Tag Archives: Antiretroviral drug

Prayer is good, prayer and medication is better!

Pastor Elizabeth was told that prayer was all she needed to fight HIV, she stopped taking her medication after faith leaders insisted she cease taking anti-HIV and life saving drugs.  She wrestled with the decision and is now an advocate for taking medication.  She says “If you are sick, and someone tells you not to take medication, they are misleading you.  Pastor Elizabeth realises this and wishes to share that HIV is simply an illness which requires medication.

At the beginning of the HIV epidemic in the early eighties, some faith leaders preached that only ‘sinners’ contracted the virus, advising that the only solution for those living with HIV was to pray hard for forgiveness. While many faith leaders have since realised that HIV is simply a virus that can affect anyone, unfortunately some haven’t. In fact, a few have gone even further, telling those in their congregations who are living with HIV to stop taking their Antiretroviral treatment (ARVs) and instead concentrate on praying because that’s the only way they will experience emotional and physical healing.

Whether praying to be healed from HIV is being preached in select churches, or some church-goers living with HIV are misinterpreting what their faith leaders are telling them, a number of HIV positive people have died as a result of stopping their HIV medication. What remains unclear is how many people are being converted to this way of thinking. Is this a big problem warranting a global intervention, or are we making a mountain out of a molehill? I personally don’t know the definitive answers to these questions, but what I can say is that where prayer and HIV healing are concerned, I have witnessed and have heard of some pretty bizarre behaviour among people living with HIV, particularly within African communities in the UK and in some parts of Africa.

It was reported in October 2011 that blind faith in prayer claimed the lives of three people who were HIV positive.  At least three people in London with HIV died after they stopped taking life saving drugs on the advice of their Evangelical Christian pastors.

The women died after attending churches in London where they were encouraged to stop taking the antiretroviral drugs in the belief that God would heal them, their friends and a leading HIV doctor said.

HIV prevention charity African Health Policy Network (AHPN) says a growing number of London churches have been telling people the power of prayer will “cure” their infections.

“This is happening through a number of churches. We’re hearing about more cases of this,” AHPN chief Francis Kaikumba said.

Whether you believe in religion or not, there is absolutely nothing wrong with prayer to help you with HIV, however there is everything wrong with discontinuing medication in favour of prayer.  Take time to consider the different mechanises to combat HIV.  Prayer may help the soul and medication will help the body.  There are a lot of people of all faiths in within research and development who would hope you look after your body too.

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The Reason Why Experimental HIV Vaccines Backfire

"This study shows that if a vaccine induces high levels of activated CD4+ T cells in mucosal tissues, any potential protective effect of the vaccine may be hampered," senior author Guido Silvestri explains.

“This study shows that if a vaccine induces high levels of activated CD4+ T cells in mucosal tissues, any potential protective effect of the vaccine may be hampered,” senior author Guido Silvestri explains.

HIV Vaccines Should Avoid Viral Target Cells, Primate Model Study Suggests
Vaccines designed to protect against HIV can backfire and lead to increased rates of infection. This unfortunate effect has been seen in more than one vaccine clinical trial.Scientists at Yerkes National Primate Research Center, Emory University, have newly published results that support a straightforward explanation for the backfire effect: vaccination may increase the number of immune cells that serve as viral targets. In a nonhuman primate model of HIV transmission, higher levels of viral target cells in gateway mucosal tissues were associated with an increased risk of infection.The findings, published in Proceedings of the National Academy of Sciences , suggest that vaccine researchers, when evaluating potential HIV/AIDS vaccines, may need to steer away from those that activate too many viral target cells in mucosal tissues.

“One of the reasons why it has been so difficult to make an AIDS vaccine is that the virus infects the very cells of the immune system that any vaccine is supposed to induce,” says senior author Guido Silvestri, chief of microbiology and immunology at Yerkes National Primate Research Center.

Silvestri is also a professor of pathology and laboratory medicine at Emory University School of Medicine and a Georgia Research Alliance Eminent Scholar. The first author of the paper is senior research specialist Diane Carnathan, PhD, and colleagues from the Wistar Institute, Inovio Pharmaceuticals and the University of Pennsylvania contributed to the study.

