms.
It came to be known as the Swiss statement.
The morning after Vernazza published his statement, Seth Kalichman, a professor of psychology at the University of Connecticut and editor of the journalAIDS and Behavior, called the World Health Organization headquarters in Switzerland.
“I called and asked them what they thought was going on,” Kalichman said. “They said they were in the middle of writing a response.” Sure enough, on February 1, WHO announced that it still recommended that all HIV-positive people use condoms to prevent the spread of the virus.
For Kalichman, Vernazza’s statement was premature. Vernazza hadn’t published any of the data from his work with HIV-mixed status couples. He hadn’t conducted a trial like the one underway at the University of North Carolina. Researchers like Kalichman, or the HIV doctor down the street, had no data on which to base a change in practice that would conflict with the CDC’s ban on unprotected sex for HIV-positive people.

"We have an epidemic, and suggesting that some people with HIV can have sex without a condom will only make it worse"

“It was going to be easily misinterpreted by the masses,” Kalichman said.

Kalichman lived in a very different HIV world than Vernazza and his highly compliant, monogamous couples. He spent his days working with HIV-positive people who scored high on the sexual compulsivity scale he had developed, on one hand, and paranoid AIDS deniers, on the other. His book, Denying AIDS: Conspiracy Theories, Pseudoscience, and Human Tragedy, would come out the following year.
Kalichman has spent the last seven years studying how well people with HIV stick to their treatment regimens. Verdict: not well. They feel good, so they don’t take their medications. They have substance abuse or mental health problems, so they don’t take their medications. Or they simply forget.

“If you meet the criteria of the Swiss statement, what the statement is advertising is true. The problem is, it only applies to a very small minority of people,” Kalichman said. “Most people with HIV infection don’t know they have the infection. If they know they are infected, they aren’t necessarily accessing treatment. Those that are accessing treatment are not necessarily adherent. Those who are adherent often will have an undetectable viral load, but that doesn’t mean it’s undetectable in the semen. And it’s not just another STI that increases the chance of transmission. It’s any inflammation in the genital tract.”
Vernazza disputes Kalichman’s argument about lack of data, saying that he based the Swiss statement not solely on his own patients, but on literature that showed there had been no HIV transmission in HIV-discordant couples when the HIV-positive partner’s viral load was undetectable.
Back at UNC, meanwhile, Myron Cohen wasn’t prepared to share his protégé Vernazza’s optimism. At the time, Cohen was three years into the pilot study for his clinical trial. It had taken five years to set up, and hundreds of people in Brazil, India, Thailand, Kenya, Zimbabwe, Malawi, Botswana, South Africa, and the U.S. were being monitored.
At an event before the International AIDS Conference in Mexico City later that year, Cohen said of his study, “We have an HIV epidemic, and suggesting that some people with HIV can have sex without a condom will only create confusion and make it worse."
“Pietro will tell you that he knew what the results of my study would be,” Cohen told me. “But I didn’t know. How is it that he could know the results of my study when I didn’t?”

* * * Poppy Morgan didn’t know anything about the Swiss statement. All she could think about now was sperm washing: The California legislature had finally overturned the ban on HIV-positive men donating sperm. She could finally have the procedure and, maybe, get pregnant.
And so it was that she found herself sitting in her doctor’s office, listening to him explain what would happen next.

“How it will work,” she remembered her doctor saying, “is that your husband will give me his sperm sample, we’ll send it to New York—”
“Wait, whoa,” she interjected. “Why are you going to send it to New York when sperm washing is legal here?”
Her doctor explained that there were no guidelines from the CDC on how to proceed with sperm washing. California doctors were free to counsel and work with patients on sperm washing—but few clinics in the state were willing to do the procedure themselves.
As Poppy listened, the doctor explained that Ted’s sperm sample would be frozen and sent to New York. There, it would be thawed, processed and then refrozen, shipped back to California, and thawed again.
Then another sickening thought occurred to her.
“Wait a minute,” she asked. “After all that freezing and thawing, what’s the likelihood that the sperm will be viable?” Her husband’s HIV medication already reduced his fertility.
“There’s a very low chance of viability,” the doctor replied.
Poppy burst into tears.
“What’s the point?” she asked. “’If it’s not even going to be viable, what’s the point of all this?”

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How Close Are We to a Functional Cure for HIV? #about.com

Photograph © International AIDS Vaccine Initiative (IAVI)

Written or medically reviewed by a board-certified physician. See About.com'sMedical Review Policy.

A functional cure is an evidence-based hypothesis by which HIV may be kept in check to undetectable levelswithout the use of chronic medications. Rather than asterilizing cure, in which HIV would be fully eradicated from the body, a functional cure serves more along the lines of a remission—whereby the manifestations of the disease are removed, even though traces of the infective agent remain.

There has been much enthusiasm and almost as much controversy surrounding the prospect of a functional cure.

