A new biomarker for chronic stress: Hair Cortisol

Main Category: Anxiety / Stress
Also Included In: Psychology / Psychiatry;  Biology / Biochemistry
Article Date: 20 Aug 2013 - 1:00 PDT Current ratings for:
A new biomarker for chronic stress: Hair Cortisol

Cortisol is a well-known stress hormone and until recently, we have only been able to understand how stressed a person has been for about the past 20 minutes or the past day. Now, with about 100 strands of hair clipped from the scalp, we can get a biological indicator of stress over the past three months. Since hair growth approximately 1 cm per month, with 3 cms, we capture cortisol retrospectively, so we can measure "chronic" or accumulated stress. In one of our first studies of chronic stress conducted on the University of Massachusetts, Boston campus, we included students, staff, and community members.

The present research was conducted to assess relationships between biological chronic stress as measured by CORT and perceived stress indices. Furthermore, this research examines potential differences in biological and perceived stress by racial/ethnic identity, SES, sex and age. We obtained domain-specific indices of stress (i.e. personal perceived stress, chaos in the home and neighborhood assessments) and examined associations between CORT, subjective stress and health indicators [blood pressure and waist-to-hip ratio (WHR)]. Finally, we also investigated the interactions of well-known factors associated with health disparities: racial/ethnic identity and SES with both hair CORT and the perceived stress indices as the dependent variables.

We found the highest cortisol levels in males, the group aged 18-22 (the entire sample was 18-66 yrs.), and those who identified as an ethnic minority. Critically, we also found perceived stress was positively related to hair cortisol. Specifically, when an individual was higher across several domains of stress (e.g., stress at home, stress in their neighborhood); this was associated with higher secretion of the stress hormone. One important interpretation of this is that perceiving something as stressful, whether happening or not, can be just as meaningful on our biological reactions to stress.

An unanticipated finding was that hair cortisol levels were higher for minorities in the higher socioeconomic status (SES). Much of the literature examining the SES/health gradient posits that better health is associated with higher objective and subjective status. However, there is related evidence that minority members may not always be conferred this benefit. One interpretation is that minorities in higher SES experience greater, albeit more subtle discrimination. Researchers suggest that in high SES, race becomes more salient, along with greater instances of misunderstanding cultural differences and awkwardness during interactions.

Interestingly, CORT was associated with only one of the other biomarkers of stress, higher systolic blood pressure. Waist and WHR were not significantly associated with CORT in these data. This was unexpected, since WHR is a well-known indicator of allostatic load and has been positively associated with CORT in other research (e.g.Manenschijn, et al., 2011). The relationship between CORT and health risk indicators needs further investigation. It is not yet known whether CORT will be consistently associated with chronic health issues and reliably predictive of chronic diseases associated with allostatic load.

Since hair grows approximately 1 cm per month, capturing 3 cms of hair (about 75-100 strands) can give us a retrospective window of stress levels for the past 3 months, rather than moments or days. Hair cortisol is a promising measure of cumulative or long term stress stress. And chronic stress is quickly becoming recognized as the mediator for multiple psychological and physical health outcomes.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our anxiety / stress section for the latest news on this subject.

This research was funded by an NIMHD P20 Center of Excellence (NIMHD 5P20MD002290-05).

(2013) Relationship between Hair Cortisol and Perceived Chronic Stress in a Diverse Sample. Article first published online in Wiley Online Library (wileyonlinelibrary.com) 6 DEC 2012, DOI: 10.1002/smi.2475

K. M. O'Brien, E. Z. Tronick & C. L. Moore

University of Massachusetts Boston

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

University of Massachusetts Boston. "A new biomarker for chronic stress: Hair Cortisol." Medical News Today. MediLexicon, Intl., 20 Aug. 2013. Web.
20 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'A new biomarker for chronic stress: Hair Cortisol'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Why some suffer and others are better able to cope with chronic stress

Main Category: Anxiety / Stress
Article Date: 19 Aug 2013 - 0:00 PDT Current ratings for:
Why some suffer and others are better able to cope with chronic stress

New research at Rutgers University may help shed light on how and why nervous system changes occur and what causes some people to suffer from life-threatening anxiety disorders while others are better able to cope.

