Friday, September 27, 2013

HIV spread may be prevented with discovery of new gene

Scientists have discovered a new gene that may have the ability to prevent human immunodeficiency virus (HIV) from spreading once it enters the body, according to a study published in the journal Nature.
Researchers from King's College London in the UK say the gene, called MX2, could lead to new effective and less toxic treatment against HIV - the virus that causes acquired immunodeficiency syndrome (AIDS).
For the study, the researchers conducted experiments on human cells, in which they introduced the HIV virus to two different cell lines. One cell line had the MX2 gene "switched on," while the other cell line had no MX2 expression.
On observing the effects, the researchers found that in the cells in which the MX2 gene was expressed, the HIV virus was unable to replicate, therefore stopping new viruses from being produced.
In the cell line in which the MX2 gene was switched off, the HIV virus replicated and spread.
Professor Mike Malim of the Department of Infectious Disease at King's College London, says:
"This is an extremely exciting finding which advances our understanding of how HIV virus interacts with the immune system and opens up opportunities to develop new therapies to treat the disease.
Until now, we knew very little about the MX2 gene, but now we recognize both its potent anti-viral function and a key point of vulnerability in the life cycle of HIV."
HIV virus
Researchers say a gene called MX2 may prevent the HIV virus (pictured) from spreading once in the body.
Photo credit: King's College London
According to the Mayo Clinic, HIV patients are currently recommended to take a minimum of three different anti-HIV drugs in order to avoid creating a form of drug resistance.
However, many of these drugs can cause serious side effects, including abnormal heartbeats, shortness of breath, skin rash, weakened bones and even bone death.
"Although people with HIV are living longer, healthier lives with the virus thanks to current effective treatments, they can often be toxic for the body, and drug resistance can become an issue with long-term use," says Prof. Malim.
He notes that it is important to continue finding new ways of mobilizing the body's natural defense system, and the MX2 gene appears to play an important role in initiating viral control in HIV sufferers.
"Developing drugs to stimulate the body's natural inhibitors is a very important approach because you are triggering a natural process and therefore won't have the problem of drug resistance," he adds.
"There are two possible routes - it may be possible to develop either a molecule that mimics the role of MX2 or a drug which activates the gene's natural capabilities."
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New rapid test could distinguish viral infections

A new blood test shows promise as a rapid way to help doctors determine whether a respiratory infection is viral or bacterial and thus reduce inappropriate use of antibiotics, which only work against bacteria.
The study is published in the journal Science Translational Medicine.
Study co-author Geoffrey Ginsburg, a professor at Duke University School of Medicine, says:
"Current tests require knowledge of the pathogen to confirm infection, because they are strain-specific. But our test could be used right away when a new, unknown pathogen emerges."
He explains the new test would be especially useful for spotting new viruses before they spread into outbreaks.
For example, in the case of pandemic flu or MERS, the new coronavirus that has erupted in the Middle East, it would be very important to diagnose new cases quickly, much faster than current diagnostic tests.
The new test uses a different approach to traditional diagnostics: instead of testing the pathogen, it tests the immune response in the infected person.
Image of a virus
The new rapid test was able to detect viral infections with 90% accuracy by determining how strongly genes in immune cells and other blood cells were switched on.
Using an approach called "reverse transcription polymerase chain reaction (RT-PCR)," the test evaluates how strongly certain genes in immune cells and other cells in the blood are switched on.
Previous studies have shown these genes are more active in people with respiratory infections caused by viruses. They are not switched on in healthy people or those whose infection is caused by bacteria.
In their study, the team describes how they evaluated the test in a group of over 100 people and found it was able to identify, with nearly 90% accuracy, the ones with viral infections.
The group comprised patients (some with viral infection, the rest with bacterial infection) and healthy controls. The patients had attended a hospital emergency department complaining of fever.
The test positively identified viral infection in 89% of cases, and it correctly ruled out viral infection in 94% of cases.
The team concludes:
"These results show that RT-PCR-based detection of a host gene expression signature can classify individuals with respiratory viral infection and sets the stage for prospective evaluation of this diagnostic approach in a clinical setting."
Christopher W. Woods, co-author and an associate professor of medicine, pathology and global health at Duke and the Durham VA Medical Center, says bacterial resistance, which is largely driven by overuse of antibiotics, is a big global public health problem, causing infections that are increasingly difficult to manage:
"A tool that enables us to accurately identify viral infections could curb the indiscriminate use of antibiotics and reduce the development of resistant pathogens."
The US Centers for Disease Control and Prevention (CDC) says taking antibiotics for viral infections can do more harm than good, citing for instance, that where children are concerned, antibiotics are the most common cause of emergency department visits for adverse drug events in the US.
The team is now working to reduce the time it takes for the test to report results.
It currently takes 12 hours to analyze 30 genes, so Prof. Ginsburg says there is scope to reduce both the time and the number of genes.
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Antidepressants linked to higher risk of type 2 diabetes