Françoise Barré-Sinoussi, the co-discover of HIV, fully believes that it is likely possible "within the space of the next 30 years." Meanwhile, Robert Gallo (also credited with discovering HIV) considers the concept flawed and believes that parts of the theory are "not likely to work."

How a Functional Cure Might Work

One of the biggest facing challenges facing researchers has been the cells and tissues of the body (called "reservoirs") where HIV can persist even the face of complete viral suppression.Hidden within these cellular reservoirs is the genetic code of HIV, which the immune system is unable to detect.

Since the virus is not actively replicating—but is rather carried along passively as the host cell replicates—it is largely unaffected by antiretroviral therapy (since antiretrovirals work by interrupting a stage in the virus' replication cycle).

There are several models being explored to address this:

**Purge the viral reservoirs. Some have theorized that, by stimulating the reservoirs in such a way that it "reactivates" the virus, the HIV will be effectively exposed to the immune system. The latent reservoirs that had unwittingly shielded the virus will die out quickly and, under the pressure of antiretroviral therapy (ART), the viral activity may be able to be suppressed to such a level that ART will no longer be needed.
**Intensify ART at the time of infection. While it was mentioned that latent reservoirs are largely unaffected by ART, that shouldn't suggest that it has no effect. (Mathematical models have shown the patients on ART would eventually be able to deplete these reservoirs, but only within the space of 60-80 years.) Evidence now suggests that initiating ART at the time of infection may reduce HIV's ability to establish these reservoirs in the first place. It is further theorized that, by keeping the viral population low from the start, HIV's ability to mutate would be greatly diminished, while immune function could preserved to such a degree that a person may eventually be able to control the virus without ART.

Additionally, research into the development of therapeutic vaccines has focused on the production of broadly neutralizing antibodies, known to neutralize a wide spectrum of HIV. Scientists are exploring ways to stimulate these naturally occurring agents, the strategy of which may be applied to a functional cure.

Evidence in Support of a Functional Cure

While research into a functional cure has been on the table for some years, three specific events provided the foundational proof-of-concept:

1. **The Berlin Patient. Timothy Ray Brown, an HIV-positive American living in Berlin, was given a bone marrow transplant in 2009 to treat his acute leukemia. Doctors selected a stem cell donor with two copies of a genetic mutation called the CCR5-delta-32, known to resist HIV in a rare population of people. Routine tests performed soon after the transplant revealed that the HIV antibodies in his blood had decreased to such a level as to suggest the complete eradication of the virus from his system. Subsequent biopsies confirmed no evidence of HIV in any of Brown's tissues, making him the first person officially cured of HIV. While the risk of death is considered too high to explore bone marrow transplants as a curative option, "The Berlin Patient" at least provided the evidence that a cure was possible.
2. **HDAC Inhibitor Research. A number of different agents have been explored to elicit the "purging" of latent HIV reservoirs, but it was in 2009 that researchers from the University of North Carolina first suggested that a class of drugs called histone deacetylase (HDAC) inhibitors could reactivate HIV in latent cells. Long used as mood stabilizers, HDAC inhibitors have shown greater utility in recent years in the treatment of T-cell lymphoma (a type of non-Hodgkin lymphoma). Subsequent research has shown that other types of HDAC inhibitors—most predominantly panobinostat—may be able to induce the same effect with lower dosing and minimal toxicities.
   
   [**UPDATE** - March 23, 2014 - In a report published in the journal Nature Medicine, researchers at John Hopkins University tested a variety of HDAC drugs on white blood cells extracted from HIV-positive patients. While earlier research had shown positive results, those studies relied solely on white blood cells infected in the test tube. Using patient-derived cells, this new study had hoped to provide a "real-life" confirmation of the activation strategy. It didn't. In fact, none of the tested agents worked. In order to be considered successful, the HDAC inhibitors would need to have elicited a 100-fold increase in viral RNA production. At best, the drugs spurred a one- to 10-fold increase, falling well short of the desired target.While the setback is regarded as considerable, the researchers are aiming to examine whether a combination of HDAC inhibitors might be more effective in spurring HIV reactivation.]
3. The Case of the Mississippi Toddler and the Visconti Cohort. Two separate cases in 2013 hinted at the potential of early ART in controlling HIV. The first involved a Mississippi child who was provided ART at the time of birth, the treatment of which continued for 18 months until the mother decided to stop. Qualitative viral load test had earlier confirmed that the baby was, in fact, HIV-positive. When the child was relinked to care after a five month gap, all HIV tests were negative—leading researchers to proclaim the toddler "functionally cured" (although some, including Anthony Fauci of the National Institutes of Health, have questioned the interpretation of the findings).
   
