Monday, 26 November 2012

Embryo survival gene may fight range of diseases

HONG KONG (Reuters) - A gene that keeps embryos alive appears to control the immune system and determine how it fights chronic diseases like hepatitis and HIV, and autoimmune diseases like rheumatoid arthritis, scientists said on Monday.

Although the experts have only conducted studies on the gene Arih2 using mice, they hope it can be used as a target for drugs eventually to fight a spectrum of incurable diseases.

Lead author Marc Pellegrini at the Walter and Eliza Hall Institute of Medical Research in Australia said the gene appears to act like a switch, flipping the immune system on and off.

"If the gene is on, it dampens ... the immune response. And if you switch it off, it greatly enhances immune responses," Pellegrini said in a telephone interview.

"It is probably one of the few genes and pathways that is very targetable and could lead to a drug very quickly."
Arih2 was first identified by another group of scientists in the fruit fly but it drew the interest of Pellegrini's team because of its suspected links to the immune system.
In a paper published in Nature Immunology, Pellegrini and his team described how mice embryos died when the gene was removed.
Next, they removed the gene from adult mice and noticed how their immune systems were boosted for a short period of time. But it quickly went into an overdrive and started attacking the rodents' own healthy cells, skin and organs.

"The mice survived for six weeks quite well. Then they started developing this very hyperactive immune responses and if you leave it for too long, it starts reacting against the body itself," Pellegrini said.

Pellegrini and his colleagues hope that scientists can study the gene further and use it as a drug target to fight a large spectrum of diseases.

"It's like an accelerator. In infectious diseases, you want to slam on the brakes on this gene, and for autoimmune diseases, you want to push the accelerator to make it work much harder to stop the whole immune response," said Pellegrini.

"The more the gene works, the less of an immune response there is. And the less active the gene is, the more the immune response is."

Real Benjamin Buttons Brothers: Matthew and Michael Clark Are Aging Backwards

The Clark brothers (courtesy of Channel4)

By the looks of their home, Tony and Christine Clark are raising two rambunctious 7-year-old boys. Model train tracks and Monopoly pieces are scattered on tables and cartoons flicker on the TV set.

But the Clarks' two sons are grown men who share only the same interests and emotional fluctuations of little boys. Like the character portrayed by Brad Pitt in the 2008 film "The Curious Case of Benjamin Buttons," Matthew, 39, and Michael, 42, are aging backwards.

Diagnosed with a terminal form of leukodystrophy, one of a group of extremely rare genetic disorders that attack the Myelin, or white matter, in the nervous system, spinal cord, and brain. In the Clarks' case, the condition has not only eroded their physical capacities, but their emotional and mental states as well. Only six years ago, both brothers were holding down jobs and growing their families. Today, they spend their days in the care of their parents, both in their sixties, playing with Mr. Potato Head, fighting over Monopoly, and in rare lucid moments, struggling to understand why their lives have changed so dramatically.
&lt;/ifra e&gt;&lt;/div&gt;&lt;p class=&quot;legend&quot;&gt;&lt;b&gt;The 2008 fantasy movie is one of the few popular frames of reference for a very real and frightening disorder. &lt;/b&gt;&lt;/p&gt;

Before the Clark Brothers were diagnosed, they were living independent lives. Michael served in the Royal Air Force and later became a cabinet maker. Matthew worked in a factory and was raising a teenage daughter. Tony and Christine, meanwhile, had retired and moved from the UK to Spain. Then in 2007, both of their sons fell off the radar. They stopped returning their parents' calls and texts, and as the Clark brothers' conditions developed, their lives fell apart.

Should parents get their kids' genome sequenced?
Michael surfaced in a soup kitchen, and was referred to medical experts by social workers. After an MRI scan, he was diagnosed with the incurable degenerative disorder. Soon after Matthew received the same news. In the U.S. alone, about 1 in 40,000 children are born with a form of the neurodegenerative disease, according to Dr. William Kintner, President of the United Leukodystrophy Foundation. While some forms of the disorder are potentially treatable if discovered in the earliest stages and not all cause an emotional regression, the brothers are unlikely to be cured. "It's very difficult to do anything once progression has occurred," Dr. Kintner tells Yahoo! Shine.

