The Road Ahead for HIV Cure Research

Today, with better understanding of the complex task at hand, cure researchers are investigating multiple avenues and taking the long view.  This article comes from Benjamin Ryan and was first presented online in Poz.com on January 7, 2019

Cure research and the potential for a cure is still front and centre in many of our lives and this article talks about the road ahead and some of the setbacks that have been suffered along the way.


HIV cure researchers received some disappointing news at the July 2018 International AIDS Conference in Amsterdam. Two studies in particular offered a sobering lesson on how extraordinarily complex developing a safe and effective cure for the virus will likely be.

As conference attendees learned, researchers behind a randomized trial of an HIV cure method, the largest such study to date, recently found that their efforts failed to reduce viral DNA in human participants. The trial, called RIVER, tested the “kick and kill” strategy that seeks to roust latently infected immune cells from their slumber and then kill them off. Standard HIV medications—antiretrovirals, or ARVs—work only against cells that harbor actively replicating virus. These resting infected cells are a chief component of what is known as the viral reservoir, and it’s the stubborn persistence of this reservoir that frustrates cure efforts.

In a second study presented at the conference, an antibody treatment that had shown promise in monkeys failed to prompt what is known as posttreatment control of the virus after HIV-positive humans interrupted their ARV therapy.

As scientists in this field recalibrate their expectations, the use of the term “cure” as a goal for their research is declining. Instead, investigators may seek to induce posttreatment control of HIV, or viral remission, in which a particular therapy would not eradicate the virus from the body but rather suppress HIV over an extended period without the need for long-term ARV treatment.

Nevertheless, the overall field is generally still referred to as HIV cure research.

Taking the pulse of her fellow HIV cure researchers, Sharon R. Lewin, MD, PhD, director of The Peter Doherty Institute for Infection and Immunity at the University of Melbourne in Australia, says, “If anything, there was probably more optimism four years ago because we had tried fewer things. We now know that curing HIV is definitely not an easy task.”

Looking on the bright side, Lewin points to other promising recent cure studies conducted in primates, noting, “We definitely have been able to cure a few monkeys. That’s exciting.”

But as the antibody study presented at the Amsterdam conference indicated, disappointing outcomes among humans might follow success in primate research.

“The preclinical studies have universally shown more favorable outcomes than human studies,” says Jintanat Ananworanich, MD, PhD, who in her capacity as the associate director for therapeutics research at the U.S. Military HIV Research Program directs research in the HIV cure field. “Although no strategies have resulted in remission in clinical trials thus far, tremendous knowledge on HIV persistence and immune responses has been generated. This is important to informing future trials.”

Concerns about recent setbacks notwithstanding, Lewin remains optimistic about the future of HIV cure research. “Science can also take dramatic turns with significant discoveries too,” she says. “So you never know what may change the field dramatically.”

Lewin is the lead author of a literature review recently published in The Lancet HIV, “Barriers and Strategies to Achieve a Cure for HIV,” in which she and her three coauthors offer a comprehensive summary of the impressive number of avenues researchers are pursuing in their quest for a cure, or something close to it. Below, POZ looks at the main takeaways from their paper. We also explore a few HIV cure studies published more recently.

***

Lewin and her colleagues note that the only person ever cured of HIV remains Timothy Ray Brown. As a component of his treatment for leukemia, Brown received stem cell transplants a decade ago from a donor with a genetic mutation that confers natural resistance to the virus—the surface of the donor’s immune cells lacked the CCR5 coreceptor to which most HIV attaches in order to infect the cells. As far as researchers can tell, Brown benefited from a sterilizing cure. There is no evidence in his body of any virus with the capacity to replicate, and his viral load has never rebounded. (Today, Brown actually takes Truvada [tenofovir disoproxil fumarate/emtricitabine] as pre-exposure prophylaxis [PrEP] to ensure he does not contract HIV again.)

Otherwise, in the realm of posttreatment control of HIV, quite a few people with the virus have been able to suppress their viral load for long stretches, sometimes for years, after interrupting standard ARV treatment. A recently published paper found that those who began ARVs very soon after contracting the virus are more likely to achieve such a prolonged state of viral remission after eventually going off their meds. It is likely that beginning on ARVs so promptly after infection keeps the viral reservoir relatively small, thus reducing the likelihood of latently infected cells springing to life at any given moment following a treatment interruption.

