Progress made toward universal flu vaccine

May 20, 2010 By Leave a Comment

Washington, May 20 (ANI): Scientists have come up with a novel influenza vaccine that could represent the next step towards a universal influenza vaccine eliminating the need for seasonal immunizations.

“Current influenza vaccines are effective against only a narrow range of influenza virus strains. It is for this reason that new vaccines must be generated and administered each year. We now report progress toward the goal of an influenza virus vaccine which would protect against multiple strains,” said study’s author Peter Palese, from Mt. Sinai School of Medicine.

The main reason the current seasonal vaccine is so strain-specific is that the antibodies it induces are targeted at the globular head of the hemaglutinin (HA) molecule on the surface of the influenza virus.

This globular head is highly variable and constantly changing from strain to strain.

In this study, the researchers constructed a vaccine using HA without its globular head. Mice immunized with the headless HA vaccine showed a broader, more robust immune response than mice immunized with full-length HA, and that immune response was enough to protect them against a lethal viral challenge.

“Our results suggest that the response induced by headless HA vaccines is sufficiently potent to warrant their further development toward a universal influenza virus vaccine. Through further development and testing, we predict that a single immunization with a headless HA vaccine will offer effective protection through several influenza epidemics,” said Palese.

The findings have been reported in the inaugural issue of mBio, the first online, open-access journal published by the American Society for Microbiology. (ANI)

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Genetic variants that increase infectious diseases risk identified

May 20, 2010 By Leave a Comment

Washington, May 20 (ANI): Scientists have identified new genetic variants that increase susceptibility to several infectious diseases including tuberculosis and malaria.

With greater understanding of the role of the gene implicated, researchers from the Wellcome Trust Centre for Human Genetics at the University of Oxford, Singapore”s Agency for Science, Technology and Research (A*STAR) and National University Health System (NUHS) hope that the findings could one day lead to better therapies and vaccines.

Environmental factors such as malnutrition and poor hygiene can account for a large proportion of an individual person”s susceptibility to infectious diseases, but it”s clear that this is not the whole story. Studies of twins and adopted persons indicate that genetics also plays a role.

The team analysed genes from over 8,000 people at clinical sites in Malawi, Kenya, Vietnam, Hong Kong and The Gambia, over a period of 5 years. In particular, they were looking for genetic variants that might contribute to susceptibility to tuberculosis, malaria and serious bacterial infections of the blood, or bacteraemia.

Their findings reveal a striking association with a gene called CISH and increased risk of susceptibility to these infectious diseases.

CISH encodes a protein that is involved in the immune response to infectious diseases. It plays a role in dampening down messaging signals between cells of the immune system.

A panel of five different genetic variants was identified within the CISH gene. Within the population studied, having just one of these variants increased susceptibility to disease by 18 percent compared with somebody who does not have any ”risk” variants.

One variant in particular accounted for most of the genetic association with disease. Functional studies carried out in Singapore showed that blood cells from healthy Chinese volunteers carrying that variant had lower levels of the CISH protein overall than individuals with the normal variant.

This suggests that CISH exerts a significant genetic influence on our immune response.

Dr Chiea C. Khor from A*STAR”s Singapore Institute for Clinical Sciences (SICS), who co-led the studies in Singapore, commented: “It”s not clear from our study why having a reduced level of CISH associates with increased susceptibility to multiple infectious diseases, but it does suggest that CISH is a key regulator of the immune system. We hope that our findings will encourage clinical research to better understand the immunological processes that are going on, with a view to identifying targets for therapeutic intervention and the development of better therapies and vaccines.” (ANI)

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Cheese boosts seniors” immune systems

May 14, 2010 By Leave a Comment

Washington, May 14 (ANI): Cheese can help preserve and enhance the immune system of the elderly by acting as a carrier for probiotic bacteria, say scientists in Finland.

The research, published in FEMS Immunology & Medical Microbiology, reveals that daily consumption of probiotic cheese helps to tackle age-related changes in the immune system.

“The increase in the proportion of aged individuals in modern society makes finding innovative ways to thwart the deterioration of the immune system a priority,” said lead author Dr Fandi Ibrahim from the University of Turku in Finland. “The intake of probiotic bacteria has been reported to enhance the immune response through other products and now we have discovered that cheese can be a carrier of the same bacteria.”

Dr Ibrahim”s team believes that the daily intake of probiotic cheese can tackle the age-related deterioration of the immune system known as immunosenescene.

This deterioration means the body is unable to kill tumour cells and reduces the immune response to vaccinations and infections. Infectious diseases, chronic inflammation disorders and cancer are hallmarks of Immunosenescene.