Maureen Barr, a professor in the Department of Genetics, and a team of researchers, found that the architectural structure of the six sensory brain cells in the roundworm, responsible for receiving information, undergo major changes and become much more elaborate when the worm is put into a high stress environment.

Scientists have known for some time that changes in the tree-like dendrite structures that connect neurons in the human brain and enable our thought processes to work properly can occur under extreme stress, alter brain cell development and result in anxiety disorders like depression and Post Traumatic Stress Disorder affecting millions of Americans each year.

What scientists don't understand for sure, Barr says, is the cause behind these molecular changes in the brain.

"This type of research provides us necessary clues that ultimately could lead to the development of drugs to help those suffering with severe anxiety disorders," Barr says.

In the study published in Current Biology, scientists at Rutgers have identified six sensory nerve cells in the tiny, transparent roundworm, known as the C. elegans and an enzyme called KPC-1/furin which triggers a chemical reaction in humans that is needed for essential life functions like blood-clotting.

While the enzyme also appears to play a role in the growth of tumors and the activation of several types of virus and diseases in humans, in the roundworm the enzyme enables its simple neurons to morph into new elaborately branched shapes when placed under adverse conditions.

Normally, this one-millimeter long worm develops from an embryo through four larval stages before molting into a reproductive adult. Put it under stressful conditions of overcrowding, starvation and high temperature and the worm transforms into an alternative larval stage known as the dauer that becomes so stress-resistant it can survive almost anything - including the Space Shuttle Columbia disaster in 2003 of which they were the only living things to survive.

"These worms that normally have a short life cycle turn into super worms when they go into the dauer stage and can live for months, although they are no longer able to reproduce," Barr says.

What is so interesting to Barr is that when a perceived threat is over, these tiny creatures and their IL2 neurons transform back to a normal lifespan and reproductive state like nothing had ever happened. Under a microscope, the complicated looking tree-like connectors that receive information are pruned back and the worm appears as it did before the trauma occurred.

This type of neural reaction differs in humans who can suffer from extreme anxiety months or even years after the traumatic event even though they are no longer in a threatening situation.

The ultimate goal, Barr says, is to determine how and why the nervous system responds to stress. By identifying molecular pathways that regulate neuronal remodeling, scientists may apply this knowledge to develop future therapeutics.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our anxiety / stress section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

University, Rutgers. "Why some suffer and others are better able to cope with chronic stress." Medical News Today. MediLexicon, Intl., 19 Aug. 2013. Web.
19 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Why some suffer and others are better able to cope with chronic stress'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Study reveals target for drug development for temporomandibular joint disorder (TMJD) - a chronic jaw pain disorder

Main Category: Dentistry
Also Included In: Pain / Anesthetics
Article Date: 05 Aug 2013 - 1:00 PDT Current ratings for:
Study reveals target for drug development for temporomandibular joint disorder (TMJD) - a chronic jaw pain disorder

Temporomandibular joint disorder (TMJD) is the most common form of oral or facial pain, affecting over 10 million Americans. The chronic disorder can cause severe pain often associated with chewing or biting down, and lacks effective treatments.

In a study in mice, researchers at Duke Medicine identified a protein that is critical to TMJD pain, and could be a promising target for developing treatments for the disorder. Their findings are published in the August issue of the journal PAIN.

Aside from cases related to trauma, little is known about the root cause of TMJD. The researchers focused on TRPV4, an ion channel protein that allows calcium to rapidly enter cells, and its role in inflammation and pain associated with TMJD.

