Mice show pain via facial expressions, just like humans

London, May 10 (ANI): Just like humans, mice too express pain through facial expressions, revealed a new study by researchers from McGill University and the University of British Columbia.

McGill Psychology Prof. Jeffrey Mogil, UBC Psychology Prof. Kenneth Craig and their respective teams have discovered that when subjected to moderate pain stimuli, mice showed discomfort through facial expressions in the same way humans do.

The study also details the development of a Mouse Grimace Scale that could inform better treatments for humans and improve conditions for lab animals.

Because pain research relies heavily on rodent models, an accurate measurement of pain is paramount in understanding the most pervasive and important symptom of chronic pain, namely spontaneous pain, said Mogil.

“The Mouse Grimace Scale provides a measurement system that will both accelerate the development of new analgesics for humans, but also eliminate unnecessary suffering of laboratory mice in biomedical research. There are also serious implications for the improvement of veterinary care more generally,” Nature quoted Mogil as saying.

This is the first time researchers have successfully developed a scale to measure spontaneous responses in animals that resemble human responses to those same painful states.

For the study, the researchers analysed images of mice before and during moderate pain stimuli – for example, the injection of dilute inflammatory substances, as are commonly used around the world for testing pain sensitivity in rodents.

Researchers said that the level of pain studied could be comparable to a headache or the pain associated with an inflamed and swollen finger easily treated by common analgesics like Aspirin or Tylenol.

Then, the researchers sent the images to Craig”s lab at UBC, where facial pain coding experts used them to develop the scale.

They proposed that five facial features be scored: orbital tightening (eye closing), nose and cheek bulges and ear and whisker positions according to the severity of the stimulus.

Craig”s laboratory had previously established studying facial expression as the standard for assessing pain in human infants and others with verbal communication limitations.

This work is an example of successful “bedside-to-bench” translation, where a technique known to be relevant in our species is adapted for use in laboratory experiments.

Further research will investigate whether the scale works equally well in other species, whether analgesic drugs given to mice after surgical procedures work well at their commonly prescribed doses, and whether mice can respond to the facial pain cues of other mice.

The study has been published in the journal Nature Methods. (ANI)

Revolutionary capsule offers hope to diabetics

London, March 29 (ANI): A revolutionary technique that has been found to successfully treat the symptoms of gout could result in a new form of therapy for a range of other medical conditions – such as diabetes and obesity, say experts.

Gout is caused by a build up of uric acid in the bloodstream, which results in crystals of uric acid being deposited in the kidneys and joints, leading to bouts of extreme pain.

Professor Martin Fussenegger of the Swiss Federal Institute of Technology in Zurich designed a ‘molecular prosthesis’ to treat gout, which is made from human cells designed to detect an increase in levels of uric acid and to respond by secreting an enzyme called urate oxydase, which destroys uric acid.

The treatment consists of implanting a small plastic capsule under the skin, which is loaded with genetically engineered cells taken from the patients themselves.

The capsule effectively works as a synthetic organ balancing the body”s chemicals and hormones.

“We have constructed a synthetic genetic circuitry that can detect uric acid in the bloodstream and process this information to produce a therapeutic response,” the Independent quoted Fussenegger as saying.

Tests on laboratory mice have proved the efficacy of the new technique.

According to scientists, human clinical trials could begin in two years.

The researchers hope to adapt the technique so that the genetically engineered human cells living in the plastic capsules can be programmed to deal with a range of other metabolic disorders, such as the hormonal imbalances leading to diabetes and obesity.

The new research has been published in the journal Nature Biotechnology. (ANI)

Why eczema often leads to asthma

Washington, May 19 (ANI): Many young children who get a severe skin rash develop asthma later. Now, researchers from Washington University have shed light on what leads to progression from eczema, or atopic dermatitis, to breathing problems.

The doctors call this progression the atopic march.

In the new study, researchers have shown that a substance secreted by damaged skin circulates through the body and triggers asthmatic symptoms in allergen-exposed laboratory mice.

Early treatment of skin rash and inhibition of the trigger substance might block asthma development in young patients with eczema.

“Over the years, the clinical community has struggled to explain atopic march,” said study author Dr Raphael Kopan, professor of developmental biology and of dermatology.

“So when we found that the skin of mice with an eczema-like condition produced a substance previously implicated in asthma, we decided to investigate further.