To tackle immunosenescene the team targeted the gastrointestinal tract, which is the main entry for bacteria cells into the body through food and drink and is also the site where 70 percent of vital immunoglobulin cells are created.

The team asked volunteers aged between 72 and 103, all of which lived in the same care home, to eat one slice of either placebo or probiotic Gouda cheese with their breakfast for four weeks. Blood tests where then carried out to discover the effect of probiotic bacteria contained within the cheese on the immune system.

The results revealed a clear enhancement of natural and acquired immunity through the activation of NK blood cells and an increase in phagocytic activity.

“The aim of our study was to see if specific probiotic bacteria in cheese would have immune enhancing effects on healthy older individuals in a nursing home setting,” concluded Ibrahim. “We have demonstrated that the regular intake of probiotic cheese can help to boost the immune system and that including it in a regular diet may help to improve an elderly person”s immune response to external challenges.” (ANI)

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Why some people with HIV develop AIDS and others don”t

May 6, 2010 By Leave a Comment

London, May 6 (ANI): Scientists are a step closer to understanding why some people with HIV develop full-blown AIDS, and others don”t.

Researchers in Massachusetts and California say that the answer lies in how the immune cells that recognize invaders are educated – a finding that may pave the way for new strategies for designing an HIV vaccine.

The human immune system detects foreign cells with the help of cell-surface proteins called human leukocyte antigens (HLAs). Each person”s cells carry a particular set of HLA molecules – the person”s HLA type – which bind fragments of virus or bacterial protein and ”present” them to T cells, the immune cells that recognize and attack infected cells.

But before T cells are ready to perform their killer function, they are in effect trained on fragments of the body”s own proteins – self-peptides – in an organ called the thymus.

To ”graduate” from the thymus, a T cell must be able to recognize at least one combination of HLA molecule and self-peptide, which provides the template for its subsequent immune response against a foreign peptide bound to that HLA molecule. T cells that bind to self-peptides very strongly, however, are rejected, as they would attack the body”s own cells.

Researchers began with two observations. First, HIV-infected people who manage to keep the virus in check – so-called ”elite controllers” – often carry a particular HLA gene variant, HLA B571. Second, people with this gene also have a higher risk of developing autoimmune diseases, in which the immune system does produce a harmful response against the body”s own proteins.

Arup Chakraborty, an immunologist at the Massachusetts Institute of Technology in Cambridge, and one of the lead authors of the study, thought the two observations might be related.

He had not previously studied HIV, but he had studied how T cells are selected in the thymus by their ability to recognize specific HLA molecules and the peptides bound to them. He surmised that the HLA molecules of elite controllers might be binding a relatively small number of self-peptides.

Indeed, a look through a database of the binding properties of HLA molecules revealed that HLA B57, along with HLA B27 – which also protects against HIV – binds a much smaller proportion of self-peptides than HLAs that are not protective. The researchers then used a computer algorithm to predict how this would affect T-cell maturation.

T cells that develop in people with the HLA B57 gene would be presented with a smaller variety of peptides in the thymus. Their model showed these cells have broader activity and would be likely to recognize HIV even if the virus mutates, allowing the immune system of elite controllers to keep the infection under control.

But that same property would also make them more likely to turn on the body”s own cells, explaining why HLA B57 leads to a higher risk of developing autoimmune diseases. “If you have a smaller diversity of self-peptides in the thymus,” says Chakraborty, “there”s a higher probability that T cells with a stronger reactivity and cross-reactivity” might be released.

Testing their model on data from 1,900 HIV-infected individuals with known HLA types, 1,100 of which were elite controllers, the researchers found that the progression of the disease was strongly correlated with the number of self-peptides an HLA molecule was able to bind.

The study has been published online in Nature. (ANI)

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1976 swine flu immunization might protect against pandemic H1N1 virus

April 24, 2010 By Leave a Comment

Washington, April 24 (ANI): A new American study has linked 1976 ”swine flu” shot to stronger immune response to 21st century pandemic flu.

Researchers at St. Jude Children”s Research Hospital found that individuals who reported receiving the 1976 vaccine mounted an enhanced immune response against both the 2009 pandemic H1N1 virus and a different H1N1 flu strain that circulated during the 2008-09 flu season.

Lead author Jonathan A. McCullers, an associate member of the St. Jude Infectious Diseases Department, said: “Our research shows that while immunity among those vaccinated in 1976 has waned somewhat, they mounted a much stronger immune response against the current pandemic H1N1 strain than others who did not receive the 1976 vaccine.”

McCullers said it is unclear if the response was enough to protect against the 2009 H1N1 virus, but the study points to a lingering benefit.