"TRPV4 is widely expressed in sensory neurons found in the trigeminal ganglion, which is responsible for all sensations of the head, face and their associated structures, such as teeth, the tongue and temporomandibular joint," said senior study author Wolfgang Liedtke, M.D., PhD, associate professor of neurology and neurobiology at Duke. "This pattern and the fact that TRPV4 has been found to be involved in response to mechanical stimulation made it a logical target to explore."

The researchers studied both normal mice and mice genetically engineered without the Trpv4 gene (which produces TRPV4 channel protein). They created inflammation in the temporomandibular joints of the mice, and then measured bite force exerted by the mice to assess jaw inflammation and pain, similar to how TMJD pain is gauged in human patients. Given that biting can be painful for those with TMJD, bite force lessens the more it hurts.

The mice without the Trpv4 gene had a smaller reduction in bite force - biting with almost full force - suggesting that they had less pain. In normal mice there was more TRPV4 expressed in trigeminal sensory neurons when inflammation was induced. The increase in TRPV4 corresponded with a greater reduction in bite force.

The researchers also administered a compound to normal mice that blocked TRPV4, and found that inhibiting TRPV4 also led to smaller reductions in bite force, similar to the effects of the mice engineered without the Trpv4 gene.

Surprisingly, the researchers found comparable bone erosion and inflammation in the jaw tissue across all mice, regardless whether the mice had TRPV4 or not.

"Remarkably, the damage is the same but not the pain," Liedtke said. "The mice that had the most TRPV4 appeared to have the most pain, but they all had similar evidence of temporomandibular joint inflammation and bone erosion in the jawbone as a consequence of the inflammation."

The results suggest that TRPV4 and its expression in trigeminal sensory neurons contribute to TMJD pain in mice. Given the lack of effective treatments for this chronic pain disorder, TRPV4 may be an attractive target for developing new therapies.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our dentistry section for the latest news on this subject.

In addition to Liedtke, Duke study authors include senior pain researcher Yong Chen, Ji Hee Hong, Suk Hee Lee, Puja K. Parekh and Carlene Moore of the Department of Neurology; Amy L. McNulty, Nicole E. Rothfusz and Farshid Guilak of the Department of Orthopaedic Surgery; Fan Wang of the Department of Cell Biology/Neurobiology; and Andrea B. Taylor of the Departments of Community and Family Medicine and Evolutionary Anthropology. Susan H. Williams of the Heritage College of Osteopathic Medicine at Ohio University and Robert W. Gereau IV of the Department of Anesthesiology at Washington University in St. Louis also contributed to this research.

The research was supported by the National Institutes of Health (DE018549, DE19440, DE19440S1, NS48602, AR048182 and DE018549-S); Duke Institute for Brain Sciences; Nicholas School of the Environment, Duke University; and Keimyung University School of Medicine in South Korea.

Duke University Medical Center

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Duke University Medical Center. "Study reveals target for drug development for temporomandibular joint disorder (TMJD) - a chronic jaw pain disorder." Medical News Today. MediLexicon, Intl., 5 Aug. 2013. Web.
5 Aug. 2013. APA
Duke University Medical Center. (2013, August 5). "Study reveals target for drug development for temporomandibular joint disorder (TMJD) - a chronic jaw pain disorder." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/264306.php.

Please note: If no author information is provided, the source is cited instead.

'Study reveals target for drug development for temporomandibular joint disorder (TMJD) - a chronic jaw pain disorder'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

Main Category: Arthritis / Rheumatology
Also Included In: Immune System / Vaccines;  Pediatrics / Children's Health;  Seniors / Aging
Article Date: 31 Jul 2013 - 1:00 PDT Current ratings for:
Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

The joints of children with the most common form of chronic inflammatory arthritis contain immune cells that resemble those of 90-year-olds, according to a new study led by researchers at Children's Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine. The findings, published in the August issue of Arthritis and Rheumatism, suggest that innovative treatment approaches could aim to prevent premature aging of immune cells.

