Cost Effectiveness of Current HIV Cure Approaches

• Published: November 14, 2014
• DOI: 10.1371/journal.pone.0113031

Abstract

Background

We examined efficacy, toxicity, relapse, cost, and quality-of-life thresholds of hypothetical HIV cure interventions that would make them cost-effective compared to life-long antiretroviral therapy (ART).

Methods

We used a computer simulation model to assess three HIV cure strategies: Gene Therapy, Chemotherapy, and Stem Cell Transplantation (SCT), each compared to ART. Efficacy and cost parameters were varied widely in sensitivity analysis. Outcomes included quality-adjusted life expectancy, lifetime cost, and cost-effectiveness in dollars/quality-adjusted life year ($/QALY) gained. Strategies were deemed cost-effective with incremental cost-effectiveness ratios <$100,000/QALY.

Results

For patients on ART, discounted quality-adjusted life expectancy was 16.4 years and lifetime costs were $591,400. Gene Therapy was cost-effective with efficacy of 10%, relapse rate 0.5%/month, and cost $54,000. Chemotherapy was cost-effective with efficacy of 88%, relapse rate 0.5%/month, and cost $12,400/month for 24 months. At $150,000/procedure, SCT was cost-effective with efficacy of 79% and relapse rate 0.5%/month. Moderate efficacy increases and cost reductions made Gene Therapy cost-saving, but substantial efficacy/cost changes were needed to make Chemotherapy or SCT cost-saving.

Conclusions

Depending on efficacy, relapse rate, and cost, cure strategies could be cost-effective compared to current ART and potentially cost-saving. These results may help provide performance targets for developing cure strategies for HIV.

Full paper:
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0113031

Groundbreaking HIV vaccine's effects were real – and could be made to work better

Findings from further studies using a reformulation of the only HIV vaccine that has ever worked in a large efficacy trial were presented at the recent HIV Research for Prevention conference (HIVR4P). They showed evidence of stronger antibody responses, and in-depth analysis of these responses shows that by further developing a similar vaccine it may be possible to push the immune system into generating an antibody response to HIV that is sufficiently strong to prevent most infections.
The RV144 vaccine had such a slight beneficial effect that when its results were first announced, some people wondered if they were not just a statistical fluke. It did prevent four out of ten HIV infections that would otherwise have happened in its original trial in Thailand, but the results observed were only just statistically significant. This was largely because the vaccine’s efficacy appeared to wane with time – if the trial had been stopped a year after the first injection, its efficacy would have been 60%. It also seemed to have little effect in people at higher risk of HIV such as people who inject drugs and gay men.
At last year’s AIDS Vaccine conference in Barcelona, however, several studies were presented that showed the RV144 vaccine’s effects were real and depended on a very specific kind of antibody response to HIV that developed in some, but not all, vaccine recipients.