The findings also raise hope that those vaccinated against the 2009 H1N1 pandemic strain might also enjoy a similar long-term advantage.

The study is the first to focus on whether those vaccinated against the 1976 H1N1 strain made antibodies against the 2009 pandemic flu, including antibodies that could block the virus from infecting cells.

The study involved 116 St. Jude employees and spouses age 55 and older.

The group included 46 vaccinated in 1976 against the H1N1 flu virus, known as A/New Jersey/76, which sickened more than 200 military recruits in New Jersey.

That outbreak triggered fears of a flu pandemic and led to a massive government effort to quickly produce and distribute a vaccine.

The current study was conducted in August 2009 before a vaccine was available against the pandemic H1N1 flu strain and before the virus was circulating widely in the Memphis, Tenn., metropolitan area, where study volunteers lived.

Researchers reported that nearly 90 percent of volunteers made antibodies able to recognize a key protein on the surface of both the 2009 pandemic and the 2008-09 H1N1 flu strains.

Those antibodies were present in numbers large enough to meet one federal gauge of vaccine effectiveness.

Nineteen percent of volunteers also produced antibodies that neutralized the 2009 pandemic strain and blocked it from infecting cells.

In comparison, more than 67 percent of volunteers had antibodies that neutralized the 2008-09 seasonal H1N1 strain.

Those vaccinated in 1976 were more likely to make neutralizing antibodies against the new pandemic strain.

More than 17 percent of the 1976-vaccine group made such antibodies in large quantities.

Only about 4 percent of those who had not received the 1976 shot had comparable levels of antibody production.

The difference between the two groups was statistically significant, meaning it was unlikely chance alone explained the result.

The study has been published in the online issue of the journal Clinical Infectious Diseases. (ANI)

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Slowing down immune system”s ”brakes” could perk up HIV vaccines’ efficacy

March 26, 2010 By Leave a Comment

Washington, Mar 26 (ANI): Just like a frisky driver slams the break of a car, a special class of T cells may be limiting the effectiveness of therapeutic vaccines for HIV by slowing the immune system response too soon, according to researchers at University of Pittsburgh.

The study is the first to look at the role of regulatory T cells in therapeutic HIV vaccines and could help researchers to improve the efficacy of such vaccines by devising methods to circumvent the braking mechanism of these cells.

Regulatory T cells (Treg) are critical because they prevent the immune system from turning against itself by suppressing the immune response.

Without the braking action of Treg, autoimmune disease could flourish.

However, the researchers didn’t know what would happen if these cells start shutting down the immune response before a therapeutic vaccine has had a chance to bolster immunity against HIV.

Pitt researchers sought to answer this question as follow-up to a clinical trial of a therapeutic dendritic cell-based HIV vaccine they developed to activate the CD8, or killer T cell, response.

First reported in 2008, the findings indicated only limited success of the vaccine in the 17 patients enrolled in the trial.

In the current study, the researchers went back to the freezer, removed Treg from the patients” blood cell samples and found that it was masking a two-fold increase in immune response to HIV induced by the vaccine.

“When we removed Treg from blood cells, we found a much stronger immune response to the vaccine, giving us insight into how we can develop more effective HIV vaccines,” said Dr. Charles R. Rinaldo, Jr.

“Treg normally shuts down CD8 responses once the infection has been controlled, but in this case it appears to be putting on the brakes early and possibly limiting the vaccine”s ability to do its job effectively,” he added.

One theory is that HIV-infection drives up Treg, which in turn shuts down the HIV-1- specific CD8 T cell response, he said.

“We know how to treat HIV, but are still learning how to use immunotherapy strategies to completely flush it out of the body. Our findings show Treg plays an important role, but we need to figure out how to maintain the right balance by getting around these cells without blocking them completely,” added Dr. Bernard J.C. Macatangay.

The study has been published in the current issue of PLoS ONE. (ANI)

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Optimism good for body’s immune system

March 24, 2010 By Leave a Comment

Washington, Mar 24 (ANI): Optimism may be good for your health, say researchers, claiming that feeling better about the future might help you feel better for real.

In a new study, psychological scientists Suzanne Segerstrom of the University of Kentucky and Sandra Sephton of the University of Louisville studied how law students” expectations about the future affected their immune response.

Earlier studies found that people who are optimistic about their health tend to do better, but it”s not clear how optimism affects your health — or whether pessimism makes you less healthy.

For the study, the researchers recruited first-year law students by sending them a packet during the summer before classes started.

The 124 students that participated in the research were studied at five times over six months.

Each time, they answered questions about how optimistic they felt about law school.

Then they were injected with material that should summon an immune response and two days later, they came back to have the injection site measured.

