Cold Sore Virus Linked with Memory Problems

Certain infections, including the one that causes cold sores, may increase the risk of thinking and memory problems in older adults, a new study suggests.

People in the study who'd suffered more viral and bacterial infections in the past, including infection with herpes simplex type 1 virus (HSV1), which causes cold sores, were at increased risk of scoring below average on a test of cognitive abilities, the researchers said.

The results held even after the researchers took into account factors that could affect people's test scores or brain function, such as age, education level, high blood pressure, diabetes and alcohol consumption.

The findings add to a growing body of evidence linking infections with cognitive function. For instance, previous studies have linked herpes infection with an increased risk of Alzheimer's disease in people with certain genetic mutations.

However, the new study found only an association, and cannot prove these infections were cause of cognitive impairment. It's possible other factors not accounted for by the study could explain the link, said study researcher Dr. Mira Katan of Columbia University Medical Center in New York City. Larger studies in different populations are needed to confirm the results, Katan, a neurologist, said.

Infections and cognitive impairment

Katan and colleagues previously found that past infections were linked with a higher risk of stroke.

The new study involved 1,625 adults around age 70 who lived in northern Manhattan.

Researchers tested participants' blood for evidence of previous infection withHSV1, herpes