Scientists Have Found A Way To Make Cells Resistant To HIV

TSRI Senior Staff Scientist Jia Xie was first author of the new study. (Photo by Madeline McCurry-Schmidt.)

In a remarkable step forward in the potential treatment of HIV, scientists in California have successfully created a cell population that is resistant to the disease.

The new approach, described as a form of “cellular vaccination” aims to offer long-term protection for patients by tethering HIV-fighting antibodies to their immune cells.

Jia Xie, senior staff scientist, said: “The ultimate goal will be the control of HIV in patients with AIDS without the need for other medications,” as even with antiretroviral drug treatments, people with HIV still suffer much higher incidences of cancer and other deadly diseases.

Here, cells protected from rhinovirus by membrane-tethered, receptor-blocking antibodies survive well and form colonies. Credit: Jia Xie, Lerner Lab

Joseph Alvarnas who was involved in the study, said: “HIV is treatable but not curable – this remains a disease that causes a lot of suffering. That makes the case for why these technologies are so important.”

The new technique is superior to therapies where antibodies float freely in the bloodstream at a relatively low concentration, as the antibodies hang on to the cell’s surface blocking HIV from accessing a crucial receptor and spreading infection.

Known as the ‘neighbour effect’ the team showed that resistant cells could quickly replace diseased cells, potentially curing a person of HIV through gradual displacement.

Xie said: “You don’t need to have so many molecules on one cell to be effective.”

In essence, the researchers had forced the cells to compete in Darwinian ‘survival-of-the-fittest’ selection in a lab dish. Cells without antibody protection died off, leaving protected cells to survive and multiply, passing on the protective gene to new cells.

To infect a person, all strains of HIV need to bind with a cell surface receptor called CD4, so the team at the Scripps Research Institute and City of Hope research centre near Los Angeles, tested antibodies that could potentially protect this receptor on the very immune cells normally killed by HIV.

The antibodies recognized the CD4 binding site, blocking HIV from getting to the receptor.

The next step in this research is to try engineering antibodies to protect a different receptor on the cell surface, according to Xie.

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Have you ever wondered what HIV sounds like?

The majority of us enjoy music to some degree or another, pop, classical, rock R&B but have you ever wondered what HIV would sound like?

There is a range of sound and music, which lies beyond the range of human hearing. “Sounds of HIV” is a musical translation of the genetic code of HIV, the human immunodeficiency virus. In this album, segments of the virus are assigned musical pitches that correspond to the segment’s scientific properties. In this way, the sounds reflect an accurate, musical nature of the virus. When listening from beginning to end, the listener hears the entire genome of HIV.”

You may think that expressing nucleotides of the genome of a virus as pitches of the melodic scale as a promotional stunt, why would you draw a connection between adenosine and A, between cytosine and C and so on?

University of Georgia graduate student Alexandra Pajak’s instrumental sequence ensemble which draws inspiration from the physical properties of HIV itself!

“Sounds of HIV,” is a 17-track, 52-minute long musical adaptation of HIV’s genetic code. Pajak assigned pitches to the four basic nucleotides in DNA — A for Adenine, C for Cytosine, G for Guanine and D for Thymine — but the score contains much more than these for notes

Applying scientific rigour to music is nothing new and has been done in the past with math so why not with biochemistry? Alexandra Pajak, native of Athens, Georgia studied both composition and sciences and her work reveals a fascination with both subjects. Then there is a general sense of unease, creeping in. This undeniably beautiful music expresses HIV, a virus responsible for the destruction of much beauty and art. On one hand, it’s tempting to assume that nature’s creations achieve a high level of symmetry and beauty and a virus should not be exempt from that principle.

On the other hand, what terrible beauty is there to be found should we glimpse inside the genome of the plague, syphilis, smallpox or even flu? These ruminations tend to accompany listening to this oddly-concordant composition, performed with aplomb by the Sequence Ensemble.

In a way, the strange and disturbing recording reveals itself beautiful yet disturbing as the sounds reflect the true nature of the virus. When listening from beginning to end, the listener hears the entire genome of HIV.”

Unfortunately, we’re unable to stream the full album however here’s the links to it on Google Music or Spotify, if you’re more old school, here’s the CD on Amazon.

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Something to #Celebrate: Good news in #HIV #Vaccine Research!

Scientists may have discovered a way to spur the human body to create antibodies capable of blocking the HIV virus. Researchers at institutions around the United States said in five studies published Thursday in the journals Cell, Immunity and Science that they had made an important early step toward developing a vaccine for the disease.

“It’s early work, but we’re trying to rewrite some rules of vaccine development to overcome the extraordinary challenges of HIV,” William Schief, director of vaccine design for the Neutralizing Antibody Center at the Scripps Research Institute’s International AIDs Vaccine Initiative, said. “In a collaborative effort we have reached critical milestones, including the first proof ever that immunization with designer proteins can produce broadly neutralizing antibodies against HIV. The new results strongly support further developing these approaches toward testing in clinical studies.”