A larger bump in the skin means a stronger immune response.

Immune systems are many-faceted— this test only measures the strength of the part that is responsible for fighting viral infections and some bacterial infections.

The students” general outlook on life — whether they had an optimistic disposition — didn”t account for the differences in immune responses between students.

But as each student”s expectations about law school waxed and waned, their immune response followed along.

At more optimistic times, they would have bigger immune responses, while at a more pessimistic time, a more sluggish immune response.

So, being optimistic about success in a specific, important domain may promote better immunity against some infections.

“I don”t think that I would advise people that they should revise their expectations to be unrealistic. But if people have slightly more positive views of the future than is actually true, that”s adaptive,” said Segerstrom.

The study has been published in Psychological Science, a journal of the Association for Psychological Science. (ANI)

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Optimism good for body’s immune system

March 24, 2010 By Leave a Comment

Washington, Mar 24 (ANI): Optimism may be good for your health, say researchers, claiming that feeling better about the future might help you feel better for real.

In a new study, psychological scientists Suzanne Segerstrom of the University of Kentucky and Sandra Sephton of the University of Louisville studied how law students” expectations about the future affected their immune response.

Earlier studies found that people who are optimistic about their health tend to do better, but it”s not clear how optimism affects your health — or whether pessimism makes you less healthy.

For the study, the researchers recruited first-year law students by sending them a packet during the summer before classes started.

The 124 students that participated in the research were studied at five times over six months.

Each time, they answered questions about how optimistic they felt about law school.

Then they were injected with material that should summon an immune response and two days later, they came back to have the injection site measured.

A larger bump in the skin means a stronger immune response.

Immune systems are many-faceted— this test only measures the strength of the part that is responsible for fighting viral infections and some bacterial infections.

The students” general outlook on life — whether they had an optimistic disposition — didn”t account for the differences in immune responses between students.

But as each student”s expectations about law school waxed and waned, their immune response followed along.

At more optimistic times, they would have bigger immune responses, while at a more pessimistic time, a more sluggish immune response.

So, being optimistic about success in a specific, important domain may promote better immunity against some infections.

“I don”t think that I would advise people that they should revise their expectations to be unrealistic. But if people have slightly more positive views of the future than is actually true, that”s adaptive,” said Segerstrom.

The study has been published in Psychological Science, a journal of the Association for Psychological Science. (ANI)

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Potential new target for treatment of colitis identified

March 19, 2010 By Leave a Comment

Washington, March 19 (ANI): Scientists have identified potential new target for treatment of colitis and other inflammatory bowel diseases.

They have found that a protein made by a gene already associated with a handful of human inflammatory immune diseases plays a pivotal role in protecting the intestinal tract from colitis.

St. Jude Children”s Research Hospital researchers led the study, which points to possible new strategies for combating colitis, a chronic inflammatory disease associated with colon damage, resulting in abdominal pain, bleeding and other symptoms.

Thirumala-Devi Kanneganti, assistant member of the St. Jude Department of Immunology and the paper”s senior author, said that the work also expands the link between the Nlrp3 protein and Crohn”s disease.

Researchers demonstrated that in a mouse model of colitis, Nlrp3 plays a pivotal role in keeping the intestinal tract intact, thus preventing further damage that occurs if intestinal bacteria leak into the body.

Nlrp3 works by anchoring a large, multi-protein complex known as the Nlrp3 inflammasome where the messenger protein interleukin 18 (IL-18) is made.

IL-18 belongs to a family of molecules known as cytokines, which shape the body”s immune response. In this study, researchers showed IL-18 produced by the Nlrp3 inflammasome helped mice maintain healthy colon by triggering production of more epithelial cells to compensate for those damaged or destroyed by colitis.

“This paper provides the basis for more effective, potentially disease-modifying approaches to treatment,” Kanneganti said.

The study appears in the March 18 online edition of the journal Immunity. (ANI)

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Potential new use for cancer treatment identified

March 16, 2010 By Leave a Comment

Washington, March 16 (ANI): A new study by researchers at the University of York has suggested that drugs increasingly used to treat cancer could have a major impact on a wide range of infectious diseases.

Anti-angiogenic drugs are used to try and prevent cancers from stimulating the growth of the blood vessels they need to survive and grow.

The new research has suggested that the same drugs could help in the treatment of other diseases including visceral leishmaniasis.

The findings showed that anti-angiogenic drugs can improve the structure of tissues where immune responses are generated and which are often destroyed by chronic infection or inflammation.

The resulting improvement in the immune response can increase the effectiveness of conventional treatments for leishmaniasis, allowing doctors to use lower doses of existing drugs that otherwise have harmful side effects.