Juvenile idiopathic arthritis, or JIA, is the most prevalent rheumatic condition in the world and affects one of every 1,000 children in the U.S., said senior researcher Abbe de Vallejo, Ph.D., associate professor of pediatrics and immunology, Pitt School of Medicine. It usually starts with a swollen ankle, knee or wrist that parents often assume is due to a minor injury sustained while playing.

"Untreated JIA has devastating consequences," Dr. de Vallejo said. "It can slow growth and, in extreme cases, the child can be physically disfigured. It's a degenerative disease that eats up the joints."

Doctors have long thought of JIA as an autoimmune disease, meaning the body attacks itself. But previous studies by Dr. de Vallejo of young adults with rheumatoid arthritis indicated that a certain population of cells present in the joint synovial fluid and blood displayed telltale signs of abnormal cell division and premature aging. His current team at Children's wanted to see if that was true in pediatric arthritis.

They examined immune cells called T-cells in the synovial fluid and blood from 98 children ages 1 to 17 and known to have JIA, as well as 46 blood samples from children who didn't have the disease. T-cells are the army of immune cells that eradicate infection, tumors and other dangerous agents to which people may be exposed.

The research team found about one-third of the T-cells of children with JIA had shortened telomeres and had reduced, or in some cases lost, the capacity to proliferate. Telomeres are the ends of chromosomes that don't code for proteins and, because they are not fully copied by enzyme mechanisms, are trimmed slightly during each DNA replication cycle. It is thought that aging occurs when the telomeres become too short for DNA replication and cell division to proceed normally.

"The T-cells of the children with JIA had very short telomeres, about the length we see in a 90-year-old or a young adult with rheumatoid arthritis. Those same T-cells express unusually high levels of several classic protein markers of cell aging and exhaustion," Dr. de Vallejo said. "These kids haven't lived long enough to have cells that look that old. This is the first indication that premature aging in occurring in this childhood condition."

In addition, the T-cells had become dysregulated, and their immune activity could be stimulated through atypical cell surface receptors. Much more must be learned about the unusual cells and about genetic mechanisms that might contribute to the development of JIA, Dr. de Vallejo said, but these findings could point the way to new therapies.

"JIA is typically treated with broad-spectrum drugs such as steroids and biologics that essentially paralyze the entire immune system, but only a third of the cells are affected and their abnormality seems to be premature aging, rather than autoimmune activity," he noted. "This study suggests cell-targeted treatments could be developed to prevent this premature immune aging."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our arthritis / rheumatology section for the latest news on this subject.

Co-authors of the paper include other researchers from Children’s Hospital of Pittsburgh of UPMC; Pitt School of Medicine; and the Mayo Clinic. The project was funded by the Nancy E. Taylor Foundation for Chronic Diseases, the Arthritis Foundation, and National Institutes of Health grant AR052282.

Children’s Hospital of Pittsburgh of UPMC & University of Pittsburgh Schools of the Health Sciences

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

University of Pittsburgh Medical Center. "Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says." Medical News Today. MediLexicon, Intl., 31 Jul. 2013. Web.
31 Jul. 2013. APA
University of Pittsburgh Medical Center. (2013, July 31). "Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/264123.php.

Please note: If no author information is provided, the source is cited instead.

'Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

Main Category: Arthritis / Rheumatology
Also Included In: Immune System / Vaccines;  Pediatrics / Children's Health;  Seniors / Aging
Article Date: 31 Jul 2013 - 1:00 PDT Current ratings for:
Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says

The joints of children with the most common form of chronic inflammatory arthritis contain immune cells that resemble those of 90-year-olds, according to a new study led by researchers at Children's Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine. The findings, published in the August issue of Arthritis and Rheumatism, suggest that innovative treatment approaches could aim to prevent premature aging of immune cells.