With their train set.(Courtesy of Channel4)
As of April, when the Clarks were first written about in the British press, their mental age was 10.
"We will be out walking and things which might interest a toddler interest them, the other day we were walking home when Michael saw a balloon and pointed it out to us," father Tony Clark, told The Telegraph last spring.
Today, the brothers are even younger mentally.
"Just like small children, they wake up a lot during the night," mom Christine said in an interview published in The Independent this week. "I was up seven times with them last night."
After learning of their diagnoses, Tony and Christine returned to the UK and moved in with their sons. Their daily struggles as a family have been chronicled in a British documentary, "The Curious Case of the Clark Brothers," airing Monday in the UK.

Earlier this year, Matthew became a grandfather, when his daughter had a son. But the news for the family was bittersweet, as the Clark brothers' mental age continued to creep backwards.
"There's no return to them being cute little boys," said Christine, who regularly manages their tantrums and fights over Monopoly. "They're big strong men—and that presents a quite different set of problems."
More recently, even their physical strength began deteriorating.
"A few weeks ago, they could still manage with a knife and fork, but now that's getting too difficult for them—they get the food onto their forks, but somehow it all falls off before it reaches their mouths," she said.

Donors and genetic disorders: how much do you know?
Now walking is the next hurdle; Matthew is already confined to a wheelchair.

"The likelihood that they're on a terminal course is fairly certain, but who knows?" says Dr. Kintner, who is familiar with the Clark case but didn't meet the brothers. "If they were citizens of U.S., we'd try to get them to the National Institute of Health for diagnostic work, but in the UK the system is different. There is no comparable organization with genetic diseases, so it's a little more difficult there."

Dr. Kintner estimates there are several million cases of one of the estimated 40 types of leukodystrophies in the U.S., but an exact number is hard to pinpoint. The different forms of the disorder are still being identified and tests for each known type are still being developed. "It's going to take a long time," says Dr. Kintner. "I hope in my lifetime I see a cure for some of them."

A preview for the British documentary on the Clark Brothers airing on the UK's Channel 4.

Tuesday, 20 November 2012

New risk gene for Alzheimer's

CHICAGO (Reuters) - Two international teams of scientists have identified a rare mutation in a gene linked with inflammation that significantly increases the risk for the most common form of Alzheimer's disease, the first such discovery in at least a decade.

The findings, published on Wednesday in the New England Journal of Medicine, offer new insights into the underpinnings of Alzheimer's, a deadly, brain-wasting disease that robs people of their memories, their independence and their lives.

In separate studies, teams led by privately held deCode Genetics and John Hardy of University College London found that people with a mutation in a gene called TREM2 were four times as likely to have Alzheimer's as people who did not have the gene.

"It quadruples the risk of Alzheimer's," said Dr. Kari Stefansson of Reykjavik-based deCode in a telephone interview.

The level of risk compares with ApoE4, the best-known genetic cause of late-onset Alzheimer's, the form of the disease that occurs in older adults.

But this new gene variant is 10 times more rare than ApoE4, which is present in about 40 percent of people with late-onset Alzheimer's.

Rare or not, scientists say the discovery represents a big breakthrough for Alzheimer's research.
"This is one of the most common, most devastating illnesses in humans and we still don't have a very good understanding of what causes the disease," said Dr. Allan Levey, director of the Emory Alzheimer's Disease Center of Excellence in Atlanta, which helped confirm the deCode findings.
"In my mind, this is very important. It gives us another important clue as to one of the biological factors that contribute to causing the disease," he said.
Despite numerous costly attempts, drug companies have been stymied in their efforts to develop drugs that can alter the steady course of Alzheimer's, which affects more than 5 million Americans and costs the United States more than $170 billion annually to treat.
Current research efforts have focused on removing sticky clumps of a protein called beta amyloid that accumulate in the brains of people with Alzheimer's disease. But several drugs that have been developed to remove these proteins have failed to produce a significant improvement in patients with mild to moderate forms of dementia.
With the new finding, researchers say the focus will turn on the role of inflammation in Alzheimer's disease.
INFLAMMATORY RESPONSE
TREM2 is a gene that affects a protein expressed on the surface of cells in various tissues that "clean up garbage," Stefansson said. These cells, called microglia, are often associated with inflammatory response.
A genetic mutation that alters the function of these housekeeping cells could affect how well the brain deals with an excess of toxic proteins from beta amyloid, Stefansson and others said.
And that suggests that even though TREM2 is rare, the way it works in the brain may be important for brain health.
"It is certainly plausible that TREM2 is involved in all of Alzheimer's disease," said Andrew Singleton of the National Institute on Aging, who worked on the paper with Hardy and colleagues at University College London.
"I think it may be very generalizable," Singleton said.
For their study, Hardy and colleagues used a number of gene sequencing techniques to study 988 people with Alzheimer's disease and 1,004 healthy volunteers.
The team also tested brain tissues from deceased Alzheimer's patients, and they studied the expression of the TREM2 gene in genetically engineered mice.