“While our research has focused on leishmaniasis the findings could have implications for a range of globally important diseases,” Professor Paul Kaye, Director of the Centre for Immunology and Infection, said.

“It is particularly exciting that this potential has been discovered in a class of drugs that are already well-established in clinical practice.

“Our research also identifies ways that anti-angiogenic drugs might be used more effectively in the treatment of cancers,” he added.

The study has been published online by the Journal of Clinical Investigation (ANI)

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New hope in devil disease fight

March 11, 2010 By Leave a Comment

There is new hope in the fight against the disease wiping out the Tasmanian devil.

Researchers have found a colony of devils in the state’s north-west showing signs of immunity to the deadly facial tumour disease.

The disease has killed about 70 per cent of the state’s devils, spreading from the east coast to the west.

University of Sydney and Tasmanian research has found a group of devils living about 20 kilometres from Cradle Mountain are not catching the disease.

Lead researcher with the University of Sydney, Kathy Belov, says these devils have a different genetic make up to others and could be immune to the disease.

“We’re pretty excited because it means that potentially some of these animals might be able to recognise that the cancer is foreign and mount an immune response against it,” she said.

“This might mean that some animals might survive the cancer epidemic. Up until now we’ve thought the disease would wipe out all of the Tassie devils in Tasmania.”

The Program Manager with the Save the Devil team, Andrew Sharman, says while the research is important, the disease is unpredictable and constantly evolving.

The findings are being published in a research journal today.

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Vaccine for urinary tract infections comes closer to reality

September 19, 2009 By Leave a Comment

Washington, Sept 18 (ANI): A simple vaccine may soon be available to protect against urinary tract infections, thanks to researchers from University of Michigan.

The study conducted over mice showed that the vaccine prevented infection and produced key types of immunity.

It alerts the immune system to iron receptors on the surface of Escherichia coli bacteria that perform a critical function allowing infection to spread.

Administered in the nose, it induces an immune response in the body’s mucosa, a first line of defense against invading pathogens. The response, also produced in mucosal tissue in the urinary tract, should help the body fight infection where it starts.

The researchers used novel systematic approach, combining bioinformatics, genomics and proteomics, to look for key parts of the bacterium that could be used in a vaccine to elicit an effective immune response.

The team, led by Dr. Harry L.T. Mobley, screened 5,379 possible bacterial proteins and identified three strong candidates to use in a vaccine to prime the body to fight E. coli.

Mobley’s team is currently testing more strains of E. coli obtained from women treated at U-M.

If the robust immunity achieved in mice can be reproduced in humans, it could be the first ever vaccine for urinary tract infections.

Most of the strains produce the same iron-related proteins that can be vaccine targets, an encouraging sign that the vaccine could work against many urinary tract infections.

The findings are published in the open-access journal PLoS Pathogens. (ANI)

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2009 H1N1 influenza vaccines well tolerated, induce strong immune response in adults

September 12, 2009 By Leave a Comment

Washington, September 12 (ANI): Early results from various clinical trials of 2009 H1N1 influenza vaccines in healthy adults seem to be quite encouraging, say U.S. health experts.

The National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health in the U.S., has revealed that the early data from these trials suggest that 2009 H1N1 influenza vaccines are well tolerated, and induce a strong immune response in most healthy adults, when administered in a single unadjuvanted 15-microgram dose.

It has even congratulated the companies that have carried out these trials, which it claims are an important part of the ongoing worldwide effort to develop vaccines to protect the public from 2009 H1N1 influenza.

The National Institute of Allergy and Infectious Diseases is also conducting clinical trials of 2009 H1N1 influenza vaccines, produced by Sanofi Pasteur and CSL Limited.

The trials are testing two different dosages-15 micrograms versus 30 micrograms-and evaluating the immune response to one and two doses of these vaccines.

More than 2,800 people are said to be participating in the ongoing NIAID trials of these vaccines.

The institute says that preliminary analyses of early data from its trials align with the recently announced findings, and those to be announced imminently by other companies.

Additional data from the NIAID trials are forthcoming.

“However, on the basis of these strong early data, our results are consonant with other reports that a single 15-microgram dose of unadjuvanted 2009 H1N1 influenza vaccine is well tolerated and induces a robust immune response in healthy adults between the ages of 18 and 64. For adults aged 65 and older, the immune response to 2009 H1N1 influenza vaccine is somewhat less robust, as is the case with seasonal influenza vaccines,” the institute said in a press release.