Juvenile idiopathic arthritis, or JIA, is the most prevalent rheumatic condition in the world and affects one of every 1,000 children in the U.S., said senior researcher Abbe de Vallejo, Ph.D., associate professor of pediatrics and immunology, Pitt School of Medicine. It usually starts with a swollen ankle, knee or wrist that parents often assume is due to a minor injury sustained while playing.

"Untreated JIA has devastating consequences," Dr. de Vallejo said. "It can slow growth and, in extreme cases, the child can be physically disfigured. It's a degenerative disease that eats up the joints."

Doctors have long thought of JIA as an autoimmune disease, meaning the body attacks itself. But previous studies by Dr. de Vallejo of young adults with rheumatoid arthritis indicated that a certain population of cells present in the joint synovial fluid and blood displayed telltale signs of abnormal cell division and premature aging. His current team at Children's wanted to see if that was true in pediatric arthritis.

They examined immune cells called T-cells in the synovial fluid and blood from 98 children ages 1 to 17 and known to have JIA, as well as 46 blood samples from children who didn't have the disease. T-cells are the army of immune cells that eradicate infection, tumors and other dangerous agents to which people may be exposed.

The research team found about one-third of the T-cells of children with JIA had shortened telomeres and had reduced, or in some cases lost, the capacity to proliferate. Telomeres are the ends of chromosomes that don't code for proteins and, because they are not fully copied by enzyme mechanisms, are trimmed slightly during each DNA replication cycle. It is thought that aging occurs when the telomeres become too short for DNA replication and cell division to proceed normally.

"The T-cells of the children with JIA had very short telomeres, about the length we see in a 90-year-old or a young adult with rheumatoid arthritis. Those same T-cells express unusually high levels of several classic protein markers of cell aging and exhaustion," Dr. de Vallejo said. "These kids haven't lived long enough to have cells that look that old. This is the first indication that premature aging in occurring in this childhood condition."

In addition, the T-cells had become dysregulated, and their immune activity could be stimulated through atypical cell surface receptors. Much more must be learned about the unusual cells and about genetic mechanisms that might contribute to the development of JIA, Dr. de Vallejo said, but these findings could point the way to new therapies.

"JIA is typically treated with broad-spectrum drugs such as steroids and biologics that essentially paralyze the entire immune system, but only a third of the cells are affected and their abnormality seems to be premature aging, rather than autoimmune activity," he noted. "This study suggests cell-targeted treatments could be developed to prevent this premature immune aging."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our arthritis / rheumatology section for the latest news on this subject.

Co-authors of the paper include other researchers from Children’s Hospital of Pittsburgh of UPMC; Pitt School of Medicine; and the Mayo Clinic. The project was funded by the Nancy E. Taylor Foundation for Chronic Diseases, the Arthritis Foundation, and National Institutes of Health grant AR052282.

Children’s Hospital of Pittsburgh of UPMC & University of Pittsburgh Schools of the Health Sciences

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

University of Pittsburgh Medical Center. "Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says." Medical News Today. MediLexicon, Intl., 31 Jul. 2013. Web.
31 Jul. 2013. APA
University of Pittsburgh Medical Center. (2013, July 31). "Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/264123.php.

Please note: If no author information is provided, the source is cited instead.

'Premature aging of immune cells present in joints of kids with chronic arthritis, Pitt/Children's Hospital team says'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Anti-herpesvirus drug treatment may benefit some chronic fatigue syndrome patients

Main Category: Infectious Diseases / Bacteria / Viruses
Article Date: 30 Jul 2013 - 0:00 PDT Current ratings for:
Anti-herpesvirus drug treatment may benefit some chronic fatigue syndrome patients

Many experts believe that chronic fatigue syndrome (CFS) has several root causes including some viruses. Now, lead scientists Shara Pantry, Maria Medveczky and Peter Medveczky of the University of South Florida's Morsani College of Medicine, along with the help of several collaborating scientists and clinicians, have published an article in the Journal of Medical Virology suggesting that a common virus, Human Herpesvirus 6 (HHV-6), is the possible cause of some CFS cases.