“We found that the mice also suffered from asthma-like responses to inhaled allergens, implicating the substance, called TSLP, as the link between eczema and asthma,” he added.

The researchers found that cells in damaged skin can secrete TSLP (thymic stromal lymphopoietin), a compound capable of eliciting a powerful immune response.

And because the skin is so effective in secreting TSLP into the blood system, the substance travels throughout the body. When it reaches the lungs, it triggers the hypersensitivity characteristic of asthma.

“We are excited because we’ve narrowed down the problem of atopic march to one molecule,” said Kopan.

“We’ve shown that skin can act as a signalling organ and drive allergic inflammation in the lung by releasing TSLP. Now it will be important to address how to prevent defective skin from producing TSLP. If that can be done, the link between eczema and asthma could be broken,” he added.

The findings are published in Public Library of Science Biology. (ANI)

Common virus may cause high blood pressure

Washington, May 15 (ANI): A common virus affecting 60 to 99 percent of adults worldwide can be a major cause of high blood pressure, finds a new study.
The research team from Beth Israel Deaconess Medical Center (BIDMC) showed that when combined with other risk factors for heart disease, the cytomegalovirus (CMV), can lead to the development of atherosclerosis, or hardening of the arteries.

“CMV infects humans all over the world,” said co-senior author Dr Clyde Crumpacker, an investigator in the Division of Infectious Diseases at BIDMC and Professor of Medicine at Harvard Medical School.

“This new discovery may eventually provide doctors with a whole new approach to treating hypertension, with anti-viral therapies or vaccines becoming part of the prescription,” Crumpacker added.

CMV affects all age groups and is the source of congenital infection, mononucleosis, and severe infection in transplant patients.

In the study using mouse models, the scientists examined four groups of laboratory mice.

Two groups of animals were fed a standard diet and two groups were fed a high cholesterol diet. After a period of four weeks, one standard diet mouse group and one high-cholesterol diet mouse group were infected with the CMV virus.

They found that CMV-infected mice had increased blood pressure compared with the uninfected group.

Moreover, 30 percent of the CMV-infected mice that were fed a high-cholesterol diet not only exhibited increased blood pressure, but also showed signs of having developed atherosclerosis.

“This strongly suggests that the CMV infection and the high-cholesterol diet might be working together to cause atherosclerosis,” said Crumpacker.

A second analysis found that infection of a mouse kidney cell line with murine CMV led to an increase in expression of the renin enzyme, which has been known to activate the renin-angiotensin system and lead to high blood pressure. (ANI)

‘Smart bomb’ drug delivery may boost effectiveness of prostate cancer imaging

Washington, Apr 22 (ANI): Researchers from Johns Hopkins University have identified a novel way to combine imaging with chemotherapy in a single agent for the treatment of prostate cancer.

According to lead researcher Dr John P. Sedelaar, a postdoctoral research fellow at Johns Hopkins University, conventional methods include multimodality MRI to examine the urological system for diagnosing prostate cancer.

However, this tool is mostly thought of as a prostate imaging method, rather than a prostate cancer imaging method.

“An increasing number of patients have minimal prostate cancer, and opt for either very focused treatment or the watchful waiting approach,” said Sedelaar.

“In this environment, the need for an accurate imaging tool is paramount,” he added.

The researchers have designed two imaging drugs: a PSMA and a PSA-activated pro-drug. These agents are therapeutic drugs that are modified by adding a tyrosine ring for imaging.

After administrating the drugs to laboratory mice, researchers noted a measureable reduction in prostate cancer cells.

“It’s like a smart bomb, to use a military analogy,” said Sedelaar.

“By retooling chemotherapy agents, we may be able to get more accurate treatment monitoring and follow-up,” he added.

The study showed that the imaging pro-drugs were cleaved and activated by PSMA or PSA, suggesting their viability as a prostate cancer imaging modality.

The study was presented at American Association for Cancer Research 100th Annual Meeting 2009. (ANI)

Walnuts can help keep breast cancer at bay

Washington, Apr 22 (ANI): Walnuts contain compounds that reduce the risk of breast cancer, claims a new study.

Elaine Hardman, Ph.D., associate professor of medicine at Marshall University School of Medicine, said that while her study was done with laboratory animals rather than humans, people should heed the recommendation to eat more walnuts.