“We note that the slight discrepancies seen in our trials between the Sanofi Pasteur and CSL Limited vaccines may be due to technical differences in the preliminary measurement of the amounts of antigen in the doses used in the clinical trial lots and the relatively limited numbers of samples studied to date, as well as the fact that our data are drawn from a very early time point after immunization,” the institute added. (ANI)

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Abnormal immune response to wheat linked to type 1 diabetes

August 21, 2009 By Leave a Comment

Washington, August 21 (ANI): An abnormal immune response to wheat proteins may be the cause of type 1 diabetes in about 50 per cent of its cases, according to a study.

Dr. Fraser Scott and his collaborators from the Ottawa Hospital Research Institute and the University of Ottawa tested 42 people with type 1 diabetes, and found that nearly half had an abnormal immune response to wheat proteins.

Type 1 diabetes is an autoimmune disease that occurs when the immune system mistakenly attacks the pancreas, the organ that regulates blood sugar.

Dr. Scott claims that his study is the first to show that immune cells called T cells from people with type 1 diabetes are also more likely to over-react to wheat.

His research has also shown that the over-reaction is linked to genes associated with type 1 diabetes.

“The immune system has to find the perfect balance to defend the body against foreign invaders without hurting itself or over-reacting to the environment and this can be particularly challenging in the gut, where there is an abundance of food and bacteria,” said Dr. Scott, a Senior Scientist at the Ottawa Hospital Research Institute and Professor of Medicine at the University of Ottawa.

“Our research suggests that people with certain genes may be more likely to develop an over-reaction to wheat and possibly other foods in the gut and this may tip the balance with the immune system and make the body more likely to develop other immune problems, such as type 1 diabetes,” he added.

In a commentary accompanying the study paper, diabetes expert Dr. Mikael Knip of Finland said: “These observations add to the accumulating concept that the gut is an active player in the diabetes disease process.”

In previous studies on animal models, Dr. Scott has already shown that a wheat-free diet can reduce the risk of developing diabetes.

He, however, stresses the need for more research to confirm the link, and determine possible effects of diet changes in humans.

His most recent findings have been published in the journal Diabetes. (ANI)

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Myth that fasting leads to longer life spans debunked

July 14, 2009 By Leave a Comment

Washington, July 14 (ANI): In a study on fruit flies, scientists have debunked the belief that fasting extends life spans in various organisms, including humans, when they suffer infection.

In their study, researchers at Stanford University School of Medicine wanted to see if reduced caloric intake also helps creatures cope with infection.

“Mounting a robust immune response is very energy-consuming. You might think an infected animal would be better off eating more, not less,” said Dr. David Schneider.

In the study on fruit flies, Schneider and his graduate student Janelle Ayres have shown that caloric restriction can indeed alter the flies’ response to infection, but in different directions depending on what they’ve been infected with.

The finding has potentially significant implications for humans, since flies are an excellent model system for studying certain aspects of our immune response.

In the study, the researchers measured the appetites of infected versus uninfected fruit flies, as well as the effects that restricting food intake in advance of an infection might have on flies’ response to the infection.

In an earlier research, Ayres had searched for mutant fruit flies that died faster, or more slowly, than normal flies after being infected with pathogenic bacteria.

One batch of mutant flies she identified were super-light eaters due to a faulty taste receptor.

These mutants were used for several of the experiments in the new study, and the researchers also repeated their experiments with normal flies that had been placed on caloric restriction for some time prior to being infected.

The observed results were the same in either case.

The investigators infected flies with three very different strains of bacteria, all of which can cause fatal disease in humans and then compared diet-restricted versus normally fed flies’ survival after infection.

Flies that had restricted caloric intake prior to infection with the pathogen, Enterococcus faecalis, ate no less than uninfected flies did. The “low-calorie flies” also survived for the same length of time as normal eaters.

When injected with S. typhimurium, flies on prior caloric restriction outlived normal eaters, surviving about 15 days post-infection versus eight days for the control flies.

Low-cal flies infected with L. monocytogenes, on the other hand, died faster than likewise infected normal eaters. They lived for only four days, as opposed to six or seven in the case of flies that had been on normal diets.

“There’s evidence that caloric restriction seems to rev up various individual components of the immune system. But in the few studies where diet-restricted animals actually have been infected experimentally, they fared poorly,” he said,

In their study’s conclusions, the authors write, “The work reported here should raise a cautionary flag, as it demonstrates that diet restriction can have complex effects on the realized immune response of a diet-restricted animal.”

The study has been published online in PLoS-Biology. (ANI)

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How TB bacteria remain latent in body for decades

July 10, 2009 By Leave a Comment

Washington, July 10 (ANI): Scientists from Memorial Sloan-Kettering Cancer Centre have identified a protein that helps TB bacteria resist immune response, and remain latent in the body for decades.