Vaccine produces better results in South Africa than Thailand

Glenda Gray, head of the South African Medical Research Council, presented the results from a small study, HVTN097, which gave a version of the RV144 vaccine protocol to 100 volunteers (51 men and 49 women).
The vaccine actually contains two components. One is a vaccine called ALVAC. This is a vector vaccine, consisting of HIV proteins encased in the shell of another virus. This 'fake infection' is intended to stimulate the cellular immune response (the part of the immune system that stimulates CD8 cells to attack other, infected cells). It was given in four components: zero, one, three and six months from the start of the study. The other component is called AIDSVAX. This consists of HIV envelope (sruface) proteins intended to stimulate the humoral immune response - the part of the immune system that generates the soluble proteins called antibodies that directly attack viruses. It was given at month three and month six.
Why has it taken so long to re-try a vaccine that produced positive results five years ago? The main problem is that expectations of the original study were so low that Vaxgen, the company making AIDSVAX, used all its stock and did not make more so the vaccine has had to be re-manufactured from scratch.
As was observed in the original study, the South African vaccine did not stimulate the cellular immune response to a useful degree. Some degree of immune response to HIV was stimulated in volunteers’ CD4 cells, and was more common and stronger in the South African trial: 69% of South African volunteers’ CD4 cells became sensitive to HIV as opposed to 50% of original vaccine recipients’ cells. However, there was little evidence of the desired CD8 response – only 5% of South African and 0.6% of the original Thai recipients had CD8 responses.
In contrast, and as seen in the original study, there was a strong and universal antibody response generated to the gp120 component of HIV. This protein forms the ‘knobs’ on the surface of HIV that attach to cells and is one of the components of AIDSVAX. There was also a near-universal (98.6%) response to a specific part of gp120 called the V1-V2 loop, a section of the protein chain that first attaches to cells. More analysis of the immune responses is underway and it looks as if the antibodies generated in the vaccine recipients in South Africa have a stronger effect against lab-engineered HIV viruses, being able, for instance, to neutralise (disable from reproducing) 25% more clade B viruses than Thai-recipient antibodies.
In January 2015 a new study, HVTN100, will give trial volunteers a vaccine based on RV144 but reformulated to contain proteins from the HIV subtype (clade) most common in south Africa, namely clade C instead of the Thai clade A/E. Depending on efficacy, this could then lead to a much bigger efficacy trial.

Thai vaccine boost regenerates immune response

In the original RV144 study, it had been found that an effective immune response to HIV depended on being on the right side of an antibody balance. Two different kinds of antibody response were generated, a dominant one of the antibody types called immunoglobulin A (IgA), and a less dominant one called IgG. The higher the ratio of IgG to IgA the more effective the immune response; indeed a high ratio of IgA to IgG actually enhanced vulnerability to HIV infection.
In a Thai study, RV305, volunteers for the original RV144 study were recalled and – eight years after they first received the vaccine – were given it again. Analysis showed that this boost produced a similar antibody response to the original vaccine; 70% of volunteers who received both vaccine components produced IgG antibodies to HIV and 56% of those who just received AIDSVAX, while 10% and 14% respectively had antibodies specific to the V1/V2 loop.
The IgA response was roughly ten times as strong as the IgG response but, significantly, no IgA specific to the HIV gp120 protein was found in rectal secretions. This suggests the vaccine could be ‘fine turned’ to produce more specific responses.
This immune response, however, is only active against varieties of HIV that are relatively easy to disable, so-called ‘tier 1’ viruses. The reason HIV vaccines are not more effective is that during infection, HIV and the immune system are locked into an arms race that HIV generally wins, staying one step ahead of the body’s response to it. While the body develops ever more elaborate antibodies, and about 35% of people eventually develop the so-called ‘broadly neutralising’ antibodies that can disable most transmitted viruses, the virus gets there first, always having mutations in hand of higher-tier viruses that are antibody-resistant.
Passive-immunity studies, in which volunteers are given injections of broadly neutralising antibodies, confirms that if we could get a vaccine to generate these antibodies from the start, they would be effective in repelling the vast majority of viral invaders. The problem is that cells capable of doing this are initially extremely rare and it is only the continued provocation of the presence of HIV that drives the production of broadly neutralising antibodies. An ideal vaccine would be one that would, so to speak, fool the immune system into thinking that it had already been dealing with a chronic HIV infection for ten years or more.

Could repeated vaccine boosts push the body into an effective anti-HIV response?