A large part of the HIV/AIDS vaccine effort has been focused on developing vaccines that stimulate antiviral T cells. T cells come in two main categories, defined by the molecules found on their surfaces. CD8 is a marker for “killer” cells, while CD4 is a marker for “helper” cells. CD4+ T cells are known to be primary targets for HIV and SIV (simian immunodeficiency virus) infection, while several studies have proposed that CD8+ T cells could be valuable in controlling infection.

In this study, researchers immunized rhesus macaques with five different combinations of vaccines encoding SIV proteins found on the inside of the virus only. This experimental strategy was designed to examine the effects of cell-mediated immunity, without stimulating the production of neutralizing antibodies, in what scientists refer to as a “reductionist approach”.

The monkeys received an initial immunization followed by two booster shots after 16 and 32 weeks. The monkeys were then exposed to repeated low-dose intrarectal challenge with SIV, once per week, up to 15 times. In general, the immunization regimens did not prevent SIV infection. While all the immunized monkeys had detectable levels of circulating “killer” CD8+ T cells, there was no correlation between these cells and preventing infection.

The most important result, however, was that the monkeys that became infected had higher levels of activated CD4+T cells in rectal biopsies before challenge, Silvestri says.

“This study shows that if a vaccine induces high levels of activated CD4+ T cells in mucosal tissues, any potential protective effect of the vaccine may be hampered,” he explains.

The study emphasizes the unique challenges that HIV poses in terms of vaccine development, and the importance of pursuing vaccine concepts and products that elicit strong antiviral immune responses without increasing the number of CD4+ T cells in the portals of entry for the virus.

The research was supported by the National Institute of Allergy and Infectious diseases (AI080082) and the NIH Director’s Office of Research Infrastructure Programs (Primate centers: P51OD11132).

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The NHS urgently needs to make PrEP available

preptabs

Two European studies of pre-exposure prophylaxis (PrEP), PROUD1 and IPERGAY2, reported early results in October 2014. Both studies showed that PrEP was so effective at preventing HIV transmission that everyone in these studies has now been offered PrEP. The comparison arms, which respectively offered delayed PrEP or a placebo, have been closed.

In light of this news, together with data on continued high rates of new infections3, the NHS urgently needs to make PrEP available.

Although an NHS England process to evaluate PrEP is underway, any decision to provide PrEP will probably not be implemented until early 2017, which is too long to wait. We are calling for earlier access to PrEP. The NHS must speed up its evaluation process and make PrEP available as soon as possible. Furthermore, we call for interim arrangements to be agreed now for provision of PrEP to those at the highest risk of acquiring HIV.

What is PrEP?

PrEP stands for Pre-Exposure Prophylaxis. It involves a person who doesn’t have HIV taking pills regularly to reduce their risk of HIV infection. Several studies show that PrEP works.

PrEP is currently only available in the UK to people enrolled in the PROUD study,4 but has been available in the US since 2012.

Why do we need PrEP?

There are now over 100,000 people living with HIV in the UK. 5 We need to improve HIV prevention.

Tens of thousands of HIV transmissions have been prevented by condom use.6  However many people do not use condoms all of the time and each year there are thousands of new infections. PrEP has the potential to prevent new infections among some of those at greatest risk of acquiring HIV.

Condom use will remain a core strategy in HIV prevention. PrEP gives people who already find it difficult to consistently use condoms an additional way to protect their health.

Due to the high rate of HIV infections, there is a particular need for the NHS to make PrEP available to gay men. However it should be available to all people who are at high risk of acquiring HIV.

How effective is PrEP?

Research suggests that PrEP is as effective as condoms in preventing HIV transmission, as long as the pills are taken regularly, as directed. Evidence from a large international study suggests that gay men who maintained at least four doses a week had 96% fewer infections.7 8 Preliminary results from separate studies of PrEP in the UK9 and France10 both show that PrEP substantially reduces infections among gay men. Full results are expected early in 2015. PrEP has also proven effective for heterosexual couples in which one partner is HIV positive and not on HIV treatment.11

PrEP does not prevent other sexually transmitted infections or pregnancy. It allows someone to protect their own health, irrespective of whether their partner uses a condom. Because it is taken several hours before sex, it does not rely on decision-making at the time of sex.