For the deCODE study, researchers sequenced the genomes of 2,261 Icelanders and identified variations likely to affect protein function. Then, they looked specifically for these variants in people with Alzheimer's and those with healthy brains, and found those with the TREM2 variant had a significantly higher risk.

To make sure the gene was not specific to Iceland, they replicated their findings in populations at Emory University in the United States, as well as groups in Norway, the Netherlands and Germany.

"We've essentially found exactly the same thing," said Singleton of the NIA, which is part of the National Institutes of Health. "In a way which you don't often see in science, the two studies point in the same direction.
In July, a team at deCODE discovered a rare mutation in a gene called APP that protects against Alzheimer's.

"It is a complex disease," Stefansson said. "I'm not surprised to see there are many ways to bring about this deterioration in cognitive function."

Levey said while the TREM2 mutation is rare, it is likely changing the function of brain cells.

"It helps identify the microglial cells as an important possible (drug) target," he said.

Dr. Ralph Nixon, director of the New York University Center of Excellence on Brain Aging and a scientific adviser to the Alzheimer's Association, said the findings suggest there are likely many more genes that increase the risk of Alzheimer's disease.

"It's a good illustration that we need to intensify this type of research and identify what these genes are doing so we can finally translate it into therapy," he said.

Sunday, 18 November 2012

Nice structural biology games

harryndungurank #48845

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"Sea Turtle" Lab for New Players

Dear all, Since we are getting many new players from the recent Nova program, we decided to launch a new lab puzzle, "Sea Turtle" to guide them into EteRNA lab. The problem focuses on simple design problem - you have to design RNA sequence..

EteRNA dev chat log [11/14/2012]

Dear all, Here is a log of the dev chat session today. Thanks all for participating! EteRNA team Adrien Treuille: So players... before we get started with the player/dev chat meeting. [6:02 PM] mat747: what is the topic [6:02..

Eterna 2.0 launched - please report any problem/bug here!

Dear all, We are glad to announce that Eterna 2.0 has finally been launched. As many things have changed at once, there might be bugs/problems we did not notice. Please report them here, and we'll fix them as soon as possible. Currently..

"FMN Switch 2.0" Round 4 results published

Dear all, we are glad to announce that round 4 results of "FMN Switch 2.0" have been published. The rewards have been distributed as well. Click here to see the results in the game Unfortunately we had 5 failed sequences in this round as wel..

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For those interested in computational biology, you can play while you contribute to solving real scientific problems:

What's New

Vote for a short documentary on Foldit!

A short documentary on Foldit is a semi-finalist for the FOCUS FORWARD Filmmaker Competition! You can help it win the Audience Favorite award by voting for it online. The video is here, and the "VOTE" button is in the top-right of the video.
http://vimeo.com/focusforwardfilms/semifinalists/51888393
(Thu, 11/15/2012 - 16:24 | 1 comment)

Welcome new users

Tonight on PBS, scienceNOW aired an episode highlighting Foldit. This is bringing an influx of new users to our community. You may find the website and game client running slower. Please bear with us while the servers are under heavy load.
For the new players, go here (http://fold.it/portal/node/988864) to see how to download/install the game. Then Check out the FAQ (http://fold.it/portal/info/faq) and Wiki (http://foldit.wikia.com/) for more. If you are in the game, feel free to ask questions in the chat box.
Welcome to Foldit (=
NOTE: If you get stuck on the intro levels, check out the wiki for hints: http://foldit.wikia.com/wiki/Tutorial_Puzzles
(Thu, 11/15/2012 - 05:53 | 4 comments)

New Release

Hey everyone,
We've just pushed the changes that were in the developer preview into the main game. You can find a list of the new features and fixes below:
General
* The Disable and Remove Bands buttons now have new icons
* Windows Only: Added an option to allow GUI scripts to run while the client is minimized
- "update_while_minimized" : "1"
* Hovering over the undo graph will now show the score
LayerDesign
* This is a new feature that will be enabled in some design puzzles. It is intended to give you more feedback about which amino acids are appropriate at each segment. When a certain amino acid is disabled on a segment you will see the button grayed out in the mutate tool. Please see http://fold.it/portal/node/993855 for more info.
(Mon, 11/12/2012 - 23:38 | 0 comments)

Triple Scientist Chat transcript posted

The transcript from today's Scientist Chat about Symmetry has been posted:
http://fold.it/portal/node/993836
All previous chat transcripts can be found here:
http://fold.it/portal/chats
(Wed, 10/31/2012 - 22:34 | 0 comments)

Monday, 8 October 2012

Ordinary cells of the body can be reprogrammed into stem cells

Nobel prize to Briton, Japanese for stem cell work

STOCKHOLM (AP) — A British researcher and a Japanese scientist won the Nobel Prize in physiology or medicine on Monday for discovering that ordinary cells of the body can be reprogrammed into stem cells, which then can turn into any kind of tissue — a discovery that may led to new treatments.