“Walnuts are better than cookies, french fries or potato chips when you need a snack,” said Hardman.

“We know that a healthy diet overall prevents all manner of chronic diseases,” the expert added.

To reach the conclusion, researchers studied mice that were fed a diet that they estimated was the human equivalent of two ounces of walnuts per day. A separate group of mice were fed a control diet.

Standard testing showed that walnut consumption significantly decreased breast tumor incidence, the number of glands with a tumor and tumor size.

“These laboratory mice typically have 100 percent tumor incidence at five months; walnut consumption delayed those tumors by at least three weeks,” said Hardman.

Molecular analysis showed that increased consumption of omega-3 fatty acids contributed to the decline in tumor incidence, but other parts of the walnut contributed as well.

“With dietary interventions you see multiple mechanisms when working with the whole food,” said Hardman.

“It is clear that walnuts contribute to a healthy diet that can reduce breast cancer,” the expert added.

The study has been presented at the American Association for Cancer Research 100th Annual Meeting 2009. (ANI)

Drug-combo could prevent pancreatic cancer recurrence

Washington, Apr 20 (ANI): In a study, led by an Indian-origin scientist, researchers have found a combination therapy, which could reduce cancer stem cells and stop the growth pancreatic cancer-one of the deadliest cancers.

Rajesh Kumar N.V., Ph.D., a faculty member at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, led the study.

He said that a combination therapy using tigatuzumab, a novel humanized death receptor-5 (DR-5) agonist antibody, along with gemcitabine, could result in reducing pancreatic cancer stem cells to achieve tumour remission and prevent tumour recurrence.

“Many advanced cancers, including pancreatic cancer, recur and result in patient death despite the use of chemotherapeutic and radiation modalities that initially lead to therapeutic responses,” said Kumar.

He added: “A growing body of evidence supports the concept that cancer stem cells are the seeds of the most clinically deadly form of therapy-resistant human cancers. Emerging studies show that cancer stem cells are indeed more resistant to therapy than other cancer cells and might be the reason why conventional chemotherapy, while reducing tumor size, does not result in long-term cures.”

For the study, the researchers examined the cancer stem cells in ten patient-derived tumours implanted in laboratory mice.

It was found that DR-5 is enriched in cancer stem cells compared to non-stem cell tumour populations.

The mice either received tigatuzumab alone; gemcitabine, the current clinical treatment for pancreatic cancer; or a combination of the two agents.

And it was discovered that treatment with gemcitabine alone reduced tumour size, but the tumour cells that remained were rich in pancreatic cancer stem cells. In nearly all cases, the tumours returned.

On the other hand, treatment with gemcitabine and tigatuzumab reduced pancreatic cancer stem cells, caused tumour remission, and significantly increased time-to-tumour progression in 50 percent of treated cases from a median of 54 days to 103 days.

The researchers claimed that targeting cancer-sustaining pancreatic cancer stem cells will be of paramount significance as there are few effective therapies for pancreatic cancer and most of the patients die within the first year of diagnosis.

“Clinically, this discovery could transform the way in which pancreatic cancer is treated and contribute towards making pancreatic cancer a more manageable disease,” said Kumar.

Results of the study will be presented at the American Association for Cancer Research 100th Annual Meeting 2009. (ANI)

Biphosphonates may prevent radiation-induced leukaemia

Washington, Apr 20 (ANI): A new study has revealed that treatment with biphosphonates could prevent radiation-induced leukaemia.

Lead researcher Dr Alexandra Miller, a senior scientist at the Armed Forces Radiobiology Research Institute, said that the study will not only help military and space agency personnel exposed to risky levels of radiation, it will also be beneficial for civilian populations.

“It is possible, although not yet proven, that the compound we studied could have a general effect on leukemia associated with causes other than radiation, such as age, which is much more common,” said Miller.

During the study, the research team studied biphosphonates known to scientists as ethane-1-hydroxy-1, 1-biphosphonate (EHBP) and carballylic amido bis phosphonic acid (CAPBP).

Biphosphonates have emerged as an attractive chemopreventive agent due to earlier research that suggests they prevent bone metastasis and because they have an ability to remove uranium from the body.

The researchers irradiated laboratory mice at 3.5 Gy and found that all of the mice who were not treated with either EHBP or CAPBP developed leukemia.

