Friday, October 16, 2015

People with HIV are at higher risk of several types of cancer, large study finds


Liz Highleyman
Produced in collaboration with hivandhepatitis.com
Published: 07 October 2015
 
People living with HIV remain at risk of AIDS-defining cancers in the era of effective antiretroviral therapy, and also have higher rates of several non-AIDS cancers than the general population, including lung, anal and liver cancer, according to findings from a study of more than 86,000 HIV-positive people published in the October 6 Annals of Internal Medicine.

Since the advent of effective combination antiretroviral therapy (ART) in the mid-1990s, rates of the three AIDS-defining cancers – Kaposi sarcoma, non-Hodgkin lymphoma and cervical cancer – have fallen among people with HIV. These cancers are caused by opportunistic viruses that can take hold when the immune system is damaged and CD4 T-cell counts are low, though human papillomavirus (HPV) also causes cervical and anal cancer in otherwise healthy people.

Most studies, however, have found that HIV-positive people have a higher overall risk for other non-AIDS-related cancers compared to HIV-negative populations, although data have been inconsistent about specific cancer types. In fact, cancer rates among people with HIV have risen over time as they live long enough to develop malignancies.

Michael Silverberg of Kaiser Permanente Northern California and fellow investigators evaluated trends in cumulative incidence of common cancer types by HIV status among participants in the large North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD).

This study included 86,620 people with HIV from 16 cohorts in the US and Canada, as well as 196,987 HIV-negative adults from five cohorts selected to be similar in terms of age, sex and race/ethnicity. Participants were followed between 1996 – when effective ART started to become widely available – and 2009.

About 85% of the HIV-positive NA-ACCORD participants were men, about 40% were white and 40% were black, and the median age was approximately 45 years. About 40% were men who have sex with men and about 20% had a history of injection drug use. Approximately 20% were co-infected with hepatitis C virus (HCV) while 4% also had hepatitis B virus (HBV). The proportion on ART increased from 39% during 1996-1999 to 74% during 2005-2009 and the median CD4 count rose from 309 to 382 cells/mm3.
The researchers looked at cumulative incidence (new cases) for nine types of cancer by age 75, as well as calendar trends in cumulative incidence and hazard rates, according to HIV status and taking into account the competing risk of death due to other causes.

All-cause mortality decreased over time for the HIV-positive group, falling from 5140 per 100,000 person-years during 1996-1999 to 2844 during 2005-2009. But it remained more than three times higher than that of the HIV-negative group, at 863 per 100,000 person-years during 2005-2009.
Cumulative incidence by age 75 of the two AIDS-related cancers remained higher for people with HIV compared to the HIV-negative cohorts:
  • Kaposi sarcoma: 4.4% vs 0.01%
  • Non-Hodgkin lymphoma: 4.5% vs 0.7%
Some of the non-AIDS cancers had higher rates among HIV-positive people compared to HIV-negative people, while others were about the same:
  • Lung cancer: 3.4% vs 2.8%
  • Anal cancer: 1.5% vs 0.05%
  • Colorectal cancer: 1.0% vs 1.5%
  • Liver cancer: 1.1% vs 0.4%
  • Hodgkin lymphoma: 0.9% vs 0.09%
  • Oral cavity or mouth and throat cancer: 0.8% vs 0.8%
  • Melanoma: 0.5% vs 0.6%
Anal, colorectal and liver cancer showed increasing cumulative incidence over time, but hazard rate trends were stable, so the researchers attributed the increase in cancer to decreased overall mortality, allowing more opportunity to be diagnosed with cancer.

Lung cancer, Hodgkin lymphoma and melanoma, in contrast, showed decreasing hazard rate trends, but cumulative incidence trends were not seen due to the counterbalancing effect of declining mortality.
"In the era before antiretroviral therapy, people who were infected with HIV were dying of AIDS. Now that use of this therapy is greatly increasing the lifespan of HIV-infected patients, their risk of developing other diseases, such as cancer, has increased," Silverberg said in a Kaiser Permanente press release. "These patients have a higher burden of cancer compared with the general population due to impaired immune function and chronic inflammation, as well as a higher prevalence of risk factors including smoking and viral co-infections."

"Our approach allowed us to disentangle the effects of longevity from other factors on the risk of cancer," Silverberg explained. "For example, we found that longevity was the main contribution to the increased risk over time for anal, colorectal and liver cancers. The risk for other cancers, such as lung cancer, melanoma, and Hodgkin's lymphoma, did not appear to increase over time. This was because the increased risk with longevity was compensated for by other factors, such as decreases in smoking or adverse sun exposure behaviours."

The non-AIDS cancers in this study were a mix of those caused by viruses – including anal cancer (HPV) and liver cancer (HBV and HCV) – as well as those with no confirmed viral cause, such as melanoma and lung cancer. Many HIV/HCV co-infected people are reaching the age at which HCV-related hepatocellular carcinoma, a type of liver cancer, typically develops.

The reasons for increased risk of non-infectious cancers in HIV-positive people on ART is not fully understood, but residual immune system damage that does not reverse with treatment and chronic inflammation due to persistent low-level HIV infection may play a role.

"The high cumulative incidences by age 75 years for Kaposi sarcoma, non-Hodgkin lymphoma, and lung cancer support early and sustained antiretroviral therapy and smoking cessation," the study authors concluded.

In their discussion the researchers suggested that HIV-positive smokers may benefit from new guidelines for annual lung cancer screening with low-dose computed tomography, as well as targeted smoking cessation efforts. Lung cancer incidence fell over time among both HIV-positive and HIV-negative people, presumably due to a decline in smoking. People with HIV may also need more frequent colorectal cancer screening.
Regarding the infectious cancers, they emphasised the importance of universal HBV vaccination, expanded HPV vaccination and antiviral treatment for hepatitis B and hepatitis C – the latter of which can now be cured using effective and well-tolerated interferon-free therapy.

The increased anal cancer risk highlights the need for further research on the harms and benefits of anal dysplasia screening (e.g. Pap smears).

Early and sustained antiretroviral treatment is the only known approach to prevent Kaposi sarcoma and non-Hodgkin lymphoma, and it may also play a role in reducing other cancers linked to immunosuppression or inflammation.

Reference

Silverberg MJ et al. Cumulative incidence of cancer among persons with HIV in North America: a cohort study. Annals of Internal Medicine 163, 215.
 