One of the most famous cases of such posttreatment control is that of the African child who was treated for HIV for less than a year after birth and, by the time the child’s case was reported in 2017, had spent over eight years in a state of viral remission. In 2015, news surfaced that an 18-year-old French individual had spent 12 years off ARVs and still controlled the virus. Then, of course, there was the 2013 case of “the Mississippi Child”—met with great fanfare—who spent a couple of years off ARVs during her very young life but ultimately, and disappointingly, experienced a viral rebound at 4 years old.

According to Lewin, scientists’ increasingly enriched comprehension of the posttreatment-control phenomenon has actually made designing HIV cure studies more difficult. Now researchers must take into account that some study participants might achieve control of their virus, even if for a short time, without the benefit of an investigative cure therapy, thus making it more challenging to prove that a cure treatment was the cause of viral remission or a delayed viral rebound after the interruption of ARV treatment.

***

Not only do latently infected immune cells evade ARV treatment, but also for every million such cells, perhaps only 60 harbor virus that can actually replicate; the rest contain defective virus. So finding those resting cells capable of waking up and repopulating the body with new virus in the absence of ARV treatment can be akin to finding a needle in a haystack. The immune system itself wastes considerable energy going after cells infected with dud copies of the virus.

In another of the myriad ways HIV has evolved to help ensure it sustains a lifelong infection, latently infected cells have the ability to clone themselves. Perhaps more than half of the viral reservoir cells in some people living with the virus are clones.

The matter of whether HIV continues to replicate at low levels in the face of effective ARV treatment has been the source of significant controversy in the cure field. A study presented at the 2018 Conference on Retroviruses and Opportunistic Infections in Boston found no evidence of such ongoing replication in the lymph nodes, calling into question the notable contrasting findings of a 2016 paper.

***

The lack of precise tests for measuring the viral reservoir remains a considerable obstacle for HIV researchers, both in determining the challenge they face in their quest to vanquish an infection and in assessing how well they did. Currently, scientists in the field must rely on rather crude metrics, such as changes in the overall presence of viral DNA or RNA in the blood, to gauge how a particular treatment affects the size of the reservoir. (HIV carries its genetic code in RNA, which is copied to DNA during infection of a cell.) Such metrics can underestimate the population of infected cells because most virus hides in tissues, not blood.

Scientists may also try to measure success by determining whether an HIV cure treatment is associated with a delay in viral rebound after an interruption of ARV therapy and whether such a treatment is associated with a particular level of control of the virus in the absence of standard ARV therapy for the virus.

If only scientists could identify a specific biomarker, such as a particular protein, that could predict the likelihood of a delay to viral rebound or control of the virus after a treatment interruption. Then, study participants might be spared the burden of interrupting their ARVs, a common requirement in HIV cure study designs. Asking people to stop standard HIV treatment raises ethical questions and may discourage people living with the virus from entering cure trials. That said, multiple studies have indicated that treatment interruptions in cure studies are safe.

Lewin argues that such a tidy biomarker would likely attract greater investment in the field from pharmaceutical companies. (Global funding for public sector HIV cure research increased from $88 million in 2012 to $289 million in 2017, with the lion’s share coming from the National Institutes of Health.) Such for-profit companies prefer study designs boasting a level of simplicity that will help an investigational treatment pass muster with regulatory bodies like the Food and Drug Administration. They also prefer efficient investments for their research and development dollars. So their researchers favor clearly delineated, objective means of measuring success in clinical trials of experimental agents.

Case in point: The recent discovery of a biomarker that can predict whether an individual will achieve a functional cure of hepatitis B virus (HBV) gave rise to a surge of interest from the pharmaceutical industry in researching curative therapies for HBV.

Investment in Cure Research chart

Source: “Global Investment in HIV Cure Research and Development in 2017”

Investment in Cure Research chart

Source: “Global Investment in HIV Cure Research and Development in 2017”

Avenues of Research:

Stem cell transplants

Clinicians are still trying to replicate the success of Timothy Brown’s HIV cure with similar strategies. In recent years, a number of other individuals with cancer have received stem cell transplants from donors who also have the genetic mutation related to the CCR5 coreceptor that confers resistance to the virus. One of the six such individuals whose cases have been published in scientific literature experienced a viral rebound; the other five ultimately died as a result of complications following their stem cell transplant or from their underlying cancer.

In other cases of people living with HIV who received a stem cell transplant but from a donor who lacked the CCR5-related genetic mutation, the stem cell transplant did delay the time to viral rebound by 3 to 10 months after the individuals stopped ARVs.

