Tag Archives: cure

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

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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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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

WHEN WAS YOUR LAST HIV TEST?

If all the recent news about the importance of an early HIV diagnosis is persuading you to think about having a HIV test, you should know we offer offer a completely free and confidential rapid HIV test.  This means you will get your test results within a couple of minutes, and it’s a simple simple finger prick test.  (We don’t collect blood and send it off, we do it there with you)!

We use the Insti HIV test produced by BioLytical laboratories. The test is 99.96% accurate from 90 days after  contact for detecting HIV 1 and 2 antibodies.  We also have a mobile testing van which is often out in communities providing mobile rapid HIV tests. Appointments are not necessary, call us (0116 2559995) we’re here to help.

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Baby Cured of HIV – Here’s the real message..

caduceus-and-red

Late Sunday night, the world media started to report about a baby, born with HIV had been cured.  Everybody got talking; scientists, people of faith, doctors, the public, HIV experts, me, you!

It’s easy to get caught up in the excitement of a cure, I honestly didn’t think I’d be writing the phrase ‘HIV Cure’ for at least a few more years yet, but as it were, we were given a flurry of media reports about how this case was set to change the HIV treatment paradigm, prevent babies from being infected, and, to quote the principal author of the study, Dr Deborah Persaud, “transform our current treatment practices in newborns worldwide”.

There are reports that parents and guardians are asking if this means that children who are infected at birth can stop their drugs.  People are very over-optimistic, and have been calling their doctors and specialists raising the question of whether they, or their child could also be cured!

More Data Needed

We need to slow down, and get some perspective.  The news was only announced five days ago.

To quote a famous professor of HIV pharmacology: “We need more data.” We need to take stock, get the facts right, and allow for scrutiny of the case by the scientific community.

There are many questions to be asked of the case. For instance, was the baby truly infected in the first place? From reviewing the data presented at the conference, it certainly seems possible. But how established was this infection? Had it established itself in so-called long-lived memory T cells?

Furthermore, when was the actual point of infection? This is not clear. Could it have been just prior to delivery? If so, it is possible that by serendipity the doctors intervened with drugs just as the virus was trying to become established.

A Cure, or PEP?

It’s imperative, then, that we attempt to understand when exactly this baby was infected. Was it just before birth, or several months before birth? The longer the period of time, the more interesting the case becomes.

However, if the intervention simply aborted the establishment of infection then Dr Persaud’s results are less exciting.

If drugs were introduced very shortly after infection, the treatment may have actually acted as PEP (post-exposure prophylaxis) – a strategy already used by HIV doctors to try and avoid establishment of infection

Think of a fire which has just caught alight, but has yet really to take hold. Pouring a bucket of water on it at this point may kill the fire dead. Was there actually a flame, or the presence of detectable virus, in this case? Yes, of course. But this bucket of water may not have worked had you allowed the ‘fire’ to become properly established.

The case being described by many as a ‘cure’ may in fact be like this bucket of water – effective, but only because it was delivered so early.

Taking the fire analogy further, after we have put out the flames we may still see the residues it left behind. It might even reignite at a later point in time. The Mississippi baby has been off anti-retroviral drug treatment [ARVs] for less than a year – there are currently no flames, but we are waiting to see if the embers are truly burned out.

Currently, and beyond this headline case, we have no way to completely put out the fire of HIV once it has caught hold. Our current ARV treatments, then, are the firemen who keep the flames of HIV at bay. As long as they are there, you can begin to rebuild the house – a fact born out by the fact that hundreds of thousands of our patients have been on totally suppressive regimens for up to twenty years.

Currently, it is a truth that, if you stop therapy, the virus inevitably rebounds when you –cease medication usually within two weeks. Admittedly, there are a very few rare cases where the virus may simply smoulder away at very low levels for many years (so-called “post treatment controllers”).

All of these considerations and unanswered questions mean that we have a long way to go yet before we fully understand this case. We must fully explore the baby’s immune make-up. What about the characteristics of the mother’s virus, which was curiously low for someone not on treatment? There are so many questions before we should really call this a cure.

Other than the potential of Dr Persaud’s research to stimulate further investigations, then, what is the best thing that can come of all this media frenzy?

The great hope is that this moment represents the greatest mass HIV awareness campaign since the Don’t Die of Ignorance ‘tombstone’ campaign of the 1980s. Rarely does HIV make such headlines, and we have a real chance to educate people whilst their interest is piqued.

We must tell people that the story of HIV is very different now, and we must take this opportunity to communicate new messages through the media whose attention we currently have – messages which can correct people’s out-dated misconceptions.

  • Let’s talk about testing, and the importance of early diagnosis.
  • Let’s talk about effective drugs, which when prescribed early enough can help a patient live a long and full life.
  • Let’s talk about condoms and prevention.
  • Let’s tackle stigma!

Today there is no reason for any baby to be become HIV positive, if the mother is tested and diagnosed early in pregnancy – and if she and the baby have access to effective treatments which can prevent transmission. Sadly, 590,000 babies every year are still born HIV-positive in the developing world: an unnecessary tragedy.

We can do something about that right now, with the tools we have – If we increase testing and make it more regular and consistent. In the UK, 95% of women take the HIV tests during pregnancy. And with effective treatment the chance of the baby being born positive is less than 0.5%. We should be aiming for the same success all over the world

Above and beyond a media storm about a supposed ‘cure’, there are good news stories we can make happen today.

Is the ‘cure’ story exciting? Yes. Is it scientifically plausible? Yes. Will it stimulate more research? Almost certainly. But it is extremely premature to hail it as a cure that will translate into routine clinical care any time soon. We need much more data.

So if you or your child are HIV-positive, then please… don’t stop taking your tablets. And if you have had unprotected sex, take the test. Condoms, education, testing, and access to treatment are our real weapons against HIV, and we need to learn to use these correctly if we want to make a real impact today.

When was your last HIV test?

We offer offer a completely free and confidential rapid HIV test (results within 60 seconds from a simple finger prick test)!  We use the Insti HIV test produced by BioLytical laboratories. The test is 99.96% accurate from 90 days after  contact for detecting HIV 1 and 2 antibodies.  We also have a mobile testing van which is often out in communities providing mobile rapid HIV tests. Appointments are not necessary, call us (0116 2559995) we’re here to help.

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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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What Can We Do Now to Speed Up HIV Cure Research?

As most of you know, the case of Timothy Brown (aka The Berlin patient), a person who got cured of HIV and leukemia 5 years ago, has jolted a new energy and hope into the search for a HIV cure.  But most people with HIV, policymakers and potential funding sources are not fully aware of this case and what the new movement for a search for a cure are all about. So, Nelson Vergel, writer for The Body.com decided was to travel around the country to interview key players in advancing this field and make a short video that could serve as a catalyst for awareness and change.

This short video, done with a very low budget with the help of his activist friend Greg Fowler, is only part of a longer, more detailed documentary to be finished before World AIDS Day this year, the 30-year anniversary of the first AIDS cases.

Please watch it and forward it to your friends. Please follow the suggestions made in that video and become part of the cure! Everyone can do something now to raise awareness and funds not only for research but also for advocacy and education in this important new and expanding area.

Via TheBody.com

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