How far along this road are we? Michael Moody of Duke University told the conference that a truly effective antibody response against HIV would need to have four characteristics.
It would need to generate significant numbers of antibodies to the V1/V2 loop of the HIV gp120 molecule. It would needed to be able to 'deglycosylate' gp120, which means it would have to penetrate a sticky coating of sugars that gp120 coats itself in as a defence against antibodies. It would need to have a specific affinity for two amino acids in the V1/V2 loops.
And it would need to have an unusual characteristic that only the rarest, most broadly neutralising antibodies have; this is an extended 'prong' in the part of the antibody called the third heavy-chain complementarity determining region (H-CDR3), which is able to penetrate parts of the gp120 protein that are highly specific to HIV’s ability to infect, and therefore not mutable – they are “conserved” – but which are only exposed for a fraction of a second during the infection process. (Essentially, antibodies with long H-CDR3s almost literally throw a ‘spanner in the works’ of HIV infection.)
Moody said that the vaccine boost in the RV305 study more than doubled the proportion of antibodies, from 2.56% to 5.52%, that had mutations indicative of a shift towards being able to broadly neutralise HIV. A much higher proportion (11.6% versus 1.35%) had H-CDR3 loops more than 21 amino acids long, which indicates that they may possibly have broadly neutralising ability. In addition, 2.4% of the antibodies produced had mutations specifically adapting them to particular glucose molecules and enabling them to bind very strongly to gp120. However, these were not the same antibodies as the ones with long H-CDR3s, in the main, and when these antibodies were isolated and used against a panel of viruses, it was still only the ‘tier 1’ viruses they could neutralise.
However, one specific antibody called Ab8850, which represented 2.5% of the total antibodies produced, was molecularly near-identical to an already-studied broadly neutralising antibody called CH04 – its H-CDR3 loop was just three antibodies shorter, and this made all the difference.
Moody said that so far we had not seen, in the RV144 research programme, production of an antibody with all four characteristics needed for it to fully neutralise HIV, but had progressed from producing antibodies with two of these characteristics to ones with three.
He speculated that repeated boosts of AIDSVAX or a similar vaccine could have the effect of ‘pushing’ the immune system into developing broadly neutralising antibodies that might eventually fully protect an individual against HIV – the obvious problem being that, with the vaccines we have at present, this might take several years’ worth of inoculations at considerable expense.
It might also depend on individuals’ genetic make-up too much to be widely applicable, but the principal that it is even possible to do this has now been established.

References

Gray G et al. HVTN 097: Evaluation of the RV144 Vaccine Regimen in HIV Uninfected South African Adults. HIV Research for Prevention Conference, Cape Town. Abstract OA11.06LB. 2014.See webcast here.
Akapirat S et al. HIV-specific Antibody in Rectal Secretions Following Late Boosts in RV144 Participants (RV305). HIV Research for Prevention Conference, Cape Town. Abstract OA11.05. 2014. See webcast here.
Moody M et al. Induction of Antibodies with Long Variable Heavy Third Complementarity Determining Regions by Repetitive Boosting with AIDSVAX® B/E in RV144 Vaccinees. HIV Research for Prevention Conference, Cape Town. Abstract OA12.06LB. 2014. See webcast here.

Prevalence and risk factors of sleep disturbances in a large HIV-infected adult population.

Prevalence and risk factors of sleep disturbances in a large HIV-infected adult population.

Authors

Allavena C¹, Guimard T², Billaud E³, de la Tullaye S⁴, Reliquet V¹, Pineau S³, Hüe H³, Supiot C¹,Chennebault JM⁵, Michau C⁶, Hitoto H⁷, Vatan R⁸, Raffi F¹.

Author information

Journal

J Int AIDS Soc. 2014 Nov 2;17(4 Suppl 3):19576. doi: 10.7448/IAS.17.4.19576. eCollection 2014.

Affiliation

Abstract

INTRODUCTION: Sleep disturbances are frequently reported in HIV-infected patients but there is a lack of large studies on prevalence and risk factors, particularly in the context of current improved immuno-clinical status and use of the newest antiretrovirals (ARV).

METHOD: Cross-sectional study to evaluate the prevalence and factors associated with sleep disturbance in adult HIV-infected patients in six French centres of the region "Pays de la Loire". Patients filled a self-administered questionnaire on their health behaviour, sleep attitudes (Pittsburgh Sleep Quality Index PSQI), quality of life (WHO QOL HIV BREF questionnaire) and depression (Beck depression Inventory (BDI)-II questionnaire). Socio-demographic and immunovirologic data, medical history, ARVs were collected.