However, the high fatality rate following transplantation highlights how impractical, not to mention unethical, this method of attempting to cure HIV is for anyone not already facing a high risk of death due to cancer.

Gene therapy

Seeking safer alternatives to cancer-treatment-based stem cell transplants, researchers are experimenting with gene-editing techniques that alter the DNA of an individual’s immune cells. In particular, the scientists will try to deactivate the gene that gives rise to the CCR5 coreceptor, thus robbing HIV of a means of latching onto immune cells. The modified cells are then grown outside the body and ultimately reinfused into the person’s body. The aim is to spawn a population of immune cells that are resistant to infection. As the field of gene editing rapidly evolves, it is hoped that new, even more cutting-edge technology will facilitate progress on the HIV cure front.

“Kick and kill”

The method of waking up latently infected cells (the “kick” part) and then finishing them off (the “kill” part) has yielded some notably disappointing results of late, including those of the RIVER study that was presented at the July conference in Amsterdam. Researchers pursuing this strategy have looked to various cancer drugs known as HDAC inhibitors as the kick element; but thus far, they have not been able to show such drugs can actually diminish reservoir cells.

Lewin remains cautiously optimistic about further research into these medications, noting that the RIVER trial used a less advanced and relatively weak kick agent. Recent, more preliminary studies that have examined other kick agents, such as so-called TLR agonists, have shown far greater promise.

On this front, Gilead Sciences is investigating a drug known as GS-9620 that has shown positive results in primate research.

Latency silencing: “block and lock”

Effectively the opposite of the kick and kill strategy, the “block and lock” method, also known as latency silencing, is based on the presumption that if rooting out and killing all the latently infected cells in the body is too challenging, keeping them in a silent state indefinitely may be a viable alternative. A recent study conducted in mice sought to inhibit a viral protein known as tat that acts as an on-off switch for viral replication in cells. The study successfully reduced the amount of HIV RNA expressed in tissue biopsies taken from the animals, and it delayed viral rebound after the interruption of ARV treatment.

Enhancing the immune system

Researchers are investigating whether vaccines can be used to prompt the body to better control the virus.

Scientists have also invested considerable energy into studying so-called broadly neutralizing antibodies, which are natural antibodies that boast the capacity to combat a wide array of HIV strains. Research has indicated that some of these antibodies are associated with a delay in viral rebound after an ARV treatment interruption. Recently, scientists have gone high-tech by synthesizing three such antibodies into one “trispecific” antibody—a kind of all-in-one triple combination therapy—that has already shown promise in its use as pre-exposure prophylaxis (PrEP) among primates.

Modulating the immune system

Scientists are seeking to manipulate proteins that redirect the traffic of immune-fighting cells. One such example is an antibody called vedolizumab that targets a protein on the surface of CD4 cells and stops these cells from moving into the gut, where HIV focuses much of its assault on the immune system. An initial study in monkeys reported two years ago provided hope for progress in this area of research, but scientists recently repeated the study and found that the antibody had a null impact on the second go-round. Preliminary results in humans also showed that vedolizumab did not affect the time to viral rebound after individuals interrupted their ARV treatment.

Looking to the future

In all likelihood, a successful HIV cure, or posttreatment control, strategy will rely upon a combination approach based on a number of the methods currently under investigation or those yet to be imagined.

“It is clear that achieving HIV remission will not be easy and that one should not expect any single intervention to help people get to remission,” says Jintanat Ananworanich. “We are taking small steps in discovery science.”

Any successful method will need to be safe, effective and—if it is to make a significant dent in the global epidemic—scalable. An HIV cure therapy that is extraordinarily expensive thanks to, for example, the highly involved and complex process required to provide personally tailored genetic editing of an individual’s immune cells, will have little to offer poorer nations—in particular those in sub-Saharan Africa—where the need is greatest.

Curative hepatitis C virus (HCV) treatment, for example, costs tens of thousands of dollars in the United States, which has led insurers to restrict coverage of the medications. The actual cost to manufacture such medications, however, is relatively low, which allows for a steep sliding scale elsewhere around the world.

The future of HIV cure science is also up against the phenomenal success of ARV treatment, which has set a high bar for any alternative means of suppressing the virus. The life expectancy of those on ARVs is approaching normal. What’s more, the risk of transmitting HIV is effectively zero for those who maintain a fully suppressed viral load.

However, such benefits don’t speak to the psychic costs of living with a highly stigmatized lifelong infection or how a cure therapy may alleviate such burdens. Then there are the extreme difficulty and expense of getting the global population on lifelong ARV treatment. Also, even well-treated HIV is associated with an increased risk of numerous health conditions, such as cardiovascular disease and cognitive decline.