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New Ideas About CD4 Cell Counts and When to Start Treatment



By Sean R. Hosein
From Canadian AIDS Treatment Information Exchange
August/September 2015

The results of the START study have confirmed what some researchers have suspected for some time -- the CD4+ cell count is an imperfect measure of the immune system's health. As a result of START, we expect scientists to engage in further work to find out more accurate ways of assessing the health of the immune system. To accompany that work, we present some findings from another study that raised issues about what constitutes a normal or acceptable CD4+ count and some of the immunological injury that can occur early in the course of HIV disease. This information appeared earlier this year in CATIE News and we have adapted it for presentation here.

Results from START and other research strongly suggest that starting potent combination anti-HIV therapy (ART) at the threshold of 500 cells/mm3 is insufficient for normalizing the functioning of the immune system. An American study has shown that starting ART within 12 months of becoming HIV positive results in measureable and significant immunological benefits. This study also provides insight into the normal range for CD4+ cells that has implications for therapeutic goals in HIV treatment.

What Is a Normal CD4+ Cell Count?

A team of scientists in California and Texas has reviewed studies from Australia, North America and Western Europe in the current era and sought to clarify the normal range for CD4+ cell counts among healthy HIV-negative people. To their surprise, researchers found that data from more than 16,000 people suggested that the normal range for CD4+ cells was between 700 and 1,100 cells/mm3. In this range, 900 CD4+ cells/mm3 would be considered the mid-point or average CD4+ cell count. This figure of 900 cells/mm3 is much greater than the figure of 500 cells/mm3,which was the figure used in many treatment guidelines before the results of START were known. Furthermore, it appears that the figure of 500 CD4+ cells/mm3 significantly underestimates what a normal CD4+ count should be.

Unmeasured Immunological Injury

Assessing CD4+ cell counts only captures some of the changes brought about by HIV infection. However, there are many complex and sometimes subtle changes to the immune system that historically have not received as much attention as the CD4+ cell count, including the following:
  • excessive activation and inflammation of the immune system
  • immunological exhaustion
These and other changes begin shortly after HIV infection and ultimately have an adverse effect on a person's health.

Timing

Here is another issue: Relying on CD4+ cell counts alone underestimates the injury caused to the immune system by HIV. New research suggests that delaying the initiation of ART until the CD4+ count falls to a level of 500 cells/mm3 does not reverse immunological injury caused by HIV. In other words, starting ART shortly after HIV infection may be highly beneficial because waiting for the CD4+ count to fall allows HIV more time to injure the immune system. The U.S. researchers suggest that in part this problem arises because using the CD4+ cell count as an indicator of the overall health of the immune system is not a highly accurate way to assess the subtle injury caused by HIV. What also needs to be taken into account, they say, is the duration of HIV infection. Historically, the duration of HIV infection has not been factored into the decision-making process for deciding when to start ART.

A Large Study

To gain a better understanding of the impact of HIV infection and early or delayed initiation of ART, the researchers in California and Texas also analysed health-related information from the U.S. Military HIV Natural History Study (NHS). Participants in the NHS are from the U.S. military and include spouses and children. What is important to note about the NHS is that participants received regular and extensive assessments (checkups and blood tests). As a result, the estimated dates when they became HIV positive are relatively accurate.
Researchers used data captured from 1,119 HIV-positive participants in the NHS. Most of them were male (95%) and relatively young (31 years) and came from the major ethno-racial groups in the U.S.

Timing of Therapy

In their analysis, researchers found that nearly 40% of NHS participants achieved a CD4+ count of about 900 cells/mm3 when ART was initiated within 12 months of becoming HIV positive. In contrast, among participants who began ART 12 months or more after becoming HIV positive, only about 30% were able to achieve a CD4+ count within the normal range. This difference was statistically significant; that is, not likely due to chance alone.
Sophisticated tests revealed that the closer participants' counts rose to 900 cells/mm3, the more their immune systems were like those of HIV-negative people -- with very low levels of immune activation, inflammation and immunological dysfunction. Such participants also had improved responses to vaccination against hepatitis B virus compared to HIV-positive people whose CD4+ counts did not approach the 900-cell mark. However, it is important to note that the immune systems of early initiators of ART never became identical to those of HIV-negative people.
The researchers concluded that delaying the initiation of ART beyond 12 months of the estimated date of becoming HIV positive "diminishes the likelihood of restoring immunologic health in HIV-1-infected individuals."

Close but Not There

There are likely several reasons that underlie the failure of ART to fully heal the immune system. Here are just a few:
  • ART can reduce the production of HIV in the blood; however, sophisticated research has found that ART does not fully penetrate the lymph nodes and lymphatic tissues that are a major part of the immune system. As a result, HIV can infect cells within these tissues throughout the body and continue to produce new viruses and viral proteins that impair the immune system and perhaps other organ-systems.
  • Members of the herpes virus family, including CMV (cytomegalovirus) and human herpes virus-8 (HHV-8), are likely sexually transmitted, particularly among men who have sex with men. These viruses can cause low-level infection in some HIV-positive people and scientists suspect that co-infection with CMV and/or HHV-8 may play a role in the excess inflammation seen in ART users.
  • Some scientists suspect that HIV causes subtle changes to the immune system that are difficult to fully reverse.
Teams of researchers in North America and Western Europe are busy trying to find ways to safely reduce excess inflammation in ART users. Results of some research on HIV-related inflammation appear in TreatmentUpdate 205 and additional reports will appear later on the CATIE website.

Implications of the U.S. Study

According to the research team, its findings have "broad implications for the management of care for HIV-1-infected patients, as well as public policy," as follows:

Restoring the Immune System

If a major goal of treatment is to restore the immune system, the researchers stated: "Our data indicate that normalization of CD4+ counts may be an important therapeutic target." This statement is supported by their findings that getting the CD4+ count to about 900 cells/mm3 and keeping viral loads low greatly reduces the risk of subsequently developing AIDS and also reduces immunological dysfunction and activation and inflammation of the immune system.
More studies need to be done to find safe ways to further reduce the excess inflammation that persists in ART users and to help raise their CD4+ cell counts.

Normalizing CD4+ Cell Counts

The researchers found that participants had "the capacity for CD4+ cell normalization" if the following two conditions were met:
  • the duration of untreated HIV infection is short (less than 12 months)
  • the CD4+ count when ART is initiated is 500 cells/mm3 or greater
In the U.S. study, researchers found that participants whose CD4+ counts were at least 500 cells/mm3 when they initiated ART generally had large subsequent increases in cell counts. However, the advantage of starting ART with a high CD4+ count was, according to the researchers, "greatly diminished" if participants initiated ART more than 12 months after they became HIV positive.
The present study has uncovered what some scientists and doctors had long suspected: Untreated HIV infection can cause significant injury to the immune system in a relatively short span of time, long before CD4+ counts fall and AIDS symptoms appear.