There are still some major challenges before clinical studies on humans can begin. To put it simply, HIV is difficult to combat because it attacks the very immune cells sent out to fight it. When the body is successful in fighting it (usually with the help of drugs) the virus is really good at hiding dormant until the next opportunity to stage a comeback. Traditional vaccines haven’t worked to fight HIV but this new research shows that so-called “broadly neutralizing antibodies” are capable of controlling or preventing infection from a range of HIV strains and researchers think these special antibodies are the key to formulating a vaccine.

But for it to be effective the vaccine would have to be much better than nature. Only about 10 to 20 percent of people infected with HIV develop the antibodies on their own and it can take years for them to develop. This new vaccine would have to coax the human immune system to act differently. The researchers were able to spur this kind of reaction in mice whose immune systems mimicked components of the human immune system.

Vaccines aren’t the only way scientists hope to address the HIV problem around the world. Other approaches — including one that resulted in the only known case of HIV being cured, stem cell transplants — are being looked at.

Want more?

Here’s another link on the same story: New vaccination strategies coach immune system to make HIV-neutralizing antibodies

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Science won’t stop until it beats AIDS, says HIV pioneer

Francoise Barre-Sinoussi, French virologist and director of the Regulation of Retroviral Infections Division (Unite de Regulation des Infections Retrovirales) at the Institut Pasteur, poses during an interview with Reuters, in Paris, France, October 1, 2015. REUTERS/Philippe Wojazer

Oct 9 More than 30 years after she identified one of the most pernicious viruses to infect humankind, Francoise Barre Sinoussi, who shared a Nobel prize for discovering HIV, is hanging up her lab coat and retiring.

Story via Reuters

 

She’s disappointed not to have been able to claim ultimate victory in the battle against the human immunodeficiency virus (HIV) that causes the killer disease AIDS, but also proud that in three decades, the virus has been beaten into check.

While a cure for AIDS may or may not be found in her lifetime, the 68-year-old says, achieving “remission” – where infected patients control HIV in their bodies and, crucially, can come off treatment for years – is definitely within reach.

“I am personally convinced that remission…is achievable. When? I don’t know. But it is feasible,” she told Reuters at her laboratory at Paris’s Pasteur Institute, where she and her mentor Luc Montagnier discovered HIV in 1983.

“We have ‘proof of concept’. We have…the famous Visconti patients, treated very early on. Now it is more than 10 years since they stopped their treatment and they are still doing very well, most of them.”

Sinoussi is referring to a study group of 14 French patients known as the Visconti cohort, who started on antiretroviral treatment within 10 weeks of being infected and stayed on it for an average of three years. A decade after stopping the drugs, the majority have levels of HIV so low they are undetectable.

These and other isolated cases of remission, or so-called “functional cure”, give hope to the 37 million people worldwide who, due to scientific progress, should now be able to live with, not have their lives cut short by, HIV.

In developed countries at least – and in many poorer ones too – an HIV positive diagnosis is no longer an immediate death sentence, since patients can enjoy long, productive lives in decent health by taking antiretroviral drugs to control the virus.

It’s a long way from the early 1980s, when Sinoussi remembers sick, dying HIV-positive patients coming to the doors of the Pasteur and pleading with scientists there for answers.

“They asked us: ‘What we are going to do to cure us’,” she says. At that time, she says, she knew relatively little about HIV, but what she was sure of was that these patients would never live long enough to see a treatment developed, let alone a cure. “It was very, very hard.”

Yet this interaction with real patients, and with their doctors and later their advocates, gave Sinoussi an important insight into what was needed to make her life in science one with meaning and impact — collaboration.

Working across barriers – be they scientific disciplines, cultural, religious and political divides, international borders or gender distinctions, has been and remains Sinoussi’s driving force.

In her earliest days, feeling disengaged while working on her PhD and itching for action in a real-life laboratory, she hustled her way in to working at the male-dominated Pasteur Institute for free with a virologist researching links between cancers and retroviruses in mice.

While viruses are her thing, she has throughout her career worked with, cajoled and learned from immunologists, cancer specialists, experts in diseases of aging, pharmaceutical companies, AIDS patients, campaigners, and even the pope.

“When you work in HIV, it’s not only working in HIV, it’s working far, far beyond,” she said.

Freshly armed with her Nobel award and fired up about a lack of support for proven methods of preventing HIV’s spread, Sinoussi wrote an open letter to then-Pope Benedict XVI in 2009 criticising him for saying that condoms can promote the spread of AIDS.

In what was widely seen as a modification of his stance in response to such criticism, Benedict said in a book a year later that use of condoms could sometimes be justified in certain limited cases as a way to fight AIDS.