They hope that the new discovery may lead to new drugs to eliminate those strains of mycobacterium tuberculosis that have grown resistant to therapies currently available.

“Tuberculosis can resist the host immune system and remain latent for decades,” said Michael Glickman, of the Memorial Sloan-Kettering Cancer Centre.

“To do so, the mycobacterium responsible must resist an arsenal of DNA-damaging mutagens produced within the macrophage, the immune cell in which it lives.

“It’s incompletely understood how it can do that. We’ve identified one such mechanism,” he added.

According to the researchers, secret to TB’s success is a protein called CarD.

“The mycobacterium tailors its translational machinery in response to stress within the host and we have identified CarD as a critical mediator of this response” said Glickman.

The study showed that loss of CarD is fatal to M. tuberculosis living in cell culture.

CarD depletion leaves the pathogen sensitive to killing by oxidative stress, starvation, and DNA damage as it fails to cut its transcription of rRNA.

Glickman said that they were able to show in infected mice that the mycobacterium depends on CarD not just when it is in its early, most active phase of growth, but also later in the course of infection.

He added that drugs that target CarD’s interaction with RNA polymerase could, therefore, lead to sorely needed, new TB drugs.

The study has been published in the journal Cell, a Cell Press publication. (ANI)

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Inflammation may lead to Alzheimer’s disease

July 10, 2009 By Leave a Comment

Washington, July 9 (ANI): A new study has revealed that inflammation might lead to development of Alzheimer’s disease.

Two research studies published by William A. Banks has shown how inflammation triggers disease, and how can it be treated.

It is believed that the toxic levels of amyloid beta protein, the substance responsible for Alzheimer’s disease, accumulate in the brain because a pump that pushes it into the blood and past the blood-brain barrier malfunctions.

The blood-brain barrier is a system of cells that regulates the exchange of substances between the brain and the blood.

The blood-brain barrier transporter known as LRP is the pump that removes amyloid beta protein from the brain and into the bloodstream.”LRP malfunctions like a stop light stuck on red, and keeps amyloid beta protein trapped in the brain,” said Banks.

Inflammation, which is part of the body’s natural immune response, occurs when the body activates white blood cells, and produces chemicals to fight infection and invading foreign substances.

“We induced inflammation in mice and found that it turned off the LRP pump that lets amyloid beta protein exit the brain into the bloodstream,” Banks said.

“It also revved up an entrance pump that transports amyloid beta into the brain. Both of these actions would increase the amount of amyloid beta protein in the brain,” he added.

Banks said that treatment with drug indomethacin prevented inflammation from turning off the LRP (exit pump). (ANI)

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New knockout vaccine reverses rabies in mice after just one injection

July 7, 2009 By Leave a Comment

London, July 7 (ANI): A knockout vaccine for rabies that reverses the disease after just one injection may soon hit the market, thanks to promising findings on mice.

The team of American virologists and immunologists, who have engineered the new strain of the rabies virus, say that it induces a far more potent immune response than current vaccines.

They have revealed that in mice already infected with a virulent rabies strain, a single administration of the new vaccine was enough to clear the virus from the body, even after early symptoms had appeared.

The finding attains significance considering that conventional post-exposure rabies vaccines require several injections to produce an appropriate immune response.

Virologist Bernhard Dietzschold and his team at Thomas Jefferson University in Philadelphia, Pennsylvania, say that they wanted to make the new virus strain as safe as an inactivated virus, yet able to rouse the immune response to expunge the infecting virus as quickly as possible.

To make sure the viral strain they developed did not cause disease, they injected it directly into the brains of healthy, but very young, mice.

Pups as young as five days old did not show any signs of rabies.

“This means it’s a lot safer than other live attenuated vaccines that are out there,” Nature magazine quoted study co-author Craig Hooper, also at Thomas Jefferson, as saying.

Dietzschold and his co-workers then infected adult mice with a virulent strain of rabies virus, injecting the pathogen either into muscle or directly into the brain, and found that their new vaccine could prevent onset of the disease if it was administered within three days of exposure.

“(At present) for humans, we must initiate treatment within 20 hours. We showed we might be able to administer the vaccine later because we can clear the virus even after the onset of early symptoms,” he said.

The vaccine also showed its efficacy as a pre-exposure treatment, with mice given the vaccine up to three weeks before being infected with the virus avoiding developing rabies.

“If this proves as safe as we think it is, it could be contemplated as a vaccine where one shot may protect for life,” Hooper says.

Dietzschold hopes that further testing may reveal the vaccine’s potential for eradicating the disease in dogs, and provide a cheaper and easier alternative to current vaccines for humans. (ANI)

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HIV-1 destroys immune response in the gut within days of infection

July 7, 2009 By 1 Comment

Washington, July 7 (ANI): Researchers have found that HIV-1 virus moves rapidly in the body, and damages the B-cell antibody-producing system in the gut, within days of infection.