Public Policy -- Reaping the Benefits of Early ART

Most people are not aware when they became infected with HIV. In large part this problem arises because the symptoms of initial HIV infection are generally similar to a cold or flu and in some cases can be very mild. However, if newly diagnosed people are to be in a position to take advantage of the benefits of early ART, sexually active adults need to have frequent access to barrier-free and confidential counselling and HIV testing. The U.S. researchers hope that such testing will uncover some previously unrecognized HIV infections so that "prompt initiation of ART after diagnosis occurs." According to the U.S. researchers, "such a strategy may offer the best chance for [quickly halting injury to the immune system that can otherwise occur because of untreated HIV infection]."

The researchers also stated that "an added advantage of earlier [initiation of] ART would be reductions in HIV transmission" because, in their experience, early ART quickly reduces the amount of HIV in the blood.
People who test negative for HIV need to take steps to continue to stay that way. Such steps include the correct and consistent use of condoms and, in some cases, discussion with their doctor about the use of pre-exposure prophylaxis (PrEP).

Possible Limitations

The analysis from the U.S. study is supported by the results of the START study, discussed earlier in this issue of TreatmentUpdate.

References

  1. Fletcher CV, Staskus K, Wietgrefe SW, et al. Persistent HIV-1 replication is associated with lower antiretroviral drug concentrations in lymphatic tissues. Proceedings of the National Academy of Sciences USA. 2014 Feb 11;111(6):2307-12.
  2. Okulicz JF, Le TD, Agan BK, et al. Influence of the timing of antiretroviral therapy on the potential for normalization of immune status in human immunodeficiency virus 1-infected individuals. JAMA Internal Medicine. 2015 Jan;175(1):88-99.
  3. Le T, Wright EJ, Smith DM, et al. Enhanced CD4+ T-cell recovery with earlier HIV-1 antiretroviral therapy. New England Journal of Medicine. 2013 Jan 17;368(3):218-30.
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Sunday, October 11, 2015

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Friday, October 9, 2015

Abdominal Body Fat Gains on ART and Viral Load: It Matters Where You Start


March 3, 2015, by Emily Newman

BETA reported from last week’s 2015 Conference on Retroviruses and Opportunistic Infections in Seattle.

New research presented at CROI 2015 last week gave new insight about a puzzling aspect of antiretroviral therapy (ART): lipodystrophy, or changes in body fat distribution. New findings show that people with higher viral loads when starting ART for the first time are more likely to undergo substantial body composition changes, such as an increased amount of fat in the abdominal area (called “central adiposity”), than those who start treatment with a lower viral load (abstract 140). This finding presents another reason why it’s important to start HIV treatment early.
Though it’s unclear why people on ART get lipodystrophy, protease inhibitors have, in the past, been suspected of causing body fat changes. Grace McComsey, MD, from Case Western Reserve University, presented new evidence that HIV, viral load and inflammation may also play a role in body composition changes above and beyond that which may be caused by any specific drug regimen.
In her study, treatment-naïve people with HIV who had viral loads in the highest range (over 100,000 copies/mL) before starting treatment had greater gains in abdominal fat and peripheral fat (e.g., fat on arms and legs) than people starting treatment with lower viral loads. People with higher IL-6 (a marker of immune activation) before starting treatment also had greater gains in peripheral fat.
A total of 328 people with no prior ART experience took part in the randomized controlled study, and were followed for a total of 96 weeks. Most (90%) of the participants were men, and the median age of study participants was 36. They were assigned to take tenofovir/emtricitabine (Truvada) plus one of the following combinations: 1) the protease inhibitor atazanavir and ritonavir (Reyataz and Norvir); 2) the protease inhibitor darunavir and ritonavir (Prezista and Norvir); or 3) the integrase inhibitor raltegravir (Isentress).
The researchers hypothesized that different medications would have different effects on fat gain. That’s not what they saw, however.
Using a body composition X-ray scan called DEXA, the research team found that men across all three study groups gained limb fat over the course of the study—with no differences based on the medication participants in each group were taking. Average increases per group ranged between 11% and 20%. Men also increased their abdominal fat by an average of 16% to 29% during the study—again, with no significant differences between medication groups.
Body mass increased during the study, with gains in all three study groups ranging from 3% to 3.5%.
In a question and answer session after her talk, McComsey showed concern about their findings, saying, “A 30% gain in fat after two years—that’s really bad. That’s a relatively short duration of treatment.”
Because there were no differences that seemed to be associated with the type of ART regimen, the researchers looked back to see if any of the factors they measured at baseline might be related to their findings. That’s when they realized, according to to McComsey, that viral loads prior to starting ART had an effect on later fat gain.
“Regardless of the treatment regimen, people who started at the high viral load strata gained double or triple the amount of fat than people who started at the lower viral load strata,” explained McComsey. Their findings provide another reason why it’s important to start HIV medications soon after diagnosis, and not wait until viral loads are elevated or CD4 counts are low.
The fat gains seen in the study may not necessarily be a negative consequence for people with high viral loads when they begin ART. McComsey said that the people in their study with higher viral loads prior to initiating ART, “may be sicker, in a way,” than people with lower viral loads, and that a greater gain in fat  seen during ART may mark a “return to health.”
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Thursday, October 8, 2015

How Cannabis Can Help Treat HIV/AIDS



Cannabis research might be limited, but there is no shortage of studies supporting the plant’s efficacy in eliminating nausea, vomiting, and appetite loss with a single puff. These effects can also help patients restore weight and maintain essential nutrients. Cannabis, whether inhaled or consumed as an extract, also targets neuropathic pain induced by HIV/AIDS therapy.

Marinol, a synthetic pill formulation of THC, is generally prescribed before medical marijuana. Its legal status makes it an easier target for research, but when compared to inhaled cannabis, patients see a difference. The plant contains hundreds of other therapeutic compounds known as cannabinoids and terpenoids that Marinol lacks, and Marinol has the potential to induce unpleasant side effects in some individuals.

“Not infrequently, a single Marinol capsule would make me feel ‘stoned’ for several hours, such that I was unable to function at a level at which I felt comfortable or competent,” explained an HIV/AIDS patient named Keith Vines. “Other times the Marinol put me right to sleep.”

Inhaled cannabis, either smoked or vaporized, provides patients with more flexible dosing and control over intoxicating effects. “I found that it took only two or three puffs from a marijuana cigarette for my appetite to return,” Vines added. “Moreover, the beneficial effect took place within minutes rather than hours that I sometimes waited after swallowing a Marinol capsule.”