Sinoussi says: “HIV has shown the way to go in the field of science. You can’t be isolated in your laboratory. You need to work with others.”

And this, she adds, is the “all together” spirit with which she advises her successors to continue after she’s gone.

Many will be sad to see her leave, but she has faith that her chosen field will deliver for the people who need it.

“Of course, I would love to have stopped and to see we had a vaccine against HIV and another treatment that could induce remission – but that’s life. I encourage the new generation of scientists today to continue our work.

“Science never stops,” she says. “Just because a scientist stops, the science should not stop.”

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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.

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

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

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

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Soy sauce molecules effectively fight HIV

More than a decade after a Japanese soy sauce manufacturer said it had discovered a molecule in its sauce that could be used to fight HIV, the findings have been confirmed by university scientists.

According to a team of virologists at the University of Missouri, a flavor-enhancing molecule found in soy sauce – called EFdA – is up to 70 times more powerful than typical drugs like Tenofovir, which is often used as a first line of defense before the disease builds up a resistance.

“Patients who are treated for HIV infections with Tenofovir, eventually develop resistance to the drugs that prevent an effective or successful defense against the virus,” said Stefan Sarafianos, associate professor of molecular microbiology and immunology in the University of Missouri School of Medicine, and a virologist at the Bond Life Sciences Center.

“EFdA, the molecule we are studying, is less likely to cause resistance in HIV patients because it is more readily activated and is less quickly broken down by the body as similar existing drugs.”

The discovery of the powerful molecule dates back to 1998, when Japanese soy sauce company Yamasa established a division of food scientists with the intention of studying how the body’s immune system reacted to the chemicals contained in food. According to Vocativ, the company discovered the potential of EFdA in 2001, when it noticed the make-up of the molecule bore a striking resemblance to existing HIV drugs on the market.

Thirteen years later, that research has been verified. When it comes to individuals whose bodies haven’t developed a resistance to Tenofovir, the soy sauce molecule is 10 times more effective.

“Not only does EFdA work on resistant HIV, it works better on HIV that has not become Tenofovir resistant,” Sarafianos said.

According to the University of Missouri’s science blog, EFdA’s effectiveness was also proven in monkeys by Sarafianos and other researchers like Michael Parniak of the University of Pittsburgh and the National Institutes of Health’s Hiroaki Mitsuya. In 2012, the three researchers showed that even in animals nearing death, EFdA allowed for rapid and impressive recovery.

“These animals were so lethargic, so ill, that they were scheduled to be euthanized when EFdA was administered,” Parniak told the blog. “Within a month they were bouncing around in their cages, looking very happy and their virus load dropped to undetectable levels. That shows you the activity of the molecule; it’s so active that resistance doesn’t come in as much of a factor with it.”

Moving forward, the researchers hope to apply EFdA most effectively in preventative measures, which the team sees as the best way to halt the spread of the disease. Continued research into the molecule could lead to other breakthroughs and even better ways to battle HIV.

“We want to understand how long EFdA stays in the bloodstream and cells,” Parniak said. “If we understand structurally why this drug is so potent it allows us to maybe develop additional molecules equally potent and a combination of those molecules could be a blockbuster.”

Story via RT

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Another GIANT Leap Forward in the Search for a Cure for HIV

In a breakthrough six years in the making, an international team of researchers has determined the precise atomic structure of a cell-surface receptor that’s used by most strains of HIV to infect human immune cells. The finding could result in medicines that block the process.

HIV researchers have been making great strides recently — and thank goodness for that. Since making its unwelcome debut in the early 1980s, HIV/AIDS has killed more than 28 million people worldwide, with more than 34 million people currently living with the virus infection.

Back in March, scientists functionally cured a baby infected with HIV. A week later, doctors announced that a similar technique had effectively cured 14 adults. And late last year Canadian researchers announced that their efforts to create the world’s first HIV vaccine had cleared a major hurdle after a successful Phase I trial. Relatedly, it was only yesterday that researchers from Oregon Health & Science University announced that they have developedan HIV/AIDS vaccine that can completely clear an AIDS-causing virus from the body. There’s even a drug, called Truvada, that’s proven to reduce the risk of HIV infection.

The war on HIV is clearly in full swing — and a new international study has made yet another major stride, this time by mapping out the molecular structure responsible for HIV infections.

Visualization = Understanding

The target is a receptor called CCR5 — and it’s one of two main entry points that HIV uses to launch its attack on the human immune system; CCR5 is a protein on the surface of white blood cells that’s involved in the immune system, acting as a receptor for chemokines (signalling proteins secreted by cells). After binding to it, an HIV protein fuses to the cell membrane beneath as it digs its way inside the cell. Infection ensues.