RESULTS: From November 2012 to May 2013, 1354 consecutive non-selected patients were enrolled. Patients' characteristics were: 73.5% male, median age 47 years, active employment 56.7%, France-native 83% and Africa-native 14.7%, CDC stage C 21%, hepatitis co-infection 13%, lipodystrophy 11.8%, dyslipidemia 20%, high BP 15.1%, diabetes 3%, tobacco smokers 39%, marijuana and cocaine users, 11.7% and 1.7% respectively, and excessive alcohol drinkers 9%. Median (med) duration of HIV infection was 12.4 years, med CD4 count was 604/mm(3); 94% of Patients were on ARVs, 87% had undetectable viral load. Median sleeping time was 7 hours. Sleep disturbances (defined as PSQI score >5) were observed in 47% of the patients, more frequently in female (56.4%) than in male (43.9%) and moderate to serious depressive symptoms in 19.7% of the patients. In multivariate analysis, factors associated with sleep disturbances were depression,, infection , ARV regimen containing nevirapine or efavirenz.

CONCLUSIONS: Prevalence of sleep disturbances is high in this HIV population and roughly similar to the French population. Associated factors are rather related to social and psychological status than HIV infection. Depression is frequent and should be taken in care to improve sleep quality.

Ibalizumab: First HIV Drug to Get Orphan Drug Status for Salvage Patients

Shares of TaiMed Biologics Inc, which manufactures drugs to treat AIDS, soared 12.93 percent yesterday after its new TMB-355 drug for intravenous injection was granted orphan drug status in the US.

The company’s shares closed at NT$151.2 yesterday, outperforming the over-the-counter benchmark index, which ended up 0.56 percent.

The granting of orphan status could shorten the time it takes for TMB-355 to enter the US market, TaiMed financial controller Jack Chen said over the telephone yesterday.

“By getting orphan status, we are able to negotiate with the US Food and Drug Administration to see if we can waive the phase-three clinical trials for the drug, or conduct them on a smaller scale,” Chen said.

An orphan drug is one that satisfies an unfilled medical need for a specific group of people numbering less than 200,000, TaiMed said, adding that as a result, clinical trials for such drugs do not require as many patients as those for other pharmaceuticals.

http://www.taipeitimes.com/News/biz/archives/2014/10/23/2003602680

Demystifying HIV Pre-Exposure Prophylaxis

Pre-Exposure Prophylaxis or PrEP is an HIV prevention strategy where an HIV negative person takes a daily pill to reduce their risk of contracting HIV. It's important to note that PrEP is not the same as PEP or Post-Exposure Prophylaxis, which HIV treatment given to individuals within 72 hours after exposure to HIV to prevent infection from taking hold.

The only currently approved PrEP regimen is Truvada, a two drug combo, which blocks an enzyme called HIV reverse transcriptase. HIV relies on this enzyme to make new copies of itself. So Truvada prevents the HIV virus from multiplying and establishing infection in the body. 

Because PrEP blocks an HIV enzyme, it protects against HIV infection, but it does not prevent against pregnancy or other sexually transmitted infections or STI's. Therefore, people taking PrEP should also get regular HIV testing, to make sure they haven't been recently infected. As well as STI testing and treatment if necessary. 

PrEP has been proven to reduce the risk of HIV infection in gay and bisexual men, transgender women and heterosexual men and women, as well as people who inject drugs. PrEP does not treat HIV. It's meant to prevent HIV from establishing infection so it should not be taken by someone who already has HIV. People who want to start PrEP must first be tested for HIV infection. 

PrEP has made a lot of headlines over the last two years, and the messages haven't always been clear. Let's look at three myths about PrEP, and see what the facts really are. 