Not only does cannabis reduce symptoms and side effects, it has also demonstrated some promise as an inhibitor of HIV/AIDS progression. One study, for example, observed a marijuana constituent called Denbinobin slow the replication of HIV. Though this mechanism requires further study, it opens up fascinating possibilities for improved HIV/AIDS therapies.

In today’s society, the importance of mental health is oftentimes swept under the rug. The symptoms of HIV/AIDS can take a heavy toll on patients as physical discomfort converts to emotional anguish. Depression, anxiety, and stress continue to feed physiological deterioration, and yet the euphoric relief associated with cannabis consumption has been pushed into the realm of taboo.

Peter McWilliams, a medical cannabis activist and author who died in 2000, wrote about his experiences as an AIDS and cancer patient. He spoke in depth about the role of cannabis in restoring a patient’s quality of life.

“In addition to the remarkable anti-nausea effects, medical marijuana had one additional benefit--now how do I say this without corrupting the youth of the nation?--I had forgotten how enjoyable it is being stoned,” McWilliams wrote. “I had forgotten, too, how healing enjoyment can be. Yes, pleasure is therapy. Ease to unravel disease. A deep appreciation of life as an answer to death.”

Accessing Medical Marijuana for HIV/AIDS

Patients considering medical marijuana for HIV/AIDS symptom management should always consult a physician before using cannabis, but knowing what options are available can make a world of difference.
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Monday, October 5, 2015

The Cure For HIV Is Not Around the Corner

by Benjamin Ryan
 
Cutting through the hype and hyperbole.

Click here to read a digital edition of this article.

The news broke in April 2013. Danish researchers were mere months from finding a cure for HIV. As other media outlets eagerly picked up the Telegraph’s electrifying report, word coursed lightning-swift online and through social media, stoking hopes that talk of ending the HIV epidemic, increasingly common of late, might soon become reality.

There was one snag: The U.K. paper’s astonishing headline, "Scientists on Brink of HIV Cure," wasn’t true. Researchers at the Aarhus University Hospital in Aarhus, Denmark, were, and still are, researching an HIV cure—that much was a fact. The Danish facility is one in a collection that is investigating cancer drugs known as histone deacetylase (HDAC) inhibitors as a means to flush the virus from the so-called latent reservoir where it hunkers down, craftily evading antiretroviral (ARV) treatment. But the Aarhus University research is only in an early phase of the multi-year process of human trials. And there is no guarantee that the investigators are more than scratching the surface of the daunting task of finding a broadly applicable cure for such a complex viral infection as HIV.

The Telegraph, which eventually revised the online article while the hospital released its own correction (the paper does not appear to have run one), is hardly alone in claiming, or at least implying, that an HIV cure is imminent. Nor is HIV the only health concern to inspire such erroneous hyperbole. Ever since President Richard Nixon announced the “war on cancer” in 1971, news outlets have repeatedly raised hopes of major victory on that front.

A typically tantalizing HIV-related headline comes from the website Medical Daily, which in March enthused that a functional cure—wherein the virus is not totally eliminated from the body but is under control without ARVs— was a “step closer to reality.”

However, Michael Farzan, PhD, a prominent HIV cure researcher and a professor at Scripps Research Institute in Florida, says, “It’s hard to say how far along we are, from start to finish” in the quest for an HIV cure. “Who knows; we could have moved one inch in a 100-mile race.”

Zhi Hong, PhD, head of infectious disease research at GSK (GlaxoSmithKline), which is one of several pharmaceutical companies investing in cure research, puts the matter more definitively: “There’s no illusion that [a cure] is not going to take decades to come to fruition.”

Overzealous members of the media are hardly the only ones contributing to public misperceptions of cure research. Perhaps unintentionally—his words ran contrary to all other public messaging from his global health-focused foundation—Microsoft co-founder Bill Gates told attendees of the World Economic Forum in January that both an HIV vaccine and the means to save people living with the virus from the need to take daily ARVs would arrive by 2030.

Richard Jeffreys, an HIV vaccine and cure expert at Treatment Action Group, scrutinized Gates’s words in a post on TAG’s website, reasoning that “hope does not equate to inevitability.”

“Gates’s buoyancy,” Jeffreys wrote, “does have some scientific basis—there have been encouraging signs of progress on both the vaccine and cure fronts in recent years—but the challenges that lie ahead must not be underestimated.”

Then there’s the exuberant fundraising messaging coming from amfAR, The Foundation for AIDS Research, which sends frequent emails signed by CEO Kevin Frost in which he characterizes the nonprofit’s “Countdown to a Cure” initiative as devoted to “unlocking HIV’s final mysteries” or clearing the “final hurdles” blocking an HIV cure.

A high-concept fundraising video published on the foundation’s website in April says that the fight against HIV has made it to “the final mile of an epic journey,” and that “a cure for all is so close. The end is finally in sight. All we need to do is grab the torch and take it over the finish line.” Only at the very end of the 1,000-word promotional text does amfAR pivot from its repeatedly underlined claim that the foundation’s goal is to find “a broadly applicable cure for HIV by 2020” to finally clarifying that it actually aims to help establish the “scientific underpinnings of a cure” by then. The initial amfAR news release announcing the cure initiative in February 2014 never made such a clarification.

Meanwhile, Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases (NIAID), a division of the National Institutes of Health (NIH), says that success on the cure front is a matter of “if” rather than “when.”

“That doesn’t mean that there’s any giving up on trying,” he says. “But you’ve got to realize where you are in the process.”

Bucking the trend of overly effusive reports on cure progress, CNN ran a headline on its website in July quoting the French virologist Françoise Barré-Sinoussi, PhD, co-discoverer of HIV, who argued that “to develop a cure is almost impossible.”

Headlines are by their nature reductive, certainly because of space constraints, but perhaps more so because journalists’ efforts to lure readers often subvert nuance or specificity in the text. In this case, CNN left many with the dispiriting impression—just as inaccurate as the notion that a cure is around the corner—that Barré-Sinoussi thought all hope was lost. But as the interview clarifies, the Nobel laureate’s claim was more pragmatic than pessimistic, and hinged on her description of the extreme difficulty of eliminating every last HIV-infected cell from the body. (When referring to success in such a feat, many scientists use more specific terminology, calling it a sterilizing cure.) She argued that what she called remission, in which the virus is brought to very low levels and kept there without daily meds, is a more viable goal, one that others call a functional cure.

******

Of course there is one person who has been cured of HIV: Timothy Ray Brown. The 49-year-old American is also known as the Berlin Patient, after the city in which he was treated for leukemia and given two bone marrow transplants, in 2007 and 2008, from a donor whose immune cells were naturally resistant to HIV thanks to an inherited genetic mutation about 1 percent of Caucasians possess. (Leukemia is cancer of the bone marrow, which manufactures immune cells. A bone marrow transplant gives an individual someone else’s immune system after theirs has been intentionally destroyed, typically by chemotherapy.)