Some form of HIV cure could help address these problems. However, as HIV drug development continues to progress and long-acting injectable treatments, or even very long-lasting implants, become the standard of care, emerging HIV cure treatments may cease to offer the freedom from daily medications as an advantage over standard ARV therapy. (Or perhaps by then, long-acting antibody treatments will be the norm.)

Furthermore, if someone is in a state of posttreatment control of the virus, what reassurances will there be that the virus will remain dormant indefinitely and won’t suddenly surge back and make an individual unwittingly infectious? How frequently will people benefiting from viral remission need viral load monitoring?

These pressing questions, along with HIV’s extraordinary complexity, likely make for a long and winding scientific road ahead. But thanks to the increasing funds backing such research and a growing army of top-tier scientists doggedly pursuing a cure, the future will hopefully prove bright with new developments.

Still, this field isn’t simply concerned with a binary outcome of finding the holy grail of a cure or otherwise failing to do so. Success will likely prove incremental, with scientists eventually discovering new means of further mitigating HIV’s long-term harms, further transforming a once surely fatal infection into an increasingly innocuous presence in the body and around the world.

 

HIV-NEGATIVE GAY MEN UNCOMFORTABLE RELYING ON AN UNDETECTABLE VIRAL LOAD TO PREVENT HIV

Much more confidence in PrEP

Australian HIV-negative gay men express far more confidence in pre-exposure prophylaxis (PrEP) than an undetectable viral load in preventing HIV, with only 18% agreeing that “a person with an undetectable viral load cannot pass on HIV” and 6% feeling comfortable having condomless sex with an HIV-positive partner who had an undetectable viral load, according to a pair of articles recently published in Sexually Transmitted Infections and AIDS & Behavior.

Confidence in the efficacy of PrEP was much higher.

Researchers from the Burnet Institute conducted an online survey with gay and bisexual men living in Melbourne and other parts of the state of Victoria. It included a series of questions to gauge men’s knowledge of and attitudes towards condoms, an undetectable viral load and PrEP.

Australia has a long history of promoting condom use and regular HIV testing in gay men. More recently, there has also been high-profile support for treatment as prevention and PrEP. Around the time the survey was conducted in August and September 2016, a PrEP demonstration project was scaling up in Victoria. Several Australian campaigns promoting the benefits of HIV treatment had already been run, but the international “Undetectable = Untransmittable” campaign had not yet taken off.

Half the survey participants were between the ages of 25 and 40; most identified as gay; and 20% were born outside Australia. A third reported condomless sex with a casual partner in the past six months, and half with a regular partner.

The survey was completed by 844 people, but men with diagnosed HIV were excluded from the following analyses. The data on comfort having condomless sex come from 771 HIV-negative or untested men, including 83 PrEP users (12% of the men). The data on perceptions of effectiveness come from a smaller group of 462 survey respondents who answered all relevant questions and were not using PrEP. (The researchers did not report on responses from PrEP users for these questions.)

Perceptions of effectiveness

Although this analysis excluded current PrEP users, the majority of respondents expressed confidence in PrEP’s effectiveness: 78% agreed that “PrEP is effective in preventing HIV infection” and 65% agreed that “An HIV-negative person who is on PrEP is unlikely to get HIV”. Respondents also agreed that PrEP users were “being responsible” (74%) and were “protecting themselves” (84%).

In contrast, 18% agreed that “A person with an undetectable viral load cannot pass on HIV”. A similar statement, with less definitive language was not much more popular – 20% agreed that “An HIV-positive person on treatment is unlikely to transmit the virus”.

Despite this scepticism, other findings showed that respondents were aware that HIV treatment has a prevention impact – 37% agreed that “If more HIV-positive men have an undetectable viral load, then I’m less likely to get HIV” and 82% agreed that “HIV-positive people should go on treatment to protect their partners”.

Moreover, taking treatment soon after diagnosis appears to have become a community norm – 84% agreed that “People should start treatment as soon as they are diagnosed”, while statements suggesting that people should delay until they are completely ready or until treatment is absolutely necessary were supported by fewer than 10%.

This cohort of HIV-negative men generally rejected relying on their partners using antiretrovirals in order to be protected from HIV. They suggested that their personal sexual strategies would not change in response – 16% agreed that “If more men are on PrEP, I would feel like I don’t need to use condoms to avoid getting HIV”. Similarly, 12% agreed that “Because of PrEP and HIV treatments, I’m less likely to ask my partners about their HIV status”.