A new systematic review of published studies suggests when prescribing antidepressant medication, clinicians should be extra aware that they are linked to raised risk for type 2 diabetes, although the study does not suggest the drugs are the direct cause.
Reporting their findings in the latest issue of Diabetes Care, researchers from the University of Southampton say use of antidepressants has risen sharply over recent years, and there are concerns they may have an adverse effect on glucose metabolism.
They note 46.7 million prescriptions for antidepressants were issued in 2011 in the UK.
Antidepressant use has also soared in the US, where a 2011 study found they are now the third most widely prescribed group of drugs.
Several studies have shown that antidepressant use is linked to diabetes, but the results have been varied, depending on the methods and numbers involved and also on the types of drugs themselves.
For instance, one study that found a link between antidepressants and risk for type 2 diabetes discovered the risk almost doubled in patients using two types of drugs at the same time: tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs).

Antidepressant users more likely to have type 2 diabetes

Researchers found a link between people who take antidepressants and type 2 diabetes, although it does not mean there is a direct causal effect.
For their systematic review, Southampton health psychologist Dr. Katharine Barnard and colleagues assessed 22 studies and three previous reviews that looked at the link between antidepressant use and risk for type 2 diabetes.
They found that overall, people on antidepressants were more likely to have type 2 diabetes.
Within that, however, the picture is somewhat "confused, with some antidepressants linked to worsening glucose control, particularly with higher doses and longer duration, others linked with improved control, and yet more with mixed results."
They note that although study quality was variable, the more recent, larger studies suggest a modest effect.
The researchers also propose that different types of antidepressants may be linked to different amounts of risk and call for long-term randomized, controlled trials to examine the effects of individual drugs.

Several 'plausible' explanations

While their review was not designed to investigate causes, the team says there could be several plausible explanations for the link. For instance, some antidepressants cause patients to put on weight, which in itself increases risk for type 2 diabetes.
But they also point out that some of the studies they reviewed found the raised risk for type 2 diabetes persisted when they took out the effect of weight gain, suggesting other factors could be involved.
Dr. Barnard says:
"Our research shows that when you take away all the classic risk factors of type 2 diabetes; weight gain, lifestyle etc, there is something about antidepressants that appears to be an independent risk factor."
She says that in light of rising prescriptions, "this potential increased risk is worrying," and:
"Heightened alertness to the possibility of diabetes in people taking antidepressants is necessary until further research is conducted."
Co-author Richard Holt, professor in Diabetes and Endocrinology at Southampton, adds:
"While depression is an important clinical problem and antidepressants are effective treatments for this debilitating condition, clinicians need to be aware of the potential risk of diabetes, particularly when using antidepressants in higher doses or for longer duration."
He says doctors prescribing antidepressants should be aware of this raised risk for diabetes and ensure they monitor patients for the condition, as well as take steps to reduce the risk by encouraging changes to lifestyle.
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Vitamin B may reduce risk of stroke