The study by Centre for HIV/AIDS Vaccine Immunology is the first to examine what happens to B cells in the gut in the earliest stage of HIV-1 infection.

“These new data show that damage to the antibody arm of the immune system begins quickly, within days. We know that by 80 days, half of the generative microenvironments for antibodies within the immune system in the gut are destroyed,” said Dr. Barton Haynes, senior author of the study.

The findings could solve one of the big mysteries in HIV-why the B cell, or antibody response, is so slow to arise in the first place and turns out to be so weak after it does, that it is unable to offer any kind of meaningful defence.

B cells that make antibodies against invading microbes are born in the bone marrow, but migrate out and mature in different locations throughout the body.

Some wind up in the intestine and settle in stretches of lymph node-like follicles called Payer’s patches, which are found at the bottom of the small intestine, where they wait to rise up against incoming bacteria, viruses, or other pathogens.

“Unfortunately, we found they are no match for HIV-1,” said Anthony Moody, a lead author of the study.

For the study, the researchers examined B cells in blood as early as 17 days after viral transmission, and in lymph tissue in the gut beginning at 47 days after transmission in 40 people infected with HIV-1.

They compared their findings with similar tissue from healthy controls, and found that even at the early stage, HIV-1 had already ravaged the gut’s B cell arm of the immune system.

The vast majority of the follicles in the Payer’s patches had been damaged.

“HIV-1 turns on the immune system, but turns it on in the wrong way. We found that it was churning out all sorts of B cells. Some appeared to be reactive against HIV-1, but others appeared reactive to things like influenza as well as self molecules,” said Moody.

Besides, it was found that by as early as 17 days after transmission, HIV-1 decreased the numbers of naive B cells – cells that may have had the potential to mature into potent infection-fighters.

The researchers are hoping that the findings may lead to a successful AIDS vaccine.

The study has been published in the open access journal PLoS Medicine. (ANI)

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New genes’ discovery confirms immune system may play a role in schizophrenia

July 2, 2009 By Leave a Comment

London, July 2 (ANI): An international study led by researchers at the University of California-Los Angeles and nearly 50 institutions worldwide has identified new genes that confirm that the immune system may play a role in the development of Schizophrenia.

The researchers say that they have also identified genetic anomalies that disrupt the cellular pathways involved in brain development, memory and cognition, all markers of schizophrenia.

Roel Ophoff, the co-lead author and an assistant professor at the Center for Neurobehavioral Genetics at the UCLA Semel Institute for Neuroscience and Human Behavior, has revealed that he and his collaborators performed a genome-wide scan of 2,663 people diagnosed with schizophrenia, and 13,498 controls from eight European locations.

He said that they were looking for single nucleotide polymorphisms (SNP), genetic variations that are commonly present in the general population but more often present in those suffering from the disorder.

In total, nearly 314,000 SNPs were included in the analysis, he added.

Ophoff said that their study revealed significant associations with genetic markers on the Major Histocompatibility Complex (MHC), a group of genes that controls several aspects of the immune response.

He further said that the team also found additional variations in two other genes, called NRGN and TCF4, pointing to perturbation of pathways involved in brain development, memory and cognition.

“This is another step forward in understanding the biological basis of this disorder, one that robs people of their lives,” Nature magazine quoted Ophoff, who holds a joint appointment at the University of Utrecht, The Netherlands, as saying.

“It also shows the importance of worldwide collaborations for the study of schizophrenia genetics, because it allows us to do very large numbers of scans,” he added.

Ophoff said that the findings were significant yet not without challenge since the study aimed at the “common variants” in the human genome.

“In other words, these are not rare mutations present in only a few individuals, but these genetic variants are abundantly present in the population. Anybody could carry this variant, but that doesn’t mean they will necessarily develop the disease. Yet, when you look at the population at large, these variants are more often present in patients than in healthy control subjects,” he said.

And that’s important in developing new techniques to thwart the disease, he reckons.

“Knowing these specific genes are involved in the pathway leading to schizophrenia provides unique clues as to which molecular mechanisms are involved,” he said.

While the association between schizophrenia and the immune system has long been suspected, the evidence for it has been mostly circumstantial to date.

And impaired cognitive and memory functions are increasingly being recognized as core features of schizophrenia, which are poorly addressed by current medications.

“The three common genetic variants we describe, then, which we feel predisposes certain individuals to schizophrenia, have the potential to be translated into targets for the development of new and novel medications,” Ophoff said. (ANI)

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