   [**UPDATE** - July 14, 2014 - The National Institute of Allergies and Infectious Diseases (NIAID) reported that viral rebound had occurred in the Mississippi baby... Read more]
   
   The second case involved 14 French patients who were provided ART within 10 weeks of infection, all of whom stopped treatment for various reasons after achieving viral suppression. Researchers from the French National Agency for Research on AIDS and Viral Hepatitis later discovered that the patients (who were part of the 70-participant Visconti Cohort Study) were able to control the virus to fully suppressed levels, some for as long as ten years. To some, this suggested that early intervention may have somehow stopped HIV from establishing reservoirs, although other factors (such as severe primary infection with high viral loads) were also noted.

Where Do We Go From Here?

As promising as all of the research may seem, they raise just as many questions as they do answers. Chief among them:

• Will purging HIV from its reservoirs be enough to ensure that the virus does not re-establish reservoirs in the same (or other) cells?
• How big a part might early ART play in a functional cure? Is it the major driver, or are there other genetic and/or biological factors that play a more important role?
• How certain can we be that viral rebound won't occur in the people who we've identified as being "functionally cured?"
• How important might broadly neutralizing antibodies be to a functional cure, and how far away are we from a viable approach given the setbacks we've seen in vaccine research?

While we appear to be the right track (and are certainly closer to a solution than we've ever been), it's important that we view the research with guarded optimism. Even as scientists continue to unlock the mysteries surrounding HIV, none of these advances even vaguely suggest that the rules regarding the prevention and treatment of HIV have changed.

If anything, given the evidence that early detection and intervention are key to a "cure," the imperative to remain vigilant is, perhaps, more important than ever.

Sources:

Connor, S. "A cure for HIV is now a realistic possibility." The Independent. May 19, 2013.

Andriote, J. "The Prospects for a 'Sterlizing' Cure." The Altantic. November 29, 2012.

Hütter, G.; Nowak, D.; Mossner, M.; et al. "Long-Term Control of HIV by CCR5 Delta32/Delta32 Stem-Cell Transplantation." New England Journal of Medicine. February 12, 2009; 360:692-698.

Archin, N.; Espeseth, A.; Margolis, D.; et al. "Expression of Latent HIV Induced by the Potent HDAC Inhibitor Suberoylanilide Hydroxamic Acid." AID Research of Human Retroviruses. February 2009; 25(2):207-212.

The Fold/Washington Post. "Was that toddler really cured of HIV?" Broadcast March 15, 2013.

Sáez-Cirión, A.; Bacchus, C.; Hocqueloux, L.; et al. "Post-Treatment HIV-1 Controllers with a Long-Term Virological Remission after the Interruption of Early Initiated Antiretroviral Therapy ANRS VISCONTI Study." PLoS Pathology.March 14, 2013; 0(3):e1003211.

John Hopkins University. "Drugs Fail to Reawaken Dormant HIV Infection." Baltimore, Maryland; press release issued March 24, 2014.

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Newly Diagnosed (2009) : Know Your Lab Tests

Newly Diagnosed (2009) : Know Your Lab Tests

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No New HIV Infections in San Francisco Community PrEP Clinic

By Emily Newman

From BETA

December 17, 2015

Steve Gibson, M.S.W. (Credit: Liz Highleyman)

A trailblazing pre-exposure prophylaxis (PrEP) program by the San Francisco AIDS Foundation sexual health center Magnet was lauded at the 2015 HIV Prevention Conference. The PrEP health program began as a pilot program in November, 2014 and will continue to expand when it moves into a new health and wellness center, Strut, in San Francisco's Castro neighborhood. In early December, Magnet director Steve Gibson, M.S.W., shared lessons learned about the PrEP health program -- which has seen no new HIV infections -- at the conference in Atlanta, Georgia.

With an increasing number of community and health groups interested in scaling up PrEP access programs, practitioners across the country had the opportunity to learn about Magnet's model of care and how the center has been able to successfully enroll and retain people in the program.

The program started in November 2014 as a pilot program for people at risk of HIV but has expanded into a full-fledged PrEP health program with almost 700 men screened. PrEP is a method by which HIV-negative people can take a daily pill to prevent HIV infection.

"It was great to share our success at launching a nurse-led PrEP program showing that community-based organizations can, and need to, offer PrEP services for their clients," said Gibson.

Some of the results presented at the conference appear below.

Who's enrolling in the PrEP Program?

A total of 695 people have been screened for PrEP interest and eligibility with 90% enrolling in the program. The mean age of enrolled participants is 34 years with an age range of 18 to 71. Participants reported an average of 18.5 sexual partners per year with the most common reason for initiating PrEP being condomless sex (91%) followed by having an HIV-positive partner (12%). San Francisco AIDS Foundation recently opened a PrEP clinic at their main office located between the Tenderloin and South of Market neighborhoods of San Francisco which will increase access to PrEP services for transgender women and non-gay identified men who have sex with men.

This excerpt was cross-posted with the permission of BETAblog.org. Read the full article.

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