Researchers have uncovered evidence that suggests vitamin B supplements could help to reduce the risk of stroke, according to a study published in the journal Neurology.
Vitamin B supplements are said to be beneficial for many health issues, including stress, anxiety, depression, dementia, Alzheimer's disease and heart disease.
However, according to Xu Yuming of Zhengzhou University in Zhengzhou, China, previous studies have conflicting findings regarding the use of vitamin B supplements and stroke or heart attack.
"Some studies have even suggested that the supplements may increase the risk of these events," he adds.
In order to determine the role of vitamin B supplements in the risk of stroke, Prof. Yuming and colleagues analyzed 14 randomized clinical trials involving a total of 54,913 participants.
All studies compared use of vitamin B supplements with a placebo, or a very low dosage of the vitamin. All participants were then followed for a period of 6 months.
During this time, there were 2,471 reported strokes over all of the studies.
Results of the analysis revealed that the participants taking the vitamin B supplements had a 7% reduced risk of stroke, compared with those taking the placebo supplements or a low dosage of vitamin B.
However, the findings showed that taking vitamin B supplements did not reduce the severity of strokes or the risk of death.
The researchers found that a supplemental form of folate (vitamin B9) - a vitamin frequently found in fortified cereals - actually reduced the effect of vitamin B on the risk of stroke.
Additionally, the study showed that vitamin B12 did not have any effect on the risk of stroke.
The study authors explain that their "meta-analysis demonstrated that homocysteine-lowering therapy with B vitamin supplementation significantly reduced stroke events."
They continue:
We did not find significant benefit for reduction of stroke events in subgroup analyses according to intervention dose, reduction of homocysteine level, or baseline blood vitamin B12 concentration. Further analyses of B12 limited to folate-replete participants (with background of cereal folic acid fortification) also revealed no benefit."
However, the researchers note that the effect of vitamin B on stroke risk is dependent on many underlying aspects:
"Factors including the background of folate fortification of cereal products, follow-up time, status of absorption and response to B vitamin supplementation, the existence of chronic kidney disease (CKD) or high blood pressure (HBP), and baseline participant medication use can influence the effects of B vitamins supplementation."
According to the Centers for Disease Control and Prevention (CDC), stroke is the leading cause of death in the US, killing nearly 130,000 Americans every year.
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Universal flu vaccine closer after natural immunity study

UK scientists believe they have taken a significant step closer to a universal flu vaccine that would protect against all strains of seasonal flu and curb future pandemics.
The team, led by researchers at Imperial College London, reports the achievement in Nature Medicine.
Lead investigator Professor Ajit Lalvani, from the National Heart and Lung Institute at Imperial, says:
"New strains of flu are continuously emerging, some of which are deadly, and so the Holy Grail is to create a universal vaccine that would be effective against all strains of flu."

Flu virus always changing surface proteins

Current flu vaccines spur the immune system to make antibodies that recognize proteins on the surface of the virus. When these are spotted in an immunized person, the immune system mounts an attack against the virus.
The difficulty with this approach is that the flu virus is always changing its surface proteins, so different vaccines have to be developed every year as new strains emerge, leaving vaccine developers inevitably one step behind.
But the core of the flu virus is more stable and changes little as strains evolve, and researchers conducting lab experiments have suggested some immune cells may already protect against flu because they recognize unchanging proteins in the virus.
For instance, a group of US scientists recently took a step toward a universal flu vaccine with animal tests that suggested their vaccine caused the animals' immune system to make antibodies to those parts of the flu virus that do not change from strain to strain.

'Natural experiment'

However, this latest study is the first to use a "natural experiment" in a real human pandemic, the 2009 swine flu pandemic.
Prof. Lalvani describes it as a unique opportunity to find out whether the immune system could recognize and protect us against new strains for which we lack antibodies.
He and his colleagues asked 342 volunteers to donate blood samples and undergo nasal swabs just as the pandemic got under way. They then tracked the volunteers by sending them email questionnaires about their health and any symptoms over the next two flu seasons. If any volunteers had flu symptoms, they took a nasal swab and sent it to the lab.
The team found the volunteers who caught the flu but had either no symptoms or only mild symptoms were those whose blood samples at the start of the 2009 swine flu pandemic had more CD8 T cells, a type of immune cell that kills viruses. Those who fell severely ill had fewer of these cells.