By contrast, if they were treated with six doses of EHBP only 75 percent of mice developed leukemia. Similarly, only 65 percent of mice treated with CAPBP developed leukemia.

The study was presented at the American Association for Cancer Research 100th Annual Meeting 2009. (ANI)

Biochemical changes that put sperm ‘in the mood’ identified

Washington, April 13 (ANI): Making a significant advance towards new infertility treatments and a male contraceptive pill, scientists at Rensselaer Polytechnic Institute have identified key biochemical changes that put sperm “in the mood” for fertilization.

Dr. Mark D. Platt, a researcher from the Department of Chemistry and Chemical Biology, notes that sperm cannot fertilize an egg immediately after entering the female reproductive tract.

He points out that sperm must acquire this ability after undergoing an activation process called “capacitation”.

He further highlights the fact that this process involves phosphorylation-common biological modification that causes cellular activities to be turned “on” by the addition of phosphate molecules to certain amino acids within proteins.

However, the specific biochemical details have been a deep mystery.

Platt and his colleagues used laboratory mice, and compared the extent of phosphorylation in both capacitated and non-capacitated sperm samples.

The researchers identified 44 peptides exhibiting differential phosphorylation, on 59 specific amino acids, suggesting that modification of those particular sites was essential for the capacitation process.

The relative ratio of phosphorylation between the capacitated and non-capacitated samples were also reported, providing the first biochemical description of what puts sperm “in the mood”.

The study appears in ACS’ Journal of Proteome Research, a monthly ublication. (ANI)

Study says marijuana chemical has anti-cancer properties

According to a study released on Thursday, Spanish researchers from the Complutense University in Madrid, together with scientists of other universities, found that tetrahydrocannabinol (THC) – the main chemical in the infamous narcotic agent, marijuana – likely helps the annihilation of brain cancer cells.

The research, which proposes to bring to improve the prospects of anti-cancer therapies, said that THC causes cancer cells to go through a process called autophagy – the breakdown that takes place when the cells fundamentally self-digest.

Based on the findings of the research, which was first carried out on the laboratory mice, and then substantiated on two patients – suffering from the highly aggressive and recurrent brain tumor, glioblastoma multiforme – in an experimental trial, the scientists came to the conclusion that THC and associated “cannabinoids” depicted properties of being “a new family of potential anti-tumoral agent.”

The study which has been published in the April edition of the US Journal of Clinical Investigation, on of the scientists, Guillermo Velasco, reported: “We found that the anti-tumoral action of THC is based on its ability to activate an intracellular signalling pathway that promotes the activation of a cellular process called `autophagy’. The activation of this pathway leads to cancer cell death.”

Scientists find new origin for a critical immune response

London, March 2 (ANI): Researchers at the Duke University Medical Center say that an immune system response, key to the first stages of fighting off viruses and harmful bacteria, has an entirely different origin than what has been thought to date.

“This finding will have important implications in vaccine science and autoimmune disease therapy development,” Nature magazine quoted said Dr. Michael Gunn, an immunologist and cardiologist at Duke, as saying.

It has been beliefved thus far that Type 1 helper (TH1) T cell immune responses, critical for the control of viruses and certain bacteria, are induced by rare immune cells, called dendritic cells.

Immunologists have generally believed that upon being activated by infection or vaccination, the dendritic cells move from peripheral tissues into lymph nodes to stimulate T cell responses.

However, the Duke researchers have discovered that the dendritic cells that stimulate TH1 responses do not come from peripheral tissues.

According to them, the dendritic cells rather arise from monocytes, a common cell type in the blood, which move directly into lymph nodes after infection.

“The result speaks to the most basic principles of immune response to pathogens. It may also explain the poor results we have seen in attempts to develop effective dendritic-cell vaccines,” Gunn said.

A previous study conducted by Gunn had led to the identification of a particular protein, known as a chemokine, that stimulates the migration of activated dendritic cells from peripheral tissues to lymph nodes.

In the current study, the researchers generated a TH1 response in laboratory mice that lacked this chemokine with influenza viruses.

“We really thought the mice would not be able to generate much of an immune response at all,” Gunn said, because they wouldn’t be able to mobilize dendritic cells.

“The mice, however, had increased TH1 responses. We knew we had to find what was really causing the response,” the researcher added.