Why take HIV treatment to avoid taking HIV treatment?

People living with HIV need to take lifelong treatment. PrEP consists of fewer drugs and people only need to take it during periods when they are at risk of HIV. Many people find that their sexual behaviour changes over time, for example when they begin or end a relationship.

Does PrEP have side-effects?

Any medicine can have side-effects, so taking PrEP is a serious decision. The drugs in PrEP have been used as part of HIV treatment for many years. This has shown that they have a low risk of serious side-effects. Most people taking PrEP don’t report side-effects. Some people have stomach problems, headaches and tiredness during the first month but these usually go away. People taking PrEP have regular check-ups at a clinic.

Does PrEP mean people take more risks?

The full results of the PROUD study will help us understand the impact of PrEP on condom use among gay men in the UK. But other studies of PrEP have consistently reported that being on PrEP did not result in people adopting riskier behaviours. 12 13  14 Instead it gives people who already find it difficult to consistently use condoms a way to protect their health.

                                                        

References

  1. http://www.proud.mrc.ac.uk/PDF/PROUD%20Statement%20161014.pdf
  2. http://www.aidsmap.com/SecondEuropeanPrEPstudyclosesplaceboarmearlyduetohigheffectiveness/page/2917367/
  3. Public Health England. HIV in the United Kingdom: 2014 Report. London: Public Health England. November 2014.
  4. For more information, http://www.proud.mrc.ac.uk
  5. Public Health England. HIV in the United Kingdom: 2014 London: Public Health England. November 2014.
  6. Phillips AN et al. Increased HIV Incidence in Men Who Have Sex with Men Despite High Levels of ARTInduced Viral Suppression: Analysis of an Extensively Documented Epidemic. PLoS ONE 8(2): e55312. doi:10.1371/journal.pone.0055312.
  7. Grant RM et al. Preexposure Chemoprophylaxis for HIV Prevention in Men Who Have Sex with Men. New England Journal of Medicine 363:2587-2599, 2010.
  8. Anderson PL et al. Emtricitabinetenofovir concentrations and preexposure prophylaxis efficacy in men who have sex with men. Science Translational Medicine 4: 151ra125, 2012.
  9. http://www.proud.mrc.ac.uk/PDF/PROUD%20Statement%20161014.pdf
  10. http://www.aidsmap.com/SecondEuropeanPrEPstudyclosesplaceboarmearlyduetohigheffectiveness/page/2917367/
  11. Baeten JM et al. Antiretroviral Prophylaxis for HIV Prevention in Heterosexual Men and Women. New England Journal of Medicine 367: 399-410, 2012.
  12. Marcus JL et al. No Evidence of Sexual Risk Compensation in the iPrEx Trial of Daily Oral HIV Preexposure PLoS ONE 8: e81997, 2013.
  13. Mugwanya KK et al. Sexual behaviour of heterosexual men and women receiving antiretroviral preexposure prophylaxis for HIV prevention: a longitudinal analysis. Lancet Infectious Diseases 13: 1021–28, 2013. 14 Grant RM et al. Uptake of preexposure prophylaxis, sexual practices, and HIV incidence in men and transgender women who have sex with men: a cohort study. Lancet Infectious Diseases 14: 820-829, 2014.

Via NAM

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HIV in the UK: 76% diagnosed, 90% on treatment, 90% undetectable

HIV test

UK achieves two out of three UNAIDS targets, but undiagnosed infection remains a major problem

The UK’s annual epidemiological report, released yesterday, shows that the country already provides HIV treatment to 90% of people attending clinical services and that 90% of those on treatment have an undetectable viral load. But the country has a long way to go in ensuring that people with HIV are aware of their HIV status – only 76% of people living with HIV have been diagnosed. The problem is particularly acute in black African communities, as only 62% of African heterosexual men and 69% of African heterosexual women living with HIV have been diagnosed.

