Tag Archives: research

So what’s the deal on sugar if you’re HIV Positive??

While we all know that sugar in moderation is best, researchers say that starving HIV of sugar may put a stop to the virus. When the virus enters an activated immune cell, it takes energy from sugar and nutrients in order to replicate. Cut off the supply of sugar, the theory goes, and HIV can’t replicate in the cell.

Now researchers at Northwestern Medicine and Vanderbilt University say they’ve found a way to cut off the sugar pipeline to the immune cell, which in effect, would starve the virus.

“It’s essential to find new ways to block HIV growth, because the virus is constantly mutating,” says Harry Taylor, a scientist at Northwestern Medicine’s HIV Translational Research Center. “A drug targeting HIV that works today may be less effective a few years down the road, because HIV can mutate itself to evade the drug.”

This new approach has several benefits, including applications to cancer treatment (another disease with a powerful sweet tooth) and reduction in organ damage in HIV-positive patients. HIV causes an abnormal proliferation of immune cells, which can cause inflammation and damage to organs over time, even in patients who are on antiretroviral treatment.

“This discovery opens news avenues for further research to solve todays persisting problems in treating HIV infection: avoiding virus resistance to medicines, decreasing the inflammation that leads to premature aging, and maybe even one day being able to cure HIV infection,” says Richard D’Aquila, director of Northwestern’s HIV Translational Research Center.

Now, we’re not advocating reducing your sugar intake to zero.  Our bodies need sugar to survive and the information above relates to clinical procedures  in the lab.  There’s lots of scaremongering in the news lately about the need to reduce sugar, the war on sugar and many people are coming out to inform us all how bad it is!

As a nation, we’re being told we need to seriously reduce our sugar intake and recent reports have destroyed the notion that it’s OK to indulge a sweet tooth, even modestly.

The World Health Organisation recommends reducing sugar to below 5 per cent of total energy intake.  The Scientific Advisory Committee on Nutrition also agree with this assessment.  Our own NHS is suggesting the maximum daily amount of sugar for an adult is the equilivent of 7 cubes.  Check out their site here: https://www.nhs.uk/change4life-beta/campaigns/sugar-smart/sugar-facts

In all cases, “sugar” here means added sugar. This is the type added to processed food and present in honey, syrups and juices, rather than lactose (the sugar in milk) and the sugars in whole fruits and vegetables.

Limited to 3 per cent of total energy, sugar intake equates to just 15g a day, or fewer than four level teaspoons. This means no more sweet treats (a slice of Battenburg contains 24g), and restricts the eating of even nutritious foods such as yogurt (a pot of the strawberry variety typically contains 14g of free sugars).

But is this recommendation actually desirable or practical?

“The claim that sugar should contribute only 3 per cent of energy is not based on good quality scientific evidence,” says registered nutritionist Sigrid Gibson.

Behind the Headlines, the section of the NHS Choices website that evaluates health news stories, agrees, writing that the BMC Public Health study has “many potential limitations, thereby reducing its reliability”.

“For tooth decay, between-meal snacking is the problem,” says Gibson.

Despite the clamour to cut sugar to help solve the obesity crisis, the evidence isn’t clear-cut here either. In fact, in many countries there is a “sugar-fat seesaw”, with those reducing their sugar intake eating more fat, which has more than twice the calories of sugar.

“Children and teenagers are eating too much sugar, with the average 11- to 18-year-old getting 15.5 per cent of their energy from sugar,” says registered dietitian Penny Hunking. “But you can still be healthy if you eat a variety of foods, and your free or added sugar intake is up to around 50g a day.”

A 50g limit allows for normal family meals, including a bowl of bran flakes, a small (150ml) glass of orange juice, pot of fruit-flavoured yogurt and a digestive biscuit every day.

“Scare-mongering messages about sugar perpetuate a myth that individual nutrients are good or bad, while we should be talking about dietary patterns as a whole,” says Gibson.

In short, yes it’s a good idea to control your sugar intake but not because of your HIV status or because there’s a push to inform people that sugar is bad. It’s important to understand sugar in context.  The best nutritional advice has always been to eat a variety of foods and that a varied diet can include sugars. While a diet high in sugars and sugar-containing foods may impact on calorie intake and weight, and therefore on diabetes and heart disease, sugar-containing foods particularly those that contain other nutrients can be included in a balanced diet.

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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

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
logo-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.

“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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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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Soy sauce molecules effectively fight HIV

soy-sauce-sq-bowl

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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Admare Jinga sentenced for ‘HIV cure’ fraud

Jinga, Admare

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:

Imagine a world where HIV can’t replicate, then start believing!

HIV capsid

The following article provides fascinating reading on the latest published research on the structure of the HIV virus itself.  Be sure to watch the video and follow up on the references at the end of the article for more information.  Excited? – We are!