Myth number one - PrEP doesn't work. In the large IPrEx study of PrEP in gay and bisexual men and transgender women, researchers found an overall 42% reduction in HIV transmission. However, when the researchers looked at levels of Truvada in the blood samples, they found that for people who took four PrEP pills per week, protection was approximately 96%. For people who took PrEP daily as recommended, protection was estimated at more than 99%. So the take home message - PrEP works if you take it as prescribed, every day. 

Myth number two - PrEP causes bad side effects. Some people in PrEP studies have reported side effects such as nausea, headaches, or weight loss in the first few weeks of taking PrEP. Most of these side effects went away on their own or when PrEP was stopped. And the majority of people didn't have them at all. For example, one clinical trial reported moderate nausea only 22 times among the 1251 people that started to take PrEP over a study period of more than two years. A recent analysis showed that some people taking PrEP can have a slight increase in serum creatinine, an indicator of reduced kidney function. But, these levels returned to normal after PrEP was stopped. Just to be safe, people who take PrEP should have regular monitoring for kidney health. Another analysis found a slight loss in bone and mineral density in study participants taking PrEP. Although this bone loss did not worsen with long term use. Truvada was chosen for use as PrEP, in part because it is safe and well tolerated. Like most drugs, some mild side effects are possible. But again, side effects reported with PrEP went away over time or when PrEP was stopped. Also, there are other drugs currently in clinical trials that may have fewer side effects.

Myth number three - PrEP is impossible to get. PrEP is available by prescription from doctors, nurse practitioners, and physicians assistants, and most health care plans cover PREP. Without insurance, Truvada PrEP can cost upwards of $1800 per month. But few people actually pay this full stickered price. There are medication assistance programs through Gilead Sciences that may be able to cover some or all of the cost of PrEP, whether or not you have insurance. Keep in mind that depending on how you are accessing PrEP, it may take several weeks to get your prescription filled the first time.

Of course, PrEP is not the only way to prevent HIV infection. When used correctly and consistently, condoms are an important tool for reducing HIV risk, as well as preventing against other STI's and pregnancy. For people who do not use condoms every time they have sex, PrEP provides effective protection against HIV. The choice to use PrEP, like the choice to use condoms is personal. The important thing is to find an HIV prevention strategy that works for you. 

This document is a transcription of a video ( https://www.youtube.com/watch?v=-Xx92whZS0o ) provided  by Youreka Science in collaboration with Beta of the San Francisco AIDS Foundation. To learn more about HIV treatment and prevention, visit Beta at BetaBlog.org.

Video: Three PrEP Myths Busted (One Pill Per Day to Prevent HIV)

The U.S. Food and Drug Administration today approved Harvoni (ledipasvir and sofosbuvir) to treat chronic hepatitis C virus (HCV) genotype 1 infection.

For Immediate Release

October 10, 2014

Release

The U.S. Food and Drug Administration today approved Harvoni (ledipasvir and sofosbuvir) to treat chronic hepatitis C virus (HCV) genotype 1 infection.

Harvoni is the first combination pill approved to treat chronic HCV genotype 1 infection. It is also the first approved regimen that does not require administration with interferon or ribavirin, two FDA-approved drugs also used to treat HCV infection.

Both drugs in Harvoni interfere with the enzymes needed by HCV to multiply. Sofosbuvir is a previously approved HCV drug marketed under the brand name Sovaldi. Harvoni also contains a new drug called ledipasvir.

“With the development and approval of new treatments for hepatitis C virus, we are changing the treatment paradigm for Americans living with the disease,” said Edward Cox, M.D., M.P.H., director of the Office of Antimicrobial Products in the FDA’s Center for Drug Evaluation and Research. “Until last year, the only available treatments for hepatitis C virus required administration with interferon and ribavirin. Now, patients and health care professionals have multiple treatment options, including a combination pill to help simplify treatment regimens.”