The figures can be compared to the ambitious targets announced by UNAIDS (the Joint United Nations Programme on HIV and AIDS) earlier in the year: for 90% of all people living with HIV to know their status, 90% of those to be on treatment and 90% of those to have an undetectable viral load. If these figures could be achieved by 2020, the global AIDS epidemic would be over by 2030, UNAIDS said.

The UK appears to have achieved two out of three of the targets, but has a significant problem due to the high rates of undiagnosed infection. Overall, 61% of all people living with HIV in the UK have an undetectable viral load. This contrasts with the 73% that would be achieved if all three of UNAIDS’ 90/90/90 targets were accomplished.

New diagnoses, overall prevalence

Public Health England reports that 6000 people were newly diagnosed with HIV in the United Kingdom in 2013. The overall figure is lower than that seen a decade ago, due to fewer diagnoses among heterosexual men and women born in high-prevalence African countries. Among gay men, the number of diagnoses is as high as ever, with 3250 cases reported in 2013. An estimated 30% of the gay men diagnosed in 2013 were recently infected with HIV (within six months of their diagnosis).

There are now almost 110,000 people living with HIV in the country, including 26,000 who don’t know they have it. This can be broken down into risk groups:

  • Gay, bisexual and other men who have sex with men (43,500 people; prevalence of 5.9%).
  • Black African heterosexual women (25,100 people; prevalence of 7.1%).
  • Black African heterosexual men (13,600 people; prevalence of 4.1%).
  • Heterosexual women of other ethnicities (10,300 people; prevalence of 0.06%).
  • Heterosexual men of other ethnicities (10,200 people; prevalence of 0.06%).
  • People who inject drugs (2400 people; prevalence of 0.7%).

High rates of undiagnosed infection, especially in black African communities

Overall, 24% of people living with HIV are unaware that they have it. The rates of undiagnosed infection are lowest among gay men (16%) and people who inject drugs (10%).

In relation to black African people, it’s worth noting that in previous epidemiological reports the description of a person as ‘black African’ primarily depended on whether they were born in an African country. In contrast, the new report focuses on a person’s ethnicity, so that someone born in the UK to Nigerian parents is considered in the ‘African’ category. As a result of this and other methodological changes, some of the figures for undiagnosed infection are not directly comparable to previous years’ – and paint a more worrying picture.

In 2013, 31% of black African heterosexual women and 38% of black African heterosexual men who had HIV were unaware of their infection. Rates of undiagnosed infection were somewhat lower among heterosexual people of other ethnicities: 27% in men and 23% in women.

The report also shows that rates of undiagnosed infection are far worse outside London, compared to the capital. Outside London, 41% and 49% of African men and women were undiagnosed. In London, 10% and 13% were undiagnosed. There is some fuzziness to these estimates: the true values could be up to 10% higher or lower than the figures given here. But a clear geographic difference would still be observed. This could reflect stronger community networks and more accessible health services, including targeted prevention, in the capital.

Another way to consider undiagnosed infection is to look at rates of late diagnosis – people diagnosed with a CD4 cell count below 350 cells/mm3. Rates of late diagnosis were highest among heterosexual men (62%) and heterosexual women (51%), with black Africans especially likely to be diagnosed late. The lowest rate of late diagnosis was seen in gay men (31%). Across all groups, older people and non-Londoners were more likely to be diagnosed late.

But progress has been made over the past decade – the overall rate of late diagnosis has gone down from 57 to 42%.

A higher uptake of HIV testing, including more frequent testing, is needed to improve the figures on undiagnosed infection and late diagnosis. The report shows that, at sexual health clinics, 86% of gay male patients take an HIV test, but only 77% of heterosexual men and 67% of heterosexual women do so. Whereas guidelines recommend that all people attending sexual health clinics are offered an HIV test, only one-in-seven clinics test at least 80% of their heterosexual patients. Public Health England recommends that clinics review their policies and training protocols.