Until Brown’s case was first reported, and then widely heralded, in 2008, a cure for HIV was the research ambition that dared not speak its name. The absence of replicating virus in Brown’s body established what scientists call a proof of principle—in this case, that a cure is possible—and it jolted the cure field to life. More scientists got on the bandwagon, and research grants flowed.

The challenge before them is formidable. The principal foe is the viral reservoir, an amorphous entity made up of cells infected with the virus in an unreplicating form, and which may also include infected cells out of reach of standard treatment, such as in the brain. Standard HIV treatment doesn’t eliminate the reservoir because ARVs only work when a cell is replicating, and because not all the meds can cross the so-called blood-brain barrier.

Unfortunately, Brown’s cure is not widely applicable. Such cancer treatments, which are highly expensive, have a steep fatality rate; post-Brown, similar efforts to cure HIV and cancer simultaneously in six others have failed, or the individuals have died before researchers could establish if the HIV cure pursuit was successful. Attempts to prepare the body for a bone marrow transplant with less potentially lethal means have also failed to vanquish HIV.

A critical obstacle facing cure efforts is that scientists haven’t developed tools refined enough to determine with absolute certainty that there are no latently infected cells hiding out in someone’s body that might years later come to life, start producing new copies of HIV and ultimately repopulate the reservoir. A major element of the search-and-discovery work that largely characterizes the cure field today is the attempt to map the reservoir, and to develop tests that can accurately measure its presence. Nascent versions of such tests are helping scientists determine the success of current attempts to at least reduce the size of the reservoir.

The disappointing case of the famed Mississippi Baby illustrates not only the pitfalls of this inability to properly detect and measure the reservoir, but also the scientific community’s lack of standards for describing an HIV cure, or anything in that general ballpark.

At the 2013 Conference on Retroviruses and Opportunistic Infections (CROI) in Atlanta, Deborah Persaud, MD, a pediatric infectious disease researcher at Johns Hopkins Children’s Center, set off a media frenzy when she announced that a then-18-month-old child in Mississippi had been functionally cured of HIV.

In some ways, the qualifier “functional” acknowledges the impossibility of declaring success in achieving a sterilizing cure. Again, a functional cure is generally defined—there is no official definition—as a case in which someone is not infectious, and although he or she still harbors HIV, the virus is under control without the need for ARVs.

After the Mississippi Baby was infected at birth by her mother, doctors quickly started her on an atypically aggressive cocktail of ARVs. Her mother eventually interrupted the treatment, and by the time Persaud first presented the case to fellow scientists, the girl had spent 10 months off ARVs without a viral rebound. Highly sensitive tests could, however, still detect traces of the virus in her body. Persaud says she used the word “functional” at the time because she felt not enough time had passed to confirm that the child was, simply, cured.

This period came to a close after 27 months, when the child’s viral load rebounded and she was put back on ARVs in 2014.

“The field has to really stop and think about terminology and expectations,” reflects Persaud, who is among the leaders of a trial seeking to replicate the Mississippi case in newborns infected at birth around the world.

There is hope that other children will fare better than the Mississippi Baby (whose case, along with other failed cure attempts, has taught scientists a great deal and helped shape and propel future research). July’s International AIDS Society Conference in Vancouver, British Columbia, heard news that an 18-year-old French woman has 12 years of remission under her belt after being born with HIV, initially receiving prophylactic treatment, and then spending six years on ARV combination therapy before quitting treatment. Researchers can still find some HIV DNA in her body, but she has no detectable viral replication in her plasma.

Another dozen French individuals, known as the Visconti cohort, have been in a state of remission for a median decade after stopping the ARV treatment all of them started within six months of contracting HIV. Scientists believe that, in each of them, such prompt treatment prevented the viral reservoir from significantly entrenching itself.

Asier Sáez-Cirión, PhD, of the Institut Pasteur in Paris, first presented data on the Visconti cohort at CROI 2011; but, in his words, the news went “almost unnoticed” at the time. In recent years it has garnered more interest, but nothing compared with the Mississippi Baby. The vast disparity in attention directed at Sáez-Cirión’s and Persaud’s respective announcements may be attributable to semantics. Sáez-Cirión has from the start eschewed the glamour and excitement of the word “cure,” with or without a qualifier, and has steadfastly insisted on characterizing these French individuals as being in a state of remission.

The word “remission,” Sáez-Cirión reasons, evokes a concept people are familiar with from cancer: The disease is gone, but there’s always a chance it could return. “When you use the term ‘functional cure,’” he adds, “sometimes the ‘functional’ part is dropped and the ‘cure’ part remains. It creates some confusion.”

Indeed, many of the headlines concerning the Mississippi Baby stated only that she was cured, thus stripping the message of any nuance. Touting its contributions to the case (another possible reason the case received so much media attention), amfAR stated in a press release that “confirmation of the cure was made possible” in part by an amfAR grant supporting Persaud’s research.

******

In marked contrast to the foundation’s fundraising pitches, amfAR’s director of research, Rowena Johnston, PhD, strikes a measured tone when describing the current state of HIV cure research, saying, “Thoughts around the key challenges are starting to coalesce. Not that [researchers] have necessarily found answers or all of the answers. But that people are really starting to agree what the challenges are.”

One major element that is increasingly coalescing is money. According to a July report from the global HIV advocacy group AVAC, worldwide public and philanthropic investment in cure research leaped by 82 percent between 2012 and 2014, from $88 million to $160 million. The lion’s share comes from the United States, mostly in the form of NIH grants, with $114 million given in 2014 and an estimated $127 million slated for 2015. AmfAR intends to rapidly scale up its annual cure funding from $4.4 million in 2014 to give researchers a total of $100 million over a six-year period starting in 2015. The Gates Foundation granted about $9 million to cure research in 2014.

Such figures are still paltry compared with recent HIV vaccine research investment; the NIH spends over half a billion dollars annually on that front. According to Fauci, the disparity between cure and vaccine funding is not a reflection of the agency’s lack of enthusiasm for the cure cause. Rather, vaccines get more money because the field is more advanced; vaccines are primarily in the development, rather than discovery, phase.

“The investment goes up once you have specific leads to pursue, and the relatively greater NIH investment in HIV vaccine research at this point in time reflects that,” Fauci says.

AVAC’s overall cure research figures don’t account for industry spending. GSK recently pledged $20 million over five years for a joint effort with the University of North Carolina (UNC), Chapel Hill. Additionally, Merck, Gilead Sciences, Janssen, and the biotech companies Sangamo BioSciences and Calimmune are all in the search.