Gunn’s team studied several different types of mice that were missing other chemokines or chemokine receptors, and found that the animals lacking the Ccr2 chemokine receptor-which controls the migration of inflammatory monocytes-had much lower accumulation of monocyte-derived dendritic cells and TH1 responses.

Based on their observations, the researchers came to the conclusion that there is a blood-derived lymph node dendritic cell type that has a key role in developing acute T-cell responses.

“For so long, dendritic cells from tissues were the obvious answer. We found out that that’s not always the case,” Gunn said.

The Duke researchers are now planning to study the blood-derived dendritic cells under different conditions, in order to determine whether they may have other activities.

“We observed the activity of these cells after TH1-inducing stimuli, like influenza. Next we’d like to study other types of immune stimuli to see how the cells respond,” Gunn said.

The researchers believes that understanding how dendritic cells stimulate different types of immune response might open the door to enhancing or inhibiting such responses, a major goal of immunologists trying to prevent infections or control autoimmune disease, Gunn said.

The study has been published in the journal Nature Immunology. (ANI)

Scientists find new origin for a critical immune response

London, March 2 (ANI): Researchers at the Duke University Medical Center say that an immune system response, key to the first stages of fighting off viruses and harmful bacteria, has an entirely different origin than what has been thought to date.

“This finding will have important implications in vaccine science and autoimmune disease therapy development,” Nature magazine quoted said Dr. Michael Gunn, an immunologist and cardiologist at Duke, as saying.

It has been beliefved thus far that Type 1 helper (TH1) T cell immune responses, critical for the control of viruses and certain bacteria, are induced by rare immune cells, called dendritic cells.

Immunologists have generally believed that upon being activated by infection or vaccination, the dendritic cells move from peripheral tissues into lymph nodes to stimulate T cell responses.

However, the Duke researchers have discovered that the dendritic cells that stimulate TH1 responses do not come from peripheral tissues.

According to them, the dendritic cells rather arise from monocytes, a common cell type in the blood, which move directly into lymph nodes after infection.

“The result speaks to the most basic principles of immune response to pathogens. It may also explain the poor results we have seen in attempts to develop effective dendritic-cell vaccines,” Gunn said.

A previous study conducted by Gunn had led to the identification of a particular protein, known as a chemokine, that stimulates the migration of activated dendritic cells from peripheral tissues to lymph nodes.

In the current study, the researchers generated a TH1 response in laboratory mice that lacked this chemokine with influenza viruses.

“We really thought the mice would not be able to generate much of an immune response at all,” Gunn said, because they wouldn’t be able to mobilize dendritic cells.

“The mice, however, had increased TH1 responses. We knew we had to find what was really causing the response,” the researcher added.

Gunn’s team studied several different types of mice that were missing other chemokines or chemokine receptors, and found that the animals lacking the Ccr2 chemokine receptor-which controls the migration of inflammatory monocytes-had much lower accumulation of monocyte-derived dendritic cells and TH1 responses.

Based on their observations, the researchers came to the conclusion that there is a blood-derived lymph node dendritic cell type that has a key role in developing acute T-cell responses.

“For so long, dendritic cells from tissues were the obvious answer. We found out that that’s not always the case,” Gunn said.

The Duke researchers are now planning to study the blood-derived dendritic cells under different conditions, in order to determine whether they may have other activities.

“We observed the activity of these cells after TH1-inducing stimuli, like influenza. Next we’d like to study other types of immune stimuli to see how the cells respond,” Gunn said.

The researchers believes that understanding how dendritic cells stimulate different types of immune response might open the door to enhancing or inhibiting such responses, a major goal of immunologists trying to prevent infections or control autoimmune disease, Gunn said.

The study has been published in the journal Nature Immunology. (ANI)

Mechanism that protects against development of Alzheimer’s identified

Washington, Feb 28 (ANI): Researchers from Johannes Gutenberg University Mainz have identified the mechanism that protects against the development of Alzheimer’s disease.

They found that the activity of the enzyme a-secretase is mainly responsible for the protective effect.

“In the past, we postulated that the enzyme a-secretase was involved in preventing the formation of cerebral plaques characteristic of Alzheimer’s disease and also enhanced cerebral functions, such as learning and memory,” said Professor Falk Fahrenholz of the Institute of Biochemistry.

“The a-secretase enzyme is a highly complex one, with many other functions. For example, it also relays signals from the intercellular space into cells and interacts with molecules on other cells,” he added.