Comfort having condomless sex

Men were asked, “How comfortable would you be having anal sex without a condom with casual partners in the following scenarios?” and were asked to respond for a number of partner types. There were important differences between the responses of PrEP users and non-users.

The 668 men who were not taking PrEP were generally uncomfortable with the idea of having condomless sex – only 7% said they would be comfortable doing so with ‘any casual partner’, 5% with a casual partner of unknown HIV status and 3% with an casual partner who was HIV positive.

It made little difference if the HIV-positive partner had an undetectable viral load – 6% would feel comfortable having sex with him.

Men appeared to be more comfortable serosorting, although this can be a risky strategy for HIV-negative men as there is always the possibility that a partner has recently acquired HIV but has not yet been diagnosed. Among men not using PrEP, 31% said they would be comfortable having condomless sex with a casual partner described as HIV negative. If the same man was taking PrEP, fewer men (23%) would be comfortable having condomless sex with him, perhaps reflecting a perception of PrEP users as risk takers.

The 83 respondents who were using PrEP were more comfortable with the idea of having condomless sex, but comfort levels were not particularly high.

PrEP users were most likely to feel comfortable having condomless sex with other HIV-negative PrEP users (72%) and HIV-negative partners not taking PrEP (64%).

The proportion who would feel comfortable having condomless sex with an HIV-positive partner (29%) was lower than for a partner of unknown HIV status (34%) or ‘any casual partner’ (40%).

And less than half of current PrEP users would be comfortable having condomless sex with an HIV-positive partner with an undetectable viral load (48%), although the respondent would be protected by two extremely effective prevention methods.

Conclusions

“While gay and bisexual men are highly supportive of pre-exposure prophylaxis, there remains some scepticism towards HIV treatment when used for prevention,” sum up the authors. “Increasing community understanding of treatment as prevention is needed to optimise treatment-based HIV prevention strategies.”

“In general, HIV-negative and untested gay and bisexual men indicated that they remained more comfortable negotiating condomless sex based on knowledge of HIV status, rather than PrEP or undetectable viral load.”

Many men continue to rely on serosorting: “HIV-negative men tend to perceive all sex with HIV-positive partners as potentially risky, regardless of condom use, HIV treatment or viral load.”

Some commentators have suggested that PrEP and understanding of undetectable viral loads could help reduce HIV stigma and the fear of partners living with HIV. However, PrEP users’ relatively high levels of discomfort with the idea of condomless sex with HIV-positive partners suggest that these hopes may be over-stated, the authors comment.

By Roger Pebody

References

Wilkinson AL et al. Measuring and understanding the attitudes of Australian gay and bisexual men towards biomedical HIV prevention using cross-sectional data and factor analyses. Sexually Transmitted Infections 94: 309-314, 2018. (Abstract.)

Holt M et al. Comfort Relying on HIV Pre-exposure Prophylaxis and Treatment as Prevention for Condomless Sex: Results of an Online Survey of Australian Gay and Bisexual Men. AIDS & Behavior, online ahead of print, 2018. (Abstract.)

Reprinted from the ETAG article published 6/6/18

Scientists Shed Light on How HIV Raises Heart Disease Risk

Researchers found a way to block a protein linked with blood clotting and inflammatory processes using a drug derived from tick saliva.

August 30, 2017 – reprinted from Poz.com

Researchers have uncovered a new pathway by which HIV leads to the chronic inflammation and immune activation associated with an increased risk of cardiovascular disease. Using an experimental drug based on an anticlotting factor in tick saliva, the scientists were able to block this pathway in primates. Such success indicates that a drug may one day be developed that helps mitigate the increased risk of heart disease associated with HIV.

Even when taking a successful antiretroviral (ARV) regimen, people with HIV have up to a two-fold increased risk of cardiovascular disease, including heart attack and stroke, compared with HIV-negative individuals. Researchers believe that the chronic inflammatory state and the persistent activation of the immune system to which the virus gives rise is likely a major driver of this increased risk.

major clinical trial called REPRIEVE is currently investigating whether a drug from the cholesterol-lowering class called statins may mitigate this risk and provide other health benefits among people with HIV who would not otherwise qualify for a statin.

Publishing their findings in Science Translational Medicine, National Institute of Allergy and Infectious Diseases (NIAID) scientists studied blood samples from people with HIV. They discovered elevated levels of immune cells known as monocytes that expressed high levels of a protein known as a tissue factor, which is linked with blood clotting and processes that give rise to inflammation.