Scientists want to build on the work by John Gurdon and Shinya Yamanaka to create replacement tissues for treating diseases like Parkinson's and diabetes, and for studying the roots of diseases in the laboratory — without the ethical dilemma posed by embryonic stem cells.

In announcing the 8 million kronor ($1.2 million) award, the Nobel committee at Stockholm's Karolinska Institute said the discovery has "revolutionized our understanding of how cells and organisms develop."

Gurdon showed in 1962 — the year Yamanaka was born — that the DNA from specialized cells of frogs, like skin or intestinal cells, could be used to generate new tadpoles. That showed the DNA still had its ability to drive the formation of all cells of the body.
At the time, the discovery had "no obvious therapeutic benefit at all," Gurdon told reporters in London.
"It was almost 50 years before the value — the potential value — of that basic scientific research comes to light," he said.
In 1997, the cloning of Dolly the sheep by other scientists showed that the same process Gurdon discovered in frogs would work in mammals.

More than 40 years after Gurdon's discovery, in 2006, Yamanaka showed that a surprisingly simple recipe could turn mature cells back into primitive cells, which in turn could be prodded into different kinds of mature cells.

Basically, the primitive cells were the equivalent of embryonic stem cells, which had been embroiled in controversy because to get human embryonic cells, human embryos had to be destroyed. Yamanaka's method provided a way to get such primitive cells without destroying embryos.
"The discoveries of Gurdon and Yamanaka have shown that specialized cells can turn back the developmental clock under certain circumstances," the committee said. "These discoveries have also provided new tools for scientists around the world and led to remarkable progress in many areas of medicine."
Just last week, Japanese scientists reported using Yamanaka's approach to turn skin cells from mice into eggs that produced baby mice.

Gurdon, 79, has served as a professor of cell biology at Cambridge University's Magdalene College and is currently at the Gurdon Institute in Cambridge, which he founded. Yamanaka, 50, worked at the Gladstone Institute in San Francisco and Nara Institute of Science and Technology in Japan. He is currently at Kyoto University and also affiliated with the Gladstone Institute. Yamanaka is the first Japanese scientist to win the Nobel medicine award since 1987.

Yamanaka told Japanese broadcaster NHK that he was at home doing chores on Monday when he got the call from Stockholm.
"Even though we have received this prize we have not really accomplished what we need to. I feel a deep sense of duty and responsibility," Yamanaka said.
Choosing Yamanaka as a Nobel winner just six years after his discovery was unusual. The Nobel committees typically reward research done more than a decade before, to make sure it has stood the test of time.
In 2010, the Nobel Prize in physics went to two researchers whose discoveries were also published six years earlier. In 2006, two American scientists won the medicine prize eight years after their work was published.
Prize committee member Juleen Zierath said Gurdon and Yamanaka's discoveries, which also earned them a Lasker award for basic research in 2009, could hold "immense potential," including in developing treatments for Parkinson's disease and in making cells that produce insulin. However, she added that therapeutic implications are still far away.
The idea of reprograming cells has also been put to work in basic research on disease, through an approach sometimes called "disease in a dish."

The reprogramming allows scientists to create particular kinds of tissue they want to study, like lung tissue for studying cystic fibrosis, or brain tissue for Huntington's disease. By reprogramming cells from patients with a particular disease, they can create new tissue with the same genetic background, and study it in the lab. That can give new insights into the roots of the problem.

In addition, that approach allows them to screen drugs in the lab for possible new medicines.

Experts welcomed the announcement, praising the duo for their groundbreaking and influential discoveries in a field riddled with ethical debates.

"Everyone who works on developmental biology and on the understanding of disease mechanisms will applaud these excellent and clear choices for the Nobel Prizes," said John Hardy, professor of Neuroscience at University College London. "Countless labs' work builds on the breakthroughs they have pioneered."