Harvoni is the third drug approved by the FDA in the past year to treat chronic HCV infection. The FDA approved Olysio (simeprevir) in November 2013 and Sovaldi in December 2013.

Hepatitis C is a viral disease that causes inflammation of the liver that can lead to diminished liver function or liver failure. Most people infected with HCV have no symptoms of the disease until liver damage becomes apparent, which may take decades.

Some people with chronic HCV infection develop scarring and poor liver function (cirrhosis) over many years, which can lead to complications such as bleeding, jaundice (yellowish eyes or skin), fluid accumulation in the abdomen, infections and liver cancer. According to the Centers for Disease Control and Prevention, about 3.2 million Americans are infected with HCV, and without proper treatment, 15-30 percent of these people will go on to develop cirrhosis.

Harvoni’s efficacy was evaluated in three clinical trials enrolling 1,518 participants who had not previously received treatment for their infection (treatment-naive) or had not responded to previous treatment (treatment-experienced), including participants with cirrhosis. Participants were randomly assigned to receive Harvoni with or without ribavirin. The trials were designed to measure whether the hepatitis C virus was no longer detected in the blood at least 12 weeks after finishing treatment (sustained virologic response, or SVR), indicating that a participant’s HCV infection has been cured.

In the first trial, comprised of treatment-naive participants, 94 percent of those who received Harvoni for eight weeks and 96 percent of those who received Harvoni for 12 weeks achieved SVR. The second trial showed 99 percent of such participants with and without cirrhosis achieved SVR after 12 weeks. And in the third trial, which examined Harvoni’s efficacy in treatment-experienced participants with and without cirrhosis, 94 percent of those who received Harvoni for 12 weeks and 99 percent of those who received Harvoni for 24 weeks achieved SVR. In all trials, ribavirin did not increase response rates in the participants.

The most common side effects reported in clinical trial participants were fatigue and headache.

Harvoni is the seventh new drug with breakthrough therapy designation to receive FDA approval. The FDA can designate a drug as a breakthrough therapy at the request of the sponsor if preliminary clinical evidence indicates the drug may demonstrate a substantial improvement over available therapies for patients with serious or life-threatening diseases. Harvoni was reviewed under the FDA’s priority review program, which provides for an expedited review of drugs that treat serious conditions and, if approved, would provide significant improvement in safety or effectiveness.

Harvoni and Sovaldi are marketed by Gilead, based in Foster City, California. Olysio is marketed by Janssen Pharmaceutical based in Raritan, New Jersey.

The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation’s food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.

###

As PrEP Becomes More Available, Couples With One HIV + Partner Consider Treatment

It has been recommended that gay and bisexual men consider taking pre-exposure prophylaxis, or PrEP, for HIV prevention, but there is one demographic that, according to many health care professionals, is an ideal candidate for this treatment: HIV-negative men with HIV-positive male partners, relationships that are referred to as serodiscordant.

For many of these couples, PrEP may offer a security in intimacy among both partners that is beneficial to physically, mentally, and emotionally, where HIV is concerned. The fear of a condom breaking during sex or not being used properly can be alleviated with the knowledge that medication taken for PrEP, when administered properly, can reduce the risk of HIV infection by 96 to 99 percent.

Read more here

What You Should Know About Ebola

Important facts summarized in this great figure.

HIV Prevention Pill (Truvada) Patient Assistance Program Now Available

More Breaking from U.S. Conference on AIDS: Gilead is raising income levels for their Assistance Program to 500% of FPL (or approx $58,350). So you may be able to get PrEP paid for if you are making below that amount and can't afford the drug. Also being told that the Co-Pay Assistance program is expanding from $200 to $300 per month. This is an important breakthrough, for ‪#‎PrEP‬ consumers!