The field is increasingly collaborative. In 2011, the NIH established the Martin Delaney Collaboratories, which has encouraged cooperation between academia and the private sector. There also is collaboration between amfAR grantees.

When it comes to research that goes beyond background study and progresses into actual curative therapies, the biggest focus is on a method known as shock and kill, or kick and kill. In the first part of this strategy—the shock or kick phase—an agent, or combination of agents, spurs the machinery of latently infected cells back into action. The subsequent challenge—the kill part—is to find ways to clear the body of those newly active cells.

Unfortunately, ARVs don’t kill HIV-infected cells. Nor does the immune system, in part because these particular cells have so few HIV antigens on their surfaces. (Antigens flag a cell as infected and help summon an immune response.) Confounding the issue, a person’s immune response to HIV may have lessened after years of taking ARVs, and the virus in latently infected cells may have mutated to resist the immune system’s primary line of attack.

The lab of Robert Siliciano, MD, PhD, at Johns Hopkins University, leads the shock-and-kill field, which includes efforts from more than two dozen groups around the world, such as the UNC-GSK team and the Danish lab that spawned those erroneous headlines. Researchers are testing at least six latency-reversing agents in humans, including the HDAC inhibitors vorinostat, panobinostat and romidepsin.

Scientists on the kill front are exploring various means of boosting the immune response in order to give rise to immune cells or antibodies that can more effectively attack the reawakened infected cells.

According to David Margolis, MD, who heads up the UNC effort, shock and kill is still in “in its infancy,” but it has enjoyed some recent advances. “The biggest limitation to forward progress right now,” Margolis says, “is that we haven’t yet really developed safe and effective ways to substantially deplete the reservoir that we can measure.” In other words, with research into the kill part of the strategy only just beginning, any results are particularly insufficient. “I think that after hopefully not too long, maybe a year or two, we will have forward motion in that regard.”

Fauci, however, is “not at all sure” that the overall shock and kill approach will prove successful.

Delving further into the realm of science-fiction-come-true is research into curative genetic therapies. Researchers are trying to recreate Tim Brown’s case (or at least partially so), but without the danger and impracticality of a traditional bone marrow transplant.

Brown’s donor had a genetic mutation that prevented development of what’s called the CCR5 coreceptor, which is located on the surface of the CD4 immune cells that HIV targets. Without CCR5, most copies of HIV can’t latch onto the immune cell, much less infect it. So scientists at Sangamo and the Fred Hutchinson Cancer Research Center, among others, are experimenting with drawing out an HIV-positive individual’s immune cells, or immune cell-producing stem cells, and editing their genetic code to ultimately prevent the development of the CCR5 coreceptor.

Sangamo has had some promising results from the company’s genetic treatment, with one 32-year-old man off ARVs for over a year and a half following an infusion of edited, HIV-resistant immune stem cells. He isn’t cured—the virus is still actively replicating—but his viral load is only about 500 and his CD4 level has remained stable.

This is an example of the partial success that researchers may build upon as they reach for the pie in the sky. Each of these individual steps may offer new and exciting health benefits to people living with HIV. Ultimately, multiple approaches may be required to beat back the virus further than ARV treatment is already able to do.

“There are many routes of attack” in the cure quest, says the Nobel prize–winning virologist David Baltimore, PhD, a professor at the California Institute of Technology and the founder of Calimmune, “and from my point of view, the word cure is perhaps misleading. What we want to do is make this a less and less debilitating disease. And what that means is limiting the effects of the virus and also moving toward forms of therapy that are less debilitating to the patient.”

Another incremental advance that cure research may achieve is to reduce the kind of low-level viral replication that occurs even in the presence of successful ARV treatment. Scientists suspect this activity from the virus may spur the immune system into a state of chronic inflammation, which is believed to contribute to the increased risk of age-related disorders among people living with the virus. Another shorter-term ambition is for treatments that would allow for periods of extended viral remission, giving HIV-positive people a safe way to take time off from the toxicities of ARVs.

Vastly shrinking but not totally eliminating the reservoir may allow for such extended remission. Case in point, the members of the Visconti cohort don’t have zero reservoir; it’s just very small in each of them. (Scientists do have the tools to determine this.) A recent study found that if someone stops taking ARVs, on average, a week will pass before at least one latently infected cell successfully reactivates and is able to kick start a viral rebound. Considering the vast number of cells in the typical reservoir, the implication is that any given cell only rarely jumps into significant action. Based on these observations, the paper’s authors estimated that a 50-to-70-fold reduction in the size of the reservoir could extend the time between stopping ARVs and a viral rebound to an average of one year. Siliciano has made his own projection that some people with HIV may experience lifelong remission with as little as a 1,000-to-10,000-fold reservoir reduction.

“We might get interventions that work a good part of the time in good sections of the people,” says amfAR’s Johnston. “And so it will be this interactive process over time until you get to an intervention that cures most people most of the time. Maybe that’s as good as we can hope for.”

Assuming such advances do come, there is the pressing question of access. The new $100,000 hepatitis C cures are threatening state Medicaid and prison health budgets nationwide, and insurers have been restricting who can receive treatment.

The process required to draw out, edit and reinfuse an HIV-positive person’s immune cells is quite expensive, and the cost can’t necessarily be brought down simply by pharmaceutical companies allowing generic production, as with ARVs used in poorer nations. (Although compared with lifelong ARV treatment, the cost for such a cure might be a bargain, especially if a one-time curative therapy is all that’s required.) With the ultimate goal of expanding such a potential opportunity to populations beyond the wealthy Western world, researchers hope that a similarly successful outcome wouldn’t require such a complicated process, and instead would come from a generalized vaccine-like shot, or maybe a series of shots.

“At the end of the day, if you have what you’re calling a cure or a sustained virologic remission, it’s got to have the three S’s: safe, simple and scalable,” says NIAID’s Fauci. “Otherwise you’re going to cure a handful of people that are going to make the front page of The New York Times, and then you can’t do much else for the 36 million other people who are infected.”

HIV Cure Research, In Short

HIV cure research is in what’s known as the discovery phase. The field is largely characterized by efforts to better understand just what scientists are up against in their quest to cure the virus.