Yamanaka deserves extra credit for overcoming fierce objections to the creation of embryos for research, reviving the field, said Julian Savulescu, director of Oxford University's Uehiro Centre for Practical Ethics.

"Yamanaka has taken people's ethical concerns seriously about embryo research and modified the trajectory of research into a path that is acceptable for all," Savulescu said. "He deserves not only a Nobel Prize for Medicine, but a Nobel Prize for Ethics."

Goran Hansson, the secretary of the prize committee, said he had reached both winners by phone before the announcement. He said they were looking forward to coming to Stockholm to collect the award in a ceremony on Dec. 10, the anniversary of prize founder Alfred Nobel's death in 1896.
The medicine award was the first Nobel Prize to be announced this year. The physics award will be announced Tuesday, followed by chemistry on Wednesday, literature on Thursday and the Nobel Peace Prize on Friday.

The economics prize, which was not among the original awards, but was established by the Swedish central bank in 1968, will be announced on Oct. 15.

______

Associated Press science writer Malcolm Ritter in New York; AP writers Cassandra Vinograd and Raphael Satter in London; and AP writer Elaine Kurtenbach in Tokyo contributed to this report.

Wednesday, 4 July 2012

'God Particle' is key to universe is it

What is the Higgs boson and why is it important?

By Nick Thompson, CNN

July 4, 2012 -- Updated 0727 GMT (1527 HKT)

STORY HIGHLIGHTS

Scientists say they've found new evidence the Higgs boson exists
The so-called "God particle" is thought to be a building block of the universe
The theoretical particle is key to understanding how universe works, experts say

(CNN) -- Scientists say they are closer to proving the existence of the Higgs boson -- a never-before-seen subatomic particle long thought to be a fundamental building block of the universe.

Researchers at the Large Hadron Collider under the Alps are unveiling their latest results on the so-called "God particle" at an eagerly awaited seminar at the CERN particle physics laboratory in Geneva, Switzerland.

Experts say finding the elusive particle would rank as one of the top scientific achievements of the past 50 years.

What is the Higgs boson?

The Standard Model of particle physics lays out the basics of how elementary particles and forces interact in the universe. But the theory crucially fails to explain how particles actually get their mass.

Particles, or bits of matter, range in size and can be larger or smaller than atoms. Electrons, protons and neutrons, for instance, are the subatomic particles that make up an atom.

Scientists believe that the Higgs boson is the particle that gives all matter its mass.

Read more: The woman at the edge of physics

Experts know that elementary particles like quarks and electrons are the foundation upon which all matter in the universe is built. They believe the elusive Higgs boson gives the particles mass and fills in one of the key holes in modern physics.

Higgs boson is the last missing piece of our current understanding of the most fundamental nature of the universe.
Physicist Martin Archer

How does the Higgs boson work?

The Higgs boson is part of a theory first proposed by physicist Peter Higgs and others in the 1960s to explain how particles obtain mass.

The theory proposes that a so-called Higgs energy field exists everywhere in the universe. As particles zoom around in this field, they interact with and attract Higgs bosons, which cluster around the particles in varying numbers.

Imagine the universe like a party. Relatively unknown guests at the party can pass quickly through the room unnoticed; more popular guests will attract groups of people (the Higgs bosons) who will then slow their movement through the room.

The speed of particles moving through the Higgs field works much in the same way. Certain particles will attract larger clusters of Higgs bosons -- and the more Higgs bosons a particle attracts, the greater its mass will be.

Why is finding the Higgs boson so important?

While finding the Higgs boson won't tell us everything we need to know about how the universe works, it will fill in a huge hole in the Standard Model that has existed for more than 50 years, according to experts.

"The Higgs boson is the last missing piece of our current understanding of the most fundamental nature of the universe," Martin Archer, a physicist at Imperial College in London, told CNN.

"Only now with the LHC [Large Hadron Collider] are we able to really tick that box off and say 'This is how the universe works, or at least we think it does'."

"It's not the be all and end all -- but in terms of what can we say practically about the world and how the world is, it actually tells us a lot."

Gordon Kane, director of the Michigan Center for Theoretical Physics, added that finding evidence of the Higgs boson would be a "very wonderful success of science and of people for four centuries."

Why is the Higgs boson called the "God particle?"

The popular nickname for the elusive particle was created for the title of a book by Nobel Prize winning physicist Leon Lederman -- reportedly against his will, as Lederman has said he wanted to call it the "Goddamn Particle" because "nobody could find the thing."