There’s no easy answer for HIV; the virus uses our own immune cells to its advantage and mutates readily to shrug off round after round of anti-retrovirals. But thanks to the efforts researchers from the University of Illinois and some heavy-duty number crunching from one of the world’s fastest petaflop supercomputers, we may be able to stop HIV right in its tracks.

The latest line of attack against HIV targets its viral casing (or capsid). Capsids lie between the virus’s spherical outer coat, a .1 micron diameter, lipid-based layer known as the viral envelope, and a bullet-shaped inner coat known as the viral core that contains the strands of HIV RNA. Capsids comprise 2,000 copies of the viral protein, p24, arranged in a lattice structure (a rough insight gleaned only from years of cryo-electron microscopy, nuclear magnetic resonance spectroscopy, cryo-EM tomography, and X-ray crystallography work). The capsid is responsible for protecting the RNA load, disabling the host’s immune system, and delivering the RNA into new cells. In other words: It’s the evil mastermind.

The lattice protein structure allows the capsid to open and close like a Hoberman Sphere.

As Dr Peijun Zhang, project lead and associate professor in structural biology at the University of Pittsburgh School of Medicine explained to the BBC:

The capsid is critically important for HIV replication, so knowing its structure in detail could lead us to new drugs that can treat or prevent the infection. The capsid has to remain intact to protect the HIV genome and get it into the human cell, but once inside, it has to come apart to release its content so that the virus can replicate. Developing drugs that cause capsid dysfunction by preventing its assembly or disassembly might stop the virus from reproducing.

But until very recently, the precise structure—how the thousands of copies of p24 actually meshed together—remained a mystery. The capsid’s (relatively) large size, non-symmetric shape, protein structure has stumped researchers’ attempts to effectively model it. Earlier research had revealed that the p24 arranged itself in either a pentagon or hexagon shape as part of the capsid structure, but how many of each and how the pieces fit together remained out of reach because science simply didn’t have the computational prowess to model this incredibly complex subatomic structure in atomic-level detail.

This problem required a petaflop-level supercomputer to solve, a class of machine that has only recently become readily available. The team turned to National Center for Supercomputing Applications at the University of Illinois at Urbana-Champaign and its resident supercomputer, Blue Waters.

The team fed electron microscopy data collected in lab experiments conducted at the University of Pittsburgh and Vanderbilt University into Blue Waters and let the $108 million, 11.5 petaflop machine do its thing: Crunch massive amounts of information with its 49,000 AMD CPUs. Blue Waters can handle one quadrillion floating point operations every second, so stitching together 1,300 proteins into an oblong molecular soccer ball was no sweat.

The team developed a novel shaping algorithm for the project, dubbed molecular dynamic flexible fitting.

“You basically simulate the physical characteristics and behavior of large biological molecules, but you also incorporate the data into the simulation so that the model actually drives itself toward agreement with the data,”

Said Professor Klaus Schulten of the University of Illinois in a press release.

“This is a big structure, one of the biggest structures ever solved,” Schulten continued. “It was very clear that it would require a huge amount of simulation — the largest simulation ever published — involving 64 million atoms.”

The team revealed the complete capsid structure in a Nature report yesterday:

The mature human immunodeficiency virus-1 (HIV-1) capsid is best described by a ‘fullerene cone’ model, in which hexamers of the capsid protein are linked to form a hexagonal surface lattice that is closed by incorporating 12 capsid-protein pentamers.

In all, the HIV capsid requires 216 protein hexagons and 12 protein pentagons to operate—arranged exactly as the predictive models said they would be. The new discovery reveals a stunningly versatile protein in p24. The protein itself is identical whether it’s shaped into a pentagon or a hexagon, only the attachment sites between p24 proteins varies between shapes. How that works remains a mystery.

“How can a single type of protein form something as varied as this thing? The protein has to be inherently flexible,” said Schulten.

New questions aside, this breakthrough illustrates precisely how the capsid works and how scientists can best attack that function to disrupt the virus’ ability to replicate. By exploiting the capsid’s structure, researchers theoretically could deliver a molecular padlock that prevents the viral core from opening and the virus from spreading. This discovery could lead to an entirely new suite of treatment alternatives and could finally outpace HIV’s ability to rapidly evolve resistance to current enzyme-based medications.

“The big problem with HIV is that it evolves so quickly that any drug you use you get drug resistance which is why we use a multi-drug cocktail,”

Professor Simon Lovell, a structural biologist at the University of Manchester, said.

“This is another target, another thing we can go after to develop a new class of drugs to work alongside the existing class.”

It’s only a matter of time until HIV goes the way of polio. And it’s thanks in no small part to one beast of a computer.

Read on for more information:

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