Over 95 percent of the population is infected with HHV-6 by age 3, but in those with normal immune systems the virus remains inactive. HHV-6 causes fever and rash (or roseola) in infants during early childhood, and is spread by saliva. In immunocompromised patients, it can reactivate to cause neurological dysfunction, encephalitis, pneumonia and organ failure.

"The good news reported in our study is that antiviral drugs improve the severe neurological symptoms, including chronic pain and long-term fatigue, suffered by a certain group of patients with CFS," said Medveczky, who is a professor of molecular medicine at USF Health and the study's principal investigator. "An estimated 15,000 to 20,000 patients with this CFS-like disease in the United States alone may ultimately benefit from the application of this research including antiviral drug therapy."

The link between HHV-6 infection and CFS is quite complex. After the first encounter, or "primary infection," all nine known human herpesviruses become silent, or "latent," but may reactivate and cause diseases upon immunosuppression or during aging. A previous study from the Medveczky laboratory showed that HHV-6 is unique among human herpesviruses; during latency, its DNA integrates into the structures at the end of chromosomes known as telomeres.

Furthermore, this integrated HHV-6 genome can be inherited from parent to child, a condition commonly referred to as "chromosomally integrated HHV-6," or CIHHV-6. By contrast, the "latent" genome of all other human herpesviruses converts to a circular form in the nucleus of the cell, not integrated into the chromosomes, and not inheritable by future generations.

Most studies suggest that around 0.8 percent of the U.S. and U.K. population is CIHHV6 positive, thus carrying a copy of HHV-6 in each cell. While most CIHHV-6 individuals appear healthy, they may be less able to defend themselves against other strains of HHV-6 that they might encounter. Medveczky reports that some of these individuals suffer from a CFS-like illness. In a cohort of CFS patients with serious neurological symptoms, the researchers found that the prevalence of CIHHV-6 was over 2 percent, or more than twice the level found in the general public. In light of this finding, the authors of the study suggest naming this sub-category of CFS "Inherited Human Herpesvirus 6 Syndrome," or IHS.

Medveczky's team discovered that untreated CIHHV-6 patients with CFS showed signs that the HHV-6 virus was actively replicating: determined by the presence of HHV-6 messenger RNA (mRNA), a substance produced only when the virus is active. The team followed these patients during treatment, and discovered that the HHV-6 mRNA disappeared by the sixth week of antiviral therapy with valganciclovir, a drug used to treat closely related cytomegalovirus (HHV-5). Of note, the group also found that short-term treatment regimens, even up to three weeks, had little or no impact on the HHV-6 mRNA level.

The investigators assumed that the integrated virus had become reactivated in these patients; however, to their surprise, they found that these IHS patients were infected by a second unrelated strain of HHV-6.

Further studies are needed to confirm that immune dysregulation, along with subsequent chronic persistence of the HHV-6 virus, is the root cause of the IHS patients' clinical symptoms, the researchers report.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject.

The USF-led study was supported by the HHV-6 Foundation and the National Institutes of Health.

Article citation: “Persistent human herpesvirus-6 infection in patients with an inherited form of the virus; ” Shara N. Pantry, Maria M. Medveczky, Jesse H. Arbuckle, Janos Luka,Jose G. Montoya, Jianhong Hu, Rolf Renne, Daniel Peterson, Joshua C. Pritchett, Dharam V. Ablashi, andPeter G. Medveczky; Journal of Medical Virology; published online July 25, 2013; DOI: 10.1002/jmv.23685

University of South Florida (USF Health)

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

University of South Florida (USF Health). "Anti-herpesvirus drug treatment may benefit some chronic fatigue syndrome patients." Medical News Today. MediLexicon, Intl., 30 Jul. 2013. Web.
30 Jul. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Anti-herpesvirus drug treatment may benefit some chronic fatigue syndrome patients'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here