The scientists further discovered that the level of such monocytes remained high regardless of whether the HIV-positive people who provided the blood samples had a fully suppressed virus thanks to ARV treatment.

Next, the researchers exposed the blood samples to an experimental drug called lxolaris, which is based on an anticlotting factor found in tick saliva. Previous research has shown that lxolaris blocks the cellular pathway that activates the tissue factor protein. The investigators found that the drug indeed shut off that particular protein in monocytes and did not otherwise affect normal cell function.

Studying monkeys infected with SIV, HIV’s simian cousin, the investigators found that the animals also had high levels of tissue-factor-expressing monocyte cells. So they treated five monkeys with lxolaris and found that this lowered levels of biomarkers that predict abnormal blood clotting and immune activation.

This finding signifies that by targeting the tissue factor pathway, lxolaris may lower some risk factors for cardiovascular disease among people with HIV. The drug has not yet been tested in humans, however, so considerable research would be needed to determine whether lxolaris may slow the inflammation and clotting processes that raise the risk of cardiovascular disease among people with HIV.

HIV Levels Before Treatment Can Predict This Immune System Indicator

HIV hides its genetic material in cells or locations in the body that remain out of reach of ARVs. This result of this overall effect is known as the viral reservoir, the existence of which prevents standard HIV treatment from curing the virus.

Publishing their findings in PLOS Pathogens, researchers from the AIDS Clinical Trials Group (ACTG) studied 101 people with HIV who had plasma and blood-cell samples taken before they started ARVs, one and four years after beginning HIV treatment, and once more between years six and 15 of treatment. All the participants achieved a viral load considered undetectable by standard laboratory measures and maintained this level of viral suppression for an average of seven years, with some doing so for more than a decade.

The participants experienced the steepest decline in measures of HIV’s genetic material (detected with highly sensitive tests) during their first four years on ARVs; afterward, they still experienced a decline, albeit at a slower pace.

Looking at the samples taken before the participants started ARVs, the researchers identified a correlation between levels of HIV and indicators of immune system activation and inflammation. However, this association ceased after the individuals started treatment for the virus. More specifically, the low levels of HIV found in the samples taken while people were on ARVs did not seem to influence the levels of immune system activation and inflammation during that time.

The investigators ultimately concluded that the levels of both immune system activation and HIV in the pretreatment samples predicted the levels of persistence of the virus and immune activation seen in the samples taken when the participants were on ARVs.

“Our findings suggest that damage to the immune system that occurs before people are started on [HIV] treatment leads to continued immune activation, even though the medicines are keeping the virus in check,” the study’s lead author, Rajesh Gandhi, MD, of the Massachusetts General Hospital Division of Infectious Diseases, said in a press release. “This suggests that diagnosing HIV and starting antiretroviral therapy as soon as possible may prevent the elevated immune activation that can lead to health problems, such as heart disease. The results also suggest that new strategies focused on reducing immune activation may need to be added to novel interventions designed to reduce and eventually eliminate HIV.”

To read the study, click here.

To read a press release about the study, click here.

Reproduced from POZ.com from 24 April 2017.

 

Australia has been invited to participate in a global survey of the needs of PLHIV and we are nearly halfway to target!

We have until the end of the month to recruit another 75 Australian participants.

 The study has been commissioned by an independent, global specialist HIV company with commitment to deliver innovative new options for the care and treatment of people living with HIV/AIDS. They have partnered with an independent market research agency in order to execute the survey.

The aims of the survey are to:

  • Gather insights around key issues and remaining needs as perceived by PLHIV and their partners/significant others. This includes recognising that certain key affected populations, including women and PLHIV over the age of 50, have distinct needs in terms of their treatment and care that need to be better understood.
  • Communicate the findings to raise awareness of the ongoing issues and needs (this may include the sharing of findings at major scientific conferences, publication to community media outlets and provision of relevant information to patient advocacy groups, etc). Note also that key study findings will be available to the public in 2017 via a dedicated portal for the initiative, via the commissioning company’s website.
  • Use the insights gathered to inform and shape future activities that provide meaningful support for PLHIV.
  • Track the key trends and shifts in the needs of PLHIV over time.

The link below allows interested participants to register their interest (once completed they would be contacted by someone from the survey company).

www.liberatingsurveys.com/en/enquire/3/orgchg

Please help us reach the target and circulate this email through your networks and connections.