"'God particle' is a nickname I don't really like," says Archer. "It's nothing to do with religion -- the only (theoretical) similarity is you're seeing something that's a field that's everywhere, in all spaces."

How are scientists searching for the Higgs boson?

For the past eighteen months scientists have searched for the Higgs boson by smashing protons together at high energy in the $10 billion Large Hadron Collider (LHC) at CERN in Geneva, Switzerland.

If we don't see [Higgs], it means the universe is more complicated than we thought.
Physicist Martin Archer

Inside the LHC, which is located 328 feet underground in a 17-mile tunnel and is the most powerful particle accelerator ever built, high speed proton collisions generate a range of even smaller particles that scientists sift through in search of a signal in the data suggesting the existence of the Higgs boson.

"You're just hoping that somewhere in these collisions that you see something ... some sort of a statistical bump," says Archer.

If Higgs bosons exist, they are elusive, popping up and then disappearing again quickly. It means, says Archer, that scientists at the LHC will only be able to observe their decaying remnants.

It has taken years for scientists to narrow down the range of mass in which they believed the Higgs boson could exist -- but during the past year a statistical bump suggests they're on the right track.

"Now they're starting to get a bump, the scientists should be able to get that result more and more," says Archer.

What if scientists don't find the Higgs boson?

The general consensus among physics academics is that the Higgs field and boson exists, according to Archer.

"It just makes sense within the framework that we've got everything set up in, given that everything else that we can describe and we can see seems to be described in this simple way," says Archer.

Nearly every scientist believes that the Large Hadron Collider will either prove or disprove the existence of the Higgs boson once and for all -- so if the LHC doesn't find it, it doesn't exist, experts say.

Martin Archer believes a failure to find the Higgs boson would be even more exciting than discovering the elusive particle.

"If we don't see it, it actually means that the universe at the most fundamental level is more complicated than we thought," says Archer, "and therefore maybe the way we've been attacking physics isn't right."

Thursday, 10 May 2012

Proteomics might be the magic bullet

Protein discovery could lead to new HIV drugs

January 27, 2012 in HIV & AIDS Protein discovery could lead to new HIV drugs

(Medical Xpress) -- A team of researchers at the Johns Hopkins Bloomberg School of Public Health recently discovered a new protein that enables HIV to destroy human cells. The finding provides scientists with a critical glimpse into the complex interactions between HIV proteins and human proteins, a discovery that could potentially lead to new HIV drug therapies. The study was published in the January 19, 2012 issue of Nature.

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HIV is a small but efficient pathogen that includes about 15 proteins which can act in various combinations with the more than 30,000 proteins in the human cell. APOBEC3G is a human protein that has the power to mutate HIV’s genome and prevent infection. However, an HIV protein called HIV-1 viral infectivity factor (Vif) typically associates itself with and degrades APOBEC3G before it can do its job.
Focusing on the interaction between Vif and APOBEC3G, researchers found that another protein called CBF-ß was a key factor needed in order for the degradation of APOBEC3G to take place.
“I’ve been working in this field for over 25 years and I am certain that there is still even more left to this story,” explained Xiao-Fang Yu, MD, DSc, professor in the Bloomberg School’s W. Harry Feinstone Department of Molecular Microbiology and Immunology and lead author of the study. “This is an exciting time to be in HIV research.”
“The identification of CBF-ß is only one piece of the puzzle, but it’s an important one,” said Sean L. Evans, a PhD candidate in the Department of Molecular Microbiology and Immunology and one author of the study. “The human protein APOBEC3G is designed to weaken HIV, and the virus has evolved a mechanism for defeating this anti-viral factor.”
There are currently more than 20 approved HIV antiviral therapies, some of which target protein interactions between the virus and humans. However, drug failure and the emergence of drug-resistant variants make it necessary to further this research and continually expand the number of HIV drugs available.
The next step, now that scientists have identified CBF-ß, will be to test various inhibitors and potential drug therapies to determine which ones disrupt the interaction between CBF-ß and Vif, and, therefore, which ones can prevent the degradation of APOBEC3G.
“Understanding these interactions is essential to the intelligent design of drugs that can fight HIV,” continued Evans. “If we can stop Vif from degrading APOBEC3G, HIV would be severely crippled.”
The study was completed in partnership with the First Hospital of Jilin University in China and was funded by the National Institutes of Health, the Chinese Ministry of Education and the Chinese Ministry of Science and Technology, as well as the Key Laboratory of Molecular Virology.
Provided by Johns Hopkins Bloomberg School of Public Health