The Truvada® for PrEP Medication Assistance Program assists eligible HIV-negative adults in the United States who do not have insurance obtain access to Truvada (emtricitabine and tenofovir disoproxil fumarate) for PrEP (pre-exposure prophylaxis). To find out if you are eligible for this medication assistance program, call 1-855-330-5479, Monday through Friday between 9:00 a.m. and 8:00 p.m. (Eastern). 

Great video that explains how a DEXA scan works for measuring bone, body fat and muscle

This video about how a full body dual-energy x-ray absorptiometry (DEXA) scan works as the best way to measure body composition.  However, few clinics provide it since they only use DEXA to measure bone density in the lower back and pelvis. It required special calibration for a full body scan. Talk to your doctor is he can find a local clinic that can do a full body DEXA scan. Your insurance may not pay for it. Out of pocket cost may be close to $200.  You only need to do it every 2-3 years for bone density if you are over 50 and HIV+. If you are a bodybuilder that expects dramatic body changes in a few months, then every 6 months to a year would be OK. The amount of X ray radiation you are exposed to is equivalent to your exposure in a transatlantic flight.

Fwd: Hot Topics: Our Inner Demons; How Bad Is Smoking?; Once-Monthly Treatment?; and More

If you have trouble reading this email, you can see the online version at: www.thebody.com/topics.html