'Blueprint' for vaccine - make more CD8 T cells

The researchers believe a vaccine that spurs the immune system to make more CD8 T cells could protect against serious disease from all flu viruses, including those that cross into human populations from birds and pigs.
Prof. Lalvani says the findings provide a "blueprint" for developing a universal flu vaccine:
"The immune system produces these CD8 T cells in response to usual seasonal flu. Unlike antibodies, they target the core of the virus, which doesn't change, even in new pandemic strains."
"We already know how to stimulate the immune system to make CD8 T cells by vaccination. Now that we know these T cells may protect, we can design a vaccine to prevent people getting symptoms and transmitting infection to others."
Such a vaccine could significantly limit seasonal flu and protect people against future pandemics, he adds.
It would be a different approach to conventional vaccines, which stimulate the immune system to develop antibodies in response to exposure to parts of a virus.
Researchers writing in PLOS Pathogens earlier this year, suggested a more effective route to a universal flu vaccine would be to combine T cell vaccines and antibody vaccines.
According to the World Health Organization (WHO), annual flu epidemics result in about three to five million cases of severe illness, and between one quarter and half a million deaths worldwide.
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Gene that triggers 'memory extinction' discovered

Many of us are the bearers of "bad" memories that, to this day, continue to affect our lives. Now, scientists say they have discovered a gene essential for "memory extinction," the process by which our brain replaces older memories with new experiences.
Researchers from the Massachusetts Institute of Technology (MIT) say the discovery could help people suffering from post-traumatic stress disorder (PTSD) by replacing "fearful" memories with more positive associations.
The gene, Tet1, has been found to play a critical role in memory extinction by controlling a small group of other genes that are necessary for the process.
For the study, published in the journal Neuron, the research team experimented on mice who had the Tet1 gene "knocked out," as well as on mice who had normal levels of the gene.
In order to measure the mice's ability to abolish memories, the mice were "conditioned" to fear a certain cage in which they received a small electric shock. Once the memory of the "cage shock" was formed, the mice were placed into the cage, but the researchers did not give them the shock.

Tet1 triggers 'memory extinction'

The researchers found that after a period of time, mice with normal Tet1 levels appeared to lose their fear of the cage, indicating that new memories replaced the old ones.
Li-Huei Tsai, director of MIT's Picower Institute for Learning and Memory, explains:
"What happens during memory extinction is not erasure of the original memory. The old trace of memory is telling the mice that this place is dangerous. But the new memory informs the mice that this place is actually safe. There are two choices of memory that are competing with each other."
However, the researchers add that the mice without the Tet1 gene remain fearful and are unable to extinguish the memory.
The team carried out another set of experiments that tested the mice's spatial memory.
These experiments showed that the mice without the Tet1 gene had the ability to learn to navigate a water maze, but they were unable to extinguish the memory of how to navigate the maze, further supporting the findings of the previous experiment.

Tet1 removes DNA methylation

The researchers explain that the Tet1 and other Tet proteins help to regulate the modifications of DNA that determine whether a certain gene will be expressed or not.
Tet1 alters the levels of DNA methylation - a modification that controls access to genes. High methylation levels prevent genes from being expressed, while low methylation levels allow them to be "switched on."
Tet1 and Tet proteins were found to remove DNA methylation, after the mice without Tet1 showed significantly lower levels of hydroxymethylation - the process leading to the removal of methylation - in both the hippocampus and cortex of the brain. These areas are key for learning and memory.