Major avenues include:
  • Characterizing the viral reservoir. What kind of cells are in the reservoir and where in the body are they located?
  • Developing tests to measure the reservoir. This is vital to be able to measure the success of attempts to reduce the size of the reservoir.
  • Determining how the reservoir manages to persist.
Current therapeutic pursuits include:
  • “Shock and kill” or “kick and kill,” in which an agent or combination of agents, such as cancer drugs called HDAC inhibitors, are used to flush the virus out of latently infected cells. Then another method is used to prompt the body to better eliminate those cells.
  • Genetic therapies. Researchers are trying to recreate the Berlin Patient’s cure by editing immune cells or immune-cell-producing stem cells to ultimately populate the body with HIV-resistant immune cells.
Common terms:
  • Sterilizing cure: totally ridding the body of HIV.
  • Functional cure: There is still some virus in the body, but it’s under control without the need for daily meds.
  • Remission: Some researchers prefer to use this term instead of “functional cure,” because it is familiar to people from the world of cancer and implies that the virus may rebound, as was the case with the Mississippi Baby.
International investment in cure research:

2012: $88 million
2013: $105 million
2014: $160 million

These figures do not reflect for-profit investment. Many biotech and pharmaceutical companies are pursuing cure strategies. For example, GSK recently pledged $20 million over five years to the University of North Carolina, Chapel Hill.
Search: HIV cure, HIV vaccine, antiretrovirals, viral reservoir, shock and kill, HDAC inhibitors, gene therapy, Berlin Patient, Timothy Brown, immune cells, sterilizing cure, functional cure, remission, Mississippi Baby, Aarhus University, Telegraph, Michael Farzan, Zhi Hong, GSK, amfAR, Bill Gates, Richard Jeffreys, Kevin Frost, Countdown to a Cure, Anthony Fauci, CNN, Françoise Barré-Sinoussi, Deborah Persaud, VISCONTI, Rowena Johnston, AVAC, The Foundation for AIDS Research, University of North Carolina, Chapel Hill, Merck, Gilead Sciences, Janssen, Sangamo BioSciences, Calimmune, Robert Siliciano, David Margolis, CCR5, David Baltimore, The New York Times, Danish.

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HIV Overview - The Stages of HIV Infection


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(Last updated 9/15/2015; last reviewed 9/15/2015)

Key Points

  • Without treatment, HIV infection advances in stages, getting worse over time.
  • The three stages of HIV infection are (1) acute HIV infection, (2) chronic HIV infection, and (3) acquired immunodeficiency syndrome (AIDS).
  • HIV can be transmitted (spread to others) during any stage of infection, but the risk is greatest during acute HIV infection.
  • There is no cure for HIV infection, but HIV medicines (called antiretroviral medicines) can prevent HIV from advancing to AIDS. HIV medicines help people with HIV live longer, healthier lives. HIV medicines also reduce the risk of HIV transmission (the spread of HIV to others).
Without treatment, HIV infection advances in stages, getting worse over time. HIV gradually destroys the immune system and eventually causes acquired immunodeficiency syndrome (AIDS).

There is no cure for HIV infection, but HIV medicines (called antiretroviral medicines) can prevent HIV from advancing to AIDS. HIV medicines help people with HIV live longer, healthier lives. HIV medicines also reduce the risk of HIV transmission (the spread of HIV to others).

There are three stages of HIV infection:

 
1.) Acute HIV Infection
Acute HIV infection is the earliest stage of HIV. Acute HIV infection generally develops within 2 to 4 weeks after a person is infected with HIV. During acute HIV infection, many people have flu-like symptoms, such as fever, headache, and rash. In this acute stage of infection, HIV multiplies rapidly and spreads throughout the body. The virus attacks and destroys the infection-fighting CD4 cells of the immune system. HIV can be transmitted during any stage of infection, but the risk is greatest during acute HIV infection.

2.) Chronic HIV Infection
The second stage of HIV infection is chronic HIV infection (also called asymptomatic HIV infection or clinical latency). During this stage of the disease, HIV continues to multiply in the body but at very low levels. People with chronic HIV infection may not have any HIV-related symptoms, but they can still spread HIV to others. Without treatment with HIV medicines, chronic HIV infection usually advances to AIDS in 10 to 12 years.

3.) AIDS 
AIDS is the final stage of HIV infection. Because HIV has destroyed the immune system, the body can’t fight off opportunistic infections and cancer. (Examples of opportunistic infections include pneumonia and tuberculosis.) AIDS is diagnosed when a person with HIV has a CD4 count of less than 200 cells/mm3 and/or one or more opportunistic infections. Without treatment, people with AIDS typically survive about 3 years.

This fact sheet is based on information from the following sources:


Find more information here:  https://aidsinfo.nih.gov
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CDC Supports New WHO Early Release HIV Treatment and PrEP Guidelines

 
Date: September 30, 2015
Source: Centers for Disease Control and Prevention (CDC)
URL: http://www.cdc.gov/media/releases/2015/s0930-hiv-prep.html

CDC welcomes today's announcement by the World Health Organization (WHO) of new Early Release HIV Treatment and Pre-Exposure Prophylaxis (PrEP) guidelines that will significantly increase the number of people eligible for life-saving anti-retroviral treatment (ART) and expand access to a powerful tool for preventing HIV among those at greatest risk.

These recommendations are a major step forward in the global fight against HIV. They have the potential to dramatically reduce transmission of HIV worldwide, increase the widespread use of PrEP among those who need it most, and help those living with HIV live longer, healthier lives.

The new WHO guidelines call for treatment for all individuals living with HIV – regardless of CD4 count. This is a dramatic shift from existing WHO guidelines that recommend ART for those with compromised immune systems (CD4 counts less than 500) and other vulnerable populations such as children, pregnant women, and people with TB. The new guidelines also recommend daily oral PrEP as an additional prevention choice for those at substantial risk for contracting HIV as part of a combination prevention approach.

Thanks to recent scientific breakthroughs, we now know unequivocally that early and effective treatment not only reduces HIV transmission but also significantly improves health outcomes for those living with HIV. The research on PrEP is also strong. PrEP has been shown in many studies and "real world" situations to reduce the risk of HIV infection by more than 90% among those who regularly take their medications.

While the science is clear, today's guidelines are a call to policymakers and the public health community worldwide to translate that science into action. The WHO Early Release Guidelines support countries in expanding access to HIV treatment and affirm the promise of PrEP as an important part of a comprehensive response to HIV.

Today's announcement aligns with two key U.S. recommendations. In 2012, the U.S. Department of Health and Human Services (HHS) issued treatment guidelines recommending ART for all patients diagnosed with HIV infection. In 2015, this was upgraded to an A1 recommendation, based on the highest quality evidence (a randomized controlled clinical trial) In 2014, CDC issued first-ever clinical guidance recommending physicians consider advising the use of PrEP for gay and bisexual men, heterosexuals, and injection drug users at substantial risk for HIV infection.