In the study involving transgenic mice, the researchers found that is the enzymatic activity alone that guarantees the protective effects.

If this activity is neutralised, the laboratory mice exhibit the symptoms that are characteristic of Alzheimer’s disease: impaired learning ability, poor memory capacity and the build-up of plaques.

It is thus possible that the enzymatic activity of a-secretase could represent the starting point for the development of future treatments.

The researchers suggest that it is not the plaque build-up itself that is responsible for the loss of memory capacity.

Prof. Fahrenholz said, “It is important to consider other aspects in addition to the plaques themselves, particularly their precursors, which are a real cause of the disease.”

The study appears in the Journal of Alzheimer’s Disease (JAD). (ANI)

Vital clues to healing arthritis caused by traumatic injury found

Washington, Feb 23 (ANI): Researchers from Duke University Medical Centre have found certain vital clues to healing arthritis caused by traumatic injury.

They have identified a strain in laboratory mice that has “superhealing” powers, which can help resist inflammation after a knee injury, and avoid developing arthritis at the injury site in the long term.

“After a patient’s traumatic injury, orthopaedic surgeons realign the joint surface as anatomically as possible and then hope for the best,” said Dr Steven A. Olson, FACS, principal investigator of the post-traumatic arthritis project and chief of the Duke orthopaedic trauma section.

“They haven’t been thinking about why patients with injuries are subsequently getting arthritis.

“Our research examines how we could possibly prevent arthritis development with growth factors and anti-inflammatory therapies after a fracture, either before or at the time of the surgery to fix it,” he added.

The scientists examined the differences in inflammatory response between two types of mice: one type known as superhealers (or MRL/MpJ) versus a strain of control mice (C57BL/6).

Previous studies have shown that superhealer mice had such regenerative powers that holes made in their ears for lab identification purposes grew over completely with no sign of scar tissue.

“The superhealer can almost regenerate tissue,” said Bridgette Furman, research analyst and lead scientist of this study.

“We thought, ‘if they can regenerate cartilage in the ear, what about cartilage in the knee?’ This happened in our pilot study, and we now have taken these results further and learned what happens in terms of inflammation.

“If you can figure out why the animal is a superhealer and apply that to people, then you may help prevent the development of arthritis,” Furman added.

During the study, the control mice showed a greater than 700-fold increase in the expression of one cytokine, interleukin(IL-1ß) in the first four hours after a fracture and 37-fold difference in that cytokine level at 7 days after the fracture.

Cytokines are signalling molecules produced by cells in response to injury. Interleukin generally promotes inflammation and an increase in temperature.

The superhealer mice showed a similar trend, but in much lower amounts.

The team also studied the mice’s joint fluid and blood serum to measure actual levels of the cytokines. Overall, the control mice again showed significantly higher serum levels and synovial (joint) fluid levels of cytokines compared with the superhealers.

The study was presented at the Orthopaedic Research Society meeting. (ANI)

Undiagnosed chronic infection may make diarrhoea fatal

Washington, Feb 13 (ANI): MIT researchers have revealed that undiagnosed gastrointestinal infections might increase the severity of and delay recovery from acute diarrhoea.

They have found that the underlying, low-level undiagnosed infection may greatly add to the severity of a significant number of fatal diarrhoea cases.

“It seemed likely that persistent enteric infection with bacterial agents would also elicit immune responses that could have similar effects. However, this had not been previously studied,” said David Schauer, MIT Professor of Biological Engineering and Comparative Medicine.

“We wanted to provide proof of principle, and begin to define the mechanism for such an interaction,” he added.

During the study, the team used laboratory mice infected first with a strain of bacteria that causes a chronic condition but produces no symptoms, and then with a second infectious agent that causes acute diarrhoea.

They found that even though the underlying chronic infection did not cause disease on its own, it did make the acute infection much worse than in a control group that was only exposed to the second agent.

About 50 percent of the world population carries a chronic infection with Helicobacter pylori, which causes stomach-lining inflammation but usually no clinical symptoms.

In the case of diarrhoea this may play a significant role.

“It may be that an individual’s infection status with these or other agents is important in determining outcome of infection, immune-mediated disease or even immunization,” said Schauer.

The research has been published in the journal Infection and Immunity. (ANI)