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Living With Our Doubts, and Our Inner Demons To the person who wrote last week about trying to commit suicide: I think that you are right that we are suffering a sort of post-traumatic stress disorder, both from the past and from the present we live. This is not a question, just insight on how some of us are not doing well out here and not knowing how to do a thing about it. Nelson Vergel responds in the "Aging With HIV" forum  Is Smoking While HIV Positive Really So Bad? I just tested positive for HIV, and I smoke one or two cigarettes a day, as well as some weed and the occasional electric cigar. How much will continuing like this worsen my situation or hurt my CD4 count? David Fawcett, Ph.D., L.C.S.W., responds in the "Substance Use and HIV" forum  Day One With HIV: Coping With an HIV Diagnosis While in College "Needless to say, my life is a mess and the future that was once so clear seems so blurred and uncertain," Jason Q writes. "I am simply looking to my graduation day, and trying to overcome the depression I have been fighting since my day one.  How Soon Will We Have Once-a-Month HIV Meds? Do you have any good guess as to when those injectable once-per-month medications I've read about will be available to treat HIV? Benjamin Young, M.D., Ph.D., responds in the "Choosing Your Meds" forum  Is It Wise to "Undo" a Regimen Switch? I was on Atripla for four years -- viral load undetectable, no drug resistance, CD4 count of 600 -- but switched to Stribild last week upon my doctor's suggestion. I am having very hard time adjusting to it. Are my symptoms normal -- and even if they are, would it be OK to switch back to Atripla so quickly? Keith Henry, M.D., responds in the "Managing Side Effects of HIV Treatment" forum  Can One Missed Dose Spell Resistance? I've been on Stribild for over four months and haven't missed a dose, but I'm scared that I'm going to miss one at some point. If I do, will it make me resistant? Benjamin Young, M.D., Ph.D., responds in the "Choosing Your Meds" forum  A Guide to Talking to Your Health Care Provider About HIV Treatment Issues We realize that, if you're doing things that hurt your ability to adhere to your HIV treatment, your HCP won't always feel like the easiest person to confide in. But if you want your treatment to work, you and your health care team have to work as partners. You don't have to do this alone.  How Do I Manage Heart Health When Statins Aren't an Option? I have been HIV positive for 30 years, and have had great results with my meds. But my total cholesterol is over 225 (LDL 150) and my triglycerides are close to 300. I have horrible side effects when using statins. At what point should I consider switching HIV meds to lower cholesterol? Keith Henry, M.D., responds in the "Managing Side Effects of HIV Treatment" forum  Can I Do Anything About Itchy Skin Bumps? When I started to take my antiretrovirals seven months ago, I developed very itchy pimple-like bumps on my scalp, face, neck, and all the way down to my legs. I always wear long sleeves or a jacket because I'm too shy too show off my arms. My doctor says it will go away, but I need help managing this now! Keith Henry, M.D., responds in the "Managing Side Effects of HIV Treatment" forum  Can Antibiotics Be Dangerous for People With HIV? I've been on HIV treatment for two years, and have also been prescribed antibiotics throughout that time. My CD4 count is 230 and climbing slowly. However, I have heard many times that antibiotics should not be "overused" -- does that go for us HIV-positive people as well? Benjamin Young, M.D., Ph.D., responds in the "Choosing Your Meds" forum  Spotlight Series on Hepatitis C We're in the midst of a dramatic evolution in hepatitis C management. TheBodyPRO.com's exclusive spotlight series on HCV captures the latest developments with a range of overviews, research updates, expert interviews, educational materials and new information. Each of us knows all too well how deeply stigma can affect the lives of people with HIV. We also know how much HIV-positive people do, day in and day out, to push back against that stigma. TheBody.com's sister site, HealthCentral, is honoring that fight against stigma with a photo contest that gives you a chance to make a statement -- and potentially win some cash in the process. The "Live Bold, Live Now" Photo Contest invites people who are living with a significant health issue to share their story by July 11; public voting will determine the winners of a $500 first prize, $250 second prize and $100 third prize. Several HIV-positive people have already submitted their stories. Visit the photo contest entry post on HealthCentral's Facebook page to see them, and to submit your own story!  How Can I Support My Newly Diagnosed Friend? Not even 24 hours ago I found out a very dear friend of mine is HIV positive. Is there anything I should know? Other than shock I don't see him any differently, but I just want to be educated in any way possible to be there for him. David Fawcett, Ph.D., L.C.S.W., responds in the "Mental Health and HIV" forum  Is HIV Treatment Truly a "Functional Cure"? I disagree with the theory that people living with HIV are already "functionally cured" if they are on antiretroviral therapy. If that's true, then why must we disclose our status even if we are undetectable and practically unable to transmit the virus? Benjamin Young, M.D., Ph.D., responds in the "Choosing Your Meds" forum  HIV Management in Depth: Exploring Key Issues in HIV Care Our flagship interview series on TheBodyPRO.com features important discussions with some of the brightest minds and most active figures in HIV treatment, research, prevention and activism. Browse our latest additions!  19 vs. 56: Is There a Difference Between Extremely Low Viral Loads? While I was volunteering for a study, I would consistently get viral load results back that were "less than 20." Most recently, though, my viral load was 56. My doctor doesn't seem concerned, but does suddenly becoming "detectable" mean I'm becoming resistant to my meds? Mark Holodniy, M.D., F.A.C.P., C.I.C., responds in the "Understanding Your Labs" forum  Can I Ever Fully Recover From a Super-Low CD4 Count? I was diagnosed in June 2011 with CD4 count of 43. Since starting treatment, my CD4 slowly climbed to around 260, where it has hovered. Why won't it keep climbing? Mark Holodniy, M.D., F.A.C.P., C.I.C., responds in the "Understanding Your Labs" forum  What's the "Real" Risk of Heterosexual Transmission? I'm HIV positive, but since I started meds I've always had an undetectable viral load. I'm also circumcised and have no other STDs. I'm wondering: What is the real percentage chance of transmitting HIV to my female partner if we don't use condoms? Shannon R. Southall responds in the "Safe Sex and HIV Prevention" forum  PEP Regimens: Do the Specific Drugs Matter? I was abroad on vacation when my condom broke during sex with a stranger. Doctors prescribed me post-exposure prophylaxis (PEP) consisting of Truvada and Kaletra, but due to drug access problems with the Truvada, they said it'd be fine to just take the Kaletra alone if I need to. Are they right? Benjamin Young, M.D., Ph.D., responds in the "Choosing Your Meds" forum Worried Your Spam Filter Might Trash Our Mailings? 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