In collaboration with other United States agencies and global partners, CDC and the National Institutes of Health, both part of HHS, have been at the forefront of PrEP research efforts. CDC also is helping to increase access to ART for those who need it around the world.

With 15 million people now on ART and recent reductions in HIV across the globe, we know that together we can make continued progress in HIV prevention and treatment. But with more than 22 million people living with HIV who are not yet on treatment and more than 2 million new infections in 2014 alone, more needs to be done. We hope these recommendations will encourage the global HIV community to act.

Find more information here: https://aidsinfo.nih.gov/news
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HIV Treatment - FDA-Approved HIV Medicines


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(Last updated 5/4/2015; last reviewed 5/4/2015)
Treatment with HIV medicines is called antiretroviral therapy (ART). ART is recommended for everyone with HIV. People on ART take a combination of HIV medicines (called an HIV regimen) every day. A person's initial HIV regimen generally includes three HIV medicines from at least two different drug classes.

ART can’t cure HIV, but HIV medicines help people with HIV live longer, healthier lives. HIV medicines also reduce the risk of HIV transmission.

The following table lists HIV medicines approved by the U.S. Food and Drug Administration (FDA) for the treatment of HIV infection in the United States. The HIV medicines are listed according to drug class and identified by generic and brand names. Click on a drug name to view information on the drug from the AIDSinfo Drug Database. Or download the AIDSinfo Drug Database app to view the information on your Apple or Android devices.


FDA-Approved HIV Medicines
Drug Class Generic Name
(Other names and acronyms)
 Brand Name FDA Approval Date
Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
NRTIs block reverse transcriptase, an enzyme HIV needs to make copies of itself. abacavir
(abacavir sulfate, ABC)		 Ziagen December 17, 1998
didanosine
(delayed-release didanosine, dideoxyinosine, enteric-coated didanosine, ddI, ddI EC)		 Videx October 9, 1991
Videx EC
(enteric-coated)		 October 31, 2000
emtricitabine
(FTC)
 Emtriva July 2, 2003
lamivudine
(3TC)		 Epivir November 17, 1995
stavudine
(d4T)		 Zerit June 24, 1994
tenofovir disoproxil
fumarate
(tenofovir DF, TDF) 		Viread October 26, 2001
zidovudine
(azidothymidine, AZT, ZDV)
 Retrovir March 19, 1987
Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
NNRTIs bind to and later alter reverse transcriptase, an enzyme HIV needs to make copies of itself.
 delavirdine
(delavirdine mesylate, DLV)
 Rescriptor
 April 4, 1997
efavirenz
(EFV)		 Sustiva September 17, 1998
etravirine
(ETR)		 Intelence
 January 18, 2008
nevirapine
(extended-release nevirapine, NVP)		 Viramune
 June 21, 1996
Viramune XR (extended release)
 March 25, 2011
rilpivirine
(rilpivirine hydrochloride, RPV)
 Edurant May 20, 2011
Protease Inhibitors (PIs)
PIs block HIV protease, an enzyme HIV needs to make copies of itself
 atazanavir
(atazanavir sulfate, ATV)
 Reyataz June 20, 2003
darunavir
(darunavir ethanolate, DRV)
 Prezista  June 23, 2006
fosamprenavir
(fosamprenavir calcium, FOS-APV, FPV)
 Lexiva October 20, 2003
indinavir
(indinavir sulfate, IDV)
 Crixivan
 March 13, 1996
nelfinavir
(nelfinavir mesylate, NFV)
 Viracept
 March 14, 1997
ritonavir
(RTV)
 Norvir
 March 1, 1996
saquinavir
(saquinavir mesylate, SQV)
 Invirase
 December 6, 1995
tipranavir
(TPV)
 Aptivus
 June 22, 2005
Fusion Inhibitors
Fusion inhibitors block HIV from entering the CD4 cells of the immune system.
 enfuvirtide
(T-20)
 Fuzeon
 March 13, 2003
Entry Inhibitors
Entry inhibitors block proteins on the CD4 cells that HIV needs to enter the cells.
 maraviroc
(MVC)
 Selzentry
 August 6, 2007
Integrase Inhibitors
Integrase inhibitors block HIV integrase, an enzyme HIV needs to make copies of itself.
 dolutegravir
(DTG)
 Tivicay
 August 13, 2013
elvitegravir
(EVG)		 Vitekta September 24, 2014
raltegravir
(raltegravir potassium, RAL)
 Isentress
 October 12, 2007
Pharmacokinetic Enhancers
Pharmacokinetic enhancers are used in HIV treatment to increase the effectiveness of an HIV medicine included in an HIV regimen.
 cobicistat
(COBI)
 Tybost
 September 24, 2014
Combination HIV Medicines
Combination HIV medicines contain two or more HIV medicines from one or more drug classes.
 abacavir and lamivudine
(abacavir sulfate / lamivudine, ABC / 3TC)
 Epzicom
 August 2, 2004
abacavir, dolutegravir, and lamivudine
(abacavir sulfate / dolutegravir sodium / lamivudine, ABC / DTG / 3TC) 		 Triumeq  August 22, 2014
abacavir, lamivudine, and zidovudine
(abacavir sulfate / lamivudine / zidovudine, ABC / 3TC / ZDV)
 Trizivir
 November 14, 2000
atazanavir and cobicistat
(atazanavir sulfate / cobicistat, ATV / COBI)
 Evotaz
 January 29, 2015
darunavir and cobicistat
(darunavir ethanolate / cobicistat, DRV / COBI)
 Prezcobix
 January 29, 2015
efavirenz, emtricitabine, and tenofovir disoproxil fumarate
(efavirenz / emtricitabine / tenofovir, efavirenz / emtricitabine / tenofovir DF, EFV / FTC / TDF)
 Atripla July 12, 2006
elvitegravir, cobicistat, emtricitabine, and tenofovir disoproxil fumarate
(QUAD, EVG / COBI / FTC / TDF)
 Stribild August 27, 2012
emtricitabine, rilpivirine, and tenofovir disoproxil fumarate
(emtricitabine / rilpivirine hydrochloride / tenofovir disoproxil fumarate, emtricitabine / rilpivirine / tenofovir, FTC / RPV / TDF)
 Complera August 10, 2011
emtricitabine and tenofovir disoproxil fumarate
(emtricitabine / tenofovir, FTC / TDF)
 Truvada August 2, 2004
lamivudine and zidovudine
(3TC / ZDV)
 Combivir September 27, 1997
lopinavir and ritonavir
(ritonavir-boosted lopinavir, LPV/r, LPV / RTV)
 Kaletra September 15, 2000

This fact sheet is based on information from the following sources:

More information can be found here: https://aidsinfo.nih.gov/
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