The other receptor that performs this feat is CXCR4. Together, the two belong to a family of receptor proteins called G-protein-coupled receptors (GPCRs) which regulate a host of functions in the human body. These receptors are crucial to scientists when designing drugs.

Until now, however, scientists haven’t been able to properly visualize the precise molecular structure of these labyrinthine receptors. Previous studies have successfully solved CXCR4’s structure, but the exact way it recognizes and binds to HIV viral proteins has remained a mystery.

Indeed, without a hi-res molecular “picture” of the receptors, designing drugs is difficult — if not impossible.

Maraviroc to the Rescue

To capture the high resolution, three-dimensional atomic structure of the receptors, a team supported by both US and Chinese research agencies (including The Scripps Research Institute in California) considered Maraviroc, an antiretroviral drug and entry inhibitor used to treat HIV-1. It’s a receptor antagonist that binds the co-receptor, making it unavailable to circulating HIV.

In this artistic impression, the HIV drug Maraviroc grabs hold of CCRF in an inactive configuration, preventing HIV from using the receptor to enter cells. (Courtesy of the Wu lab)

In the new study, the researchers demonstrated the precise spot where Maraviroc attaches to cells and blocks HIV’s entry.

Maraviroc was used by the researchers to bind an engineered CCR5 receptor. It was then purified and crystallized, resulting in a receptor/drug complex that measured 2.7 Angstroms. By looking at this bound complex at such a high resolution — where the receptor was made inactive and unresponsive to HIV — the scientists were able to catch a glimpse of the molecular pathway by which HIV fuses with cells, including the molecular-scale quirks that allow some strains of HIV to escape CCR5 inhibitors.

Image: CCR5 side-by side with alternate HIV co-receptor CXCR4. (Courtesy of the Wu lab)

The study, which appears in Science, will help scientists to both improve existing HIV drugs based on CCR5 inhibition and to design new drugs altogether.

“We hope that the structure we determined can be used to understand the molecular details of the current viral strains of HIV entry, to develop new molecules that can inhibit both CXCR4 and CCR5 receptors, and to block future strains that might emerge and be addressed with second generation HIV entry inhibitors,” noted Beili Wu, a researcher from the Chinese Academy of Sciences’ Shanghai Institute.

via i09 Read the entire study at Science Express .

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Admare Jinga sentenced for ‘HIV cure’ fraud

Admare Jinga, 31, was sentenced at Belfast Magistrates Court on Tuesday

A man who was convicted of an on-line scam selling products that claimed to ‘kill’ the HIV virus has been sentenced to 240 hours community service.

Admare Jinga used his base in Belfast to set up a company that advertised and distributed products overseas, particularly to his native Zimbabwe.

In June, he was found guilty of fraud by false representation.  He had already admitted a second charge of marketing medicines for human use without proper authorisation.

The 31-year-old University of Ulster graduate was sentenced at Belfast Magistrates Court on Tuesday.
Jinga, who now lives in Hamilton, Lanarkshire, Scotland, will carry out his community service over the next 12 months.  During the trial, Belfast Magistrates Court had heard that Jinga established a company called Savec Healthcare Ltd in 2007, when he was living in south Belfast.

Up until 2009 it marketed products as alternative forms of treatment for the HIV infection.  They claimed to be able to kill, prevent or stop Aids, according to the prosecution.

In the witness box Jinga said he became involved with pharmacists, a microbiologist and other Zimbabwean professionals concerned with the impact of HIV in their country.  Jinga claimed that no complaints were ever received from people who used his products.
The case against him was taken by the Medicines and Healthcare Products Regulatory Agency (MHRA).  In a statement issued after the sentencing, the MHRA said the case was its first ever prosecution of its kind.

The agency said it took action against Jinga after he was found to be selling a machine and accompanying medicine over the internet that he falsely claimed could cure HIV and Aids.

“There are no known cures for HIV so any claim to this effect is illegal,” the MHRA statement added.

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Are you interested in news and articles about genuine research into developing a cure for HIV? – We have some articles for you to read, take a look at these:

• Computer Simulations Help Explain Why HIV Cure Remains Elusive
• What Can We Do Now to Speed Up HIV Cure Research?
• Nobel laureate, discoverer of HIV, says a cure for HIV is in sight!
• Even without a cure, the end of the AIDS pandemic is in sight
• A Cure for HIV/AIDS Has Got a Step Closer!
• I Am Living Proof That There Could Be a Cure For AIDS!
• A Message of Hope for a HIV Cure from Timothy Brown
• MEDICAL HISTORY – Child Born with HIV Cured!
• Baby Cured of HIV – Here’s the real message..
• Early HIV drugs ‘functionally cure about one in 10
• Fighting Fire with Fire.. How HIV is Used to Cure Cancer!

 

And finally,…

Glowing cats to cure HIV? (You read that right)!