Demethylation higher in early memory genes

The researchers found that demethylation was most significant in a group of 200 genes, particularly a small subset referred to as "immediate early genes" - critical for memory formation.
In the mice without the Tet1 gene, it was found that immediate early genes were highly methylated, meaning it would be difficult for these genes to be expressed.
Previous research from MIT showed that an immediate early gene called Npas4 regulates other immediate early genes. In this study, the researchers found that in the promoter region of the Npas4 gene, methylation levels in mice without the Tet1 gene was almost 60%, compared with 8% in mice who had the Tet1 gene.
"It's a huge increase in methylation, and we think that is most likely to explain why Npas4 is so drastically downregulated in the Tet1 knockout mice," notes Prof. Tsai.
Matthew Lattai, associate professor of behavioral neuroscience at Oregon Health and Science University, who was not a part of the study, says the findings could pave the way for treatments for PTSD:
"By demonstrating some of the ways that regulatory genes are methylated in response to Tet1 knockout and behavioral experience, the authors have taken an important step in identifying potential pharmacological treatment targets for disorders such as PTSD and addiction."
Furthermore, the research team also discovered why mice without the Tet1 gene still have the ability to learn new tasks.
They found that during fear conditioning, the methylation of the Npas4 gene reduced to 20% - a level low enough for Npas4 to be expressed, therefore creating new memories.
The team hypothesize that the mice's fear is so strong that it may trigger other demethylation proteins, such as Tet2 or Tet3.
Overall, the researchers say that their findings suggest there is a threshold level needed in order for methylation to take place, and that Tet1 is responsible for maintaining low methylation to make sure that the genes needed for memory formation are ready to be "turned on" when needed.
Further research from the team will involve searching for ways to artificially increase Tet1 levels and seeing whether this could "boost" memory extinction. Additionally, they plan to determine the effects of erasing all Tet genes.
Meelad Dawlaty of MIT's Whitehead Institute, adds:
"This will not only help us further delineate epigenetic regulation of memory formation and extinction, but will also unravel other potential functions of Tets and methylation in the brain beyond memory extinction."
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Breast health linked to eating peanut butter and nuts

By eating more peanut butter during their high school years, girls could be improving their breast health in adulthood, according to a US study published recently in the journal Breast Cancer Research and Treatment.
Dr. Graham Colditz, of Washington University School of Medicine in St. Louis, and colleagues found that girls aged 9 to 15 who ate peanut butter and nuts twice a week were 39% less likely to develop benign breast disease by the age of 30 than girls who did not.
Benign breast disease includes lumps or tender spots that turn out to be fibrous tissue and/or cysts, as well as other conditions like hyperplasia, an overgrowth of the cells that line the ducts in the glandular breast tissue.
Although benign breast disease is not cancerous, it can raise the risk of developing breast cancer later in life.
Dr. Colditz, associate director for cancer prevention and control at the Alvin J. Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine, says:
"These findings suggest that peanut butter could help reduce the risk of breast cancer in women."
For their study, he and his colleagues looked at health data on over 9,000 American schoolgirls recruited to The Growing Up Today Study between 1996 and 2001. This included detailed information about food consumption as captured in food frequency questionnaires that the girls filled in on enrollment.
The data also included reports from the girls between 2005 and 2010, when they were 18 to 30 years old, that indicated whether they had ever been diagnosed with biopsy-confirmed benign breast disease.
When they compared the two sets of data, the researchers found that participants who had eaten peanut butter or nuts twice a week were 39% less likely than peers who never ate those foods to receive a diagnosis for benign breast disease.
The data suggest pulse foods - soy and other beans and lentils - and corn may also be linked to reduced risk of benign breast disease, but because they did not feature as much in the diets of these girls, the evidence was not so strong.
The researchers also note that:
"Girls with a family history of breast cancer had significantly lower risk if they consumed these foods or vegetable fat."
And they concluded that "consumption of vegetable protein, fat, peanut butter, or nuts by older girls may help reduce their risk of BBD [benign breast disease] as young women."
This is not the first study to tie diets rich in vegetable fats - such as those present in peanut butter, nuts and pulse foods - to a lower risk for benign breast disease. But it is the first to find the evidence by comparing data captured during adolescence with followed-up cases of diagnosed disease, as opposed to asking young women to recall what they ate when they were in high school.
Dr. Colditz says girls would do well to eat more peanut butter and nuts and consume less junk foods and sugary drinks, especially in view of the rise in obesity.
Funds from the Breast Cancer Research Foundation and the National Institutes of Health (NIH) helped finance the study.
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