Tag Archives: science

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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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.

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.

New discovery brings us one step closer to preventing HIV infections

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.

New discovery brings us one step closer to preventing HIV infections

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.

New discovery brings us one step closer to preventing HIV infections

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

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:

Bill to lift ban on HIV positive organ donation passes House committee

Red-Green-Organ-Donation-Ri

USA: A bill which could eventually allow the donation of HIV positive organs to HIV positive recipients has passed the House after having passed the US Senate back in June.

The HIV Organ Policy Equity Act (HOPE), which is sponsored by both Democrats and Republicans would allow organs from HIV positive people to be donated to HIV positive recipients, and more so would allow researchers to study the safety of such practice.

The Human Rights Campaign also commended the passage of the bill. Back in March, the HRC praised the passage of the bill in the Senate Committe, and in June it passed in the full Senate.

“The HOPE Act represents sound public health policy,” said HRC legislative director Allison Herwitt. “The action by the House Energy & Commerce Committee is a major step forward in removing an outdated barrier which impedes access to lifesaving transplants for persons living with HIV and AIDS.”

HIV-positive patients in the US have been lobbying for the right to receive HIV-infected transplant organs for some time. They argue that there are hundreds of HIV-infected organs available every year and that making the change would save lives and give more people the chance of a transplant.

There are more than 100,000 actively waiting for life-saving organs, and around 50,000 more are added annually, and lifting the ban could decrease waiting time for all.

Allowing organs from HIV positive donors to HIV positive recipients with liver or kidney failure could save up to 1,000 people each year.

The ban on HIV positive organ donation was put in place in 1988, and aruments for it being lifted come partly from the fact that the treatment of HIV and AIDS has advanced significantly since.

The Centers for Disease Control (CDC) issued draft Public Health Service Guidelines in September 2011, recommending research in this area, but said that in the US, federal law blocks it from taking place.

Over 40 medical and patient advocacy groups endorse the act, including the United Network for Organ Sharing, which manages the US’s organ transplant system.

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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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Early HIV drugs ‘functionally cure about one in 10’

HIV Medicine

Rapid treatment after HIV infection may be enough to “functionally cure” about a 10th of those diagnosed early, say researchers in France.

They have been analysing 14 people who stopped therapy, but have since shown no signs of the virus resurging.  It follows reports of a baby girl being effectively cured after very early treatment in the US.  However, most people infected with HIV do not find out until the virus has fully infiltrated the body.

The group of patients, known as the Visconti cohort, all started treatment within 10 weeks of being infected. The patients were caught early as they turned up in hospital with other conditions and HIV was found in their blood.

They stuck to a course of antiretroviral drugs for three years, on average, but then stopped.  The drugs keep the virus only in check, they cannot eradicate it from its hiding places inside the immune system.  Normally, when the drugs stop, the virus bounces back.

Control

This has not happened in the Visconti patients. Some have been able to control HIV levels for a decade.

Dr Asier Saez-Cirion, from the Institute Pasteur in Paris, said: “Most individuals who follow the same treatment will not control the infection, but there are a few of them who will.”  He said 5-15% of patients may be functionally cured, meaning they no longer needed drugs, by attacking the virus soon after infection.

“They still have HIV, it is not eradication of HIV, it is a kind of remission of the infection.”

Their latest study, in the journal PLoS Pathogens, analysed what happened to the immune system of the patients.  Early treatment may limit the number of unassailable HIV hideouts that are formed. However, the researchers said it was “unclear” why only some patients were functionally cured.

Dr Andrew Freedman, a reader in infectious diseases at Cardiff University School of Medicine, said the findings were “certainly interesting”.

“The presumption is that they’ve started treatment very early and the virus hasn’t spread to so many of the long-term reservoirs and that’s why it works.  Whether they’ll control it forever, or whether it’ll be for a number of years and subsequently they will progress and the virus will reappear, we don’t know.”

However, he cautioned that many patients would be diagnosed much later than in this study.

Deborah Jack, the chief executive of the National AIDS Trust said it was “exciting times” in progress towards an HIV cure, but the key was early treatment.

“This just underlines the importance of people being testing and diagnosed early. Currently half of people living with HIV in the UK are diagnosed late – indicating that they are likely to have been infected for five years.”

Analysis

There have been two stories about HIV ‘cures’ in two weeks now – yet the latest developments offer little to the majority of people living with HIV.

In the Mississippi baby case and in the Visconti cohort the infection was caught very early, within weeks, at a vulnerable stage.

This suggests that by hitting the virus hard when it first infects the body, it might be possible to live for years without needing treatment – a functional cure.

However, these patients were the lucky few who were detected in the days and weeks after infection. Most cases are detected years later. For these patients a cure looks, at best, distant.

The hope is that by investigating how patients treated early, and a group of people who are genetically resistant to HIV, can combat the virus – it will give scientists clues for developing cures for everyone else.

Original Article by James Gallagher
Health and science reporter, BBC News

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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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