But while PHE has been able to collect data on HIV testing in sexual health clinics, none are available for testing in GP surgeries, in other medical settings, or in community settings. A significant improvement in the proportion of people living with HIV who are diagnosed is thought unlikely to occur without improved provision of testing in non-specialist settings, as recommended in guidelines. The report notes that less than one in five of the black-African population attended a sexual health clinic in the previous five years.

“Reductions in undiagnosed infection can be achieved through increasing testing coverage in STI clinics, the introduction and consolidation of HIV testing in a variety of different medical services, in addition to further development of community testing, including self-sampling,” PHE comment.

Quality of care for people living with HIV

Considering the next stages of the ‘treatment cascade’ and the National Health Service’s performance in relation to UNAIDS’ targets, the report shows that 90% of people were linked to care within a month of their diagnosis (98% within three months). Moreover, 95% of those who received care in 2012 were retained in care in 2013. Results did not vary according to age, gender, ethnicity, sexuality or geographical area.

Further, 90% of people in care received antiretroviral therapy (up from 69% in 2004). This includes 92% of those with a CD4 cell count below 350 cells/mm3. Of all people taking treatment, 90% had an undetectable viral load, below 200 cells/ml.

Generally there was equality in treatment outcomes, although younger people were less likely to be taking therapy. Moreover, people in both the youngest (15-24 years) and the oldest (over 50) age groups were less likely to have an undetectable viral load.

Guidelines recommend that clinicians discuss treatment as prevention with patients, and give them the option to start treatment early for this reason. Probably as a result, average CD4 cell counts when starting treatment have risen in recent years. In 2013, 25% began treatment with a CD4 cell count between 350 and 500 cells/mm3, and a further 26% did so above 500 cells/mm3.

Article via NAM

For your full copy of the report, click here

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Human Genome Tinkering Could Be Our Best Bet to Beat HIV

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The human immunodeficiency virus (HIV) is a crafty little beast, constantly mutating to mask itself from our body’s defenses, but always entering cells through the same molecular door. The design of that cellular door is governed by our DNA, so why not change the lock by modding our genetic code?

In 2006, a minor medical miracle occurred. HIV-positive leukemia patient Timothy Ray Brown—the second Berlin Patient—received a bone marrow transplant that saved his life in more ways than one. The marrow that he received was from a donor with a unique double mutation to a gene on the 3rd chromosome known as CCR5. This gene codes for the surface protein that the HIV virus uses to gain entry into our white blood cells (specifically, CD4+ T-cells); however the double mutation shuts down these sites and provides a natural immunity to HIV. This mutation is exceptionally rare, only occurring in about one percent of Caucasians and nowhere else. It’s been hypothesized that it’s this same natural immunity that allowed a small portion of Europeans to make it through the Black Plague unscathed.

While that was fantastic news for Brown, who nearly a decade later remains off of his retroviral drug regimen and maintains an undetectable level of the virus in his system, it’s not of much use to the rest of us. With both the mutation prevalence and bone marrow compatibility matches in general being so rare, there was no effective means of using transplants as delivery vectors for this beneficial genetic condition. And it’s worth noting that the very process of becoming HIV-free nearly killed Brown. But that’s where Professor Yuet Kan’s team at UCSF comes in.

Kan figured that if integrating this double mutation wouldn’t work on the macro level—that is, replacing a patient’s bone marrow with that of a naturally HIV-immune person’s—maybe it would at the molecular level, thereby allowing researchers to confer the benefits while cutting out the marrow donation. To that end, he and a team of researchers from the University of San Francisco are employing cutting-edge genetic editing techniques to snip out the beneficial length of DNA coding and integrate it with a patient’s own genome.

The technique they’re using is known as CRISPR (Cas9) genome-editing. CRISPRs, (clustered regularly interspaced short palindromic repeats) are DNA delivery vectors that replace the existing base codes at a specific part of a specific chromosome with new base pair sets. Cas9, on the other hand are the “molecular scissors” that Kan’s team employs to first cut out the offending DNA. It sounds easy, sure—just find the string of DNA you want to replace, then snip it out with Cas9 DNA scissors, and install some new DNA using a CRISPR—however the nuts and bolts of the process are far more technically challenging.

The patient’s own blood cells would be employed as a precursor. Researchers would then have to convert those cells into induced pluripotent stem (iPS) cells by modulating a number of genetic switches, thereby instigating their regression to more basic stem cells. After that, the offending CCR5 gene would need to be knocked out and replaced with the better, double-mutated version before the now fortified blood cells were transfused back into the patient. Not only is there no chance of the body rejecting the new cells (they are the patient’s own after all), the technique also neatly sidesteps the whole embryonic stem cell issue.

While the technique is still in its early stages of development and no human trial dates have yet been set, it holds huge promise. Not just for the 35 million people annually infected by HIV, but also sufferers of sickle cell anemia and cystic fibrosis—two deadly diseases caused by a single protein deformation—could benefit from similar techniques. By figuring out which genes do what on our iPS cells, we could even theoretically grant everyone on Earth immediate immunity to any number of diseases.

Of course, being able to update and augment our genetic code opens up a whole slew of potential concerns, objections, and abuses. Just look at the ire raised over the use of embryonic stem cells in the early 2000s. People were lost their minds because they thought scientific progress was being built on the backs of fetuses. Researchers had to go and invent an entirely new way of making stem cells (the iPS lines) just to get around that one moralized sticking point, so you can bet there will be plenty of chimera, master race, and Island of Dr. Moreaureferences bandied about should we ever begin seriously discussing the prospect of upgrading our genes. And could certainly slow progress in this specific research.

That’s not to say that the hysteria that accompanies seemingly every news cycle these days is completely off base. Like cars, styrofoam, pressure cookers, and thermonuclear bombs, this technology can be used for evil just as easily as it can be for good. And while we’re not nearly as genetically complex as, say, an ear of corn, wrangling the myriad of interactions between our various genes is still an incredibly complex task and one with severe consequences should something go awry—even if we can avoid creating unwanted mutations through stringent testing and development methodology as we do with today’s pharmaceutical development. So why not turn ourselves into the ultimate GMOs? It certainly beats everyone becoming cyborgs.

Article via Gizmodo

Want more? – Read this..

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Another Major HIV Breakthrough

ProfLewin

Yesterday, the world was taken by storm when it was announced that a baby, born with HIV had been cured.  On the same day, it was announced a team from The Alfred hospital have uncovered HIV’s genetic hiding place and found a drug able to wake it up so that it can be destroyed.

The Alfred’s director of infectious diseases, Prof Sharon Lewin, said waking up HIV with doses of a highly toxic cancer drug was a huge step in curing a disease that has already claimed an estimated 30 million lives.

“What we thought would happen happened: the virus woke up, and we could measure it,” Prof Lewin said. “That is a big step.

“There are more possibilities of getting rid of it by making it visible to drugs and visible to the immune system (and) that we now know we can do.  Now the big challenge is working out, once it is visible, what are the ways to get rid of that infected cell.”

Traditional antiviral medications have been able to stop the virus infecting cells, giving patients a greater life expectancy.

But the virus remained “sleeping” in their DNA, unable to be found or treated, so patients had to take expensive medication daily to suppress its effects.

“It jumps in, buries itself into the DNA and sits there lurking. At any time, if the cell becomes active, the virus then becomes active,” Prof Lewin said.

“It is like having the embers of a fire sitting there . . . the minute you take away the anti-HIV drugs, the embers relight the fire and the whole thing gets going again.”

But by using cancer drug, Vorinostat, for two weeks, Prof Lewin had been able to turn on sleeping HIV-infected cells so they could be detected.

Researchers at The Alfred were able to bring the virus to notice in 18 of 20 HIV patients in a trial that concluded in January.

Prof Lewin hopes a new generation of drugs able to kick-start the immune system may now be able to kill the virus.

Prof Lewin and her team — which included collaboration with Monash University, the Burnet Institute, the Peter MacCallum Cancer Centre and the National Association of People Living with HIV/AIDS — will soon publish their full results.

For David Menadue, who has lived with HIV for almost 30 years, the results bring a new hope.

“Just having the existence of HIV in your body does do damage to your body every day. It puts pressure on your organs, your heart, your kidney, your liver.

“People with HIV would just love to get rid of this and go back to a normalised life. We are never really going to be able to get on top of the virus in developing countries without some sort of magical cure.”

Original Article via Herald Sun

Channel 4 news interviewed Professor Lewin yesterday, click here to see. (Sorry, we can’t embed this video)

Professor Lewin’s news isn’t new, she spoke about this at the 2012 CROI (Conference on Retroviruses and Opportunistic Infections)  – He she speaks with Matt Sharp about HIV Latency and Eradication using Vorinostat.

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Anti-HIV drug effort in South Africa yields dramatic results

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An intensive campaign to combat HIV/AIDS with costly antiretroviral drugs in rural South Africa has increased life expectancy by more than 11 years and significantly reduced the risk of infection for healthy individuals, according to new research.

The two studies, published Thursday in the journal Science, come as wealthy Western nations are debating how best to stretch limited AIDS funding at a time of economic stress.

With an annual price tag of $500 to $900 per patient, antiretroviral therapy programs have stirred frequent debate. Critics argue that adherence to the drug regimen is low and social stigma prevents some from seeking care until they are very ill and have infected others. Cheaper remedies, such as condom distribution, male circumcision and behavior modification, deserve more attention and funding, they say.

The new economic analysis of a $10.8-million campaign in KwaZulu-Natal province concluded that the drug scale-up there had been highly cost-effective.

The program was administered by nurses in rural health clinics in an impoverished region of about 100,000 people. Treatment consisted primarily of daily doses of antiretroviral therapy, or ART, drugs, which patients take every day for their entire lives. Patients picked up their medication at a rural clinic once a month.

In 2003, the year before the drugs were available, 29% of all residents were infected with HIV and half of all deaths there were caused by AIDS. Life expectancy in the region was just over 49 years.

By 2011, life expectancy had grown to 60 1/2 years — “the most rapid life expectancy gains observed in the history of public health,” said study senior author Till Barnighausen, a global health professor at the Harvard School of Public Health.

Based on that increase in longevity, researchers determined just how many years of life were effectively “gained” among residents as a result of ART intervention. They used that figure and the total expense of the program to calculate a cost-effectiveness ratio of $1,593 per life-year saved.

The World Health Organization considers medical intervention to be “highly cost-effective” if the cost per year of life saved is less than a nation’s per capita gross domestic product. The program’s ratio was well below South Africa’s 2011 per capita GDP of about $11,000.

“It’s really a slam dunk of an intervention,” said study leader Jacob Bor, a graduate student at Harvard. “These investments are worthwhile.”

The research team noted that the study period coincided with the arrival of electric power and clean water for area residents. But those alone could not explain the dramatic increase in longevity, they said.

“While mortality due to HIV declined precipitously, mortality due to other causes flat-lined,” Bor said. “These changes were almost certainly due to ART scale-up.”

In a second study from the same region, researchers followed nearly 17,000 healthy people from 2004 to 2011 to determine HIV infection rates in areas with active ART intervention programs.

Healthy individuals in those areas were 38% less likely to contract HIV than people in areas where ART drugs were not widely available, researchers found. People in extremely rural areas also fared better than those in more closely populated areas clustered around national roads.

Overall HIV prevalence increased 6% during the seven years of the study, probably because the antiretroviral drugs allowed people with the virus to live longer, according to the report.

It’s not clear how the results of the new study would translate to areas where stable, cohabiting couples were not the norm, said lead author Frank Tanser, an epidemiologist at the University of KwaZulu-Natal.

AIDS researchers who weren’t involved in the studies said they provide strong support for maintaining programs like the President’s Emergency Plan for AIDS Relief, begun by President George W. Bush in 2003.

“These papers present truly remarkable data,” said Dr. Douglas Richman, director of the Center for AIDS Research at UC San Diego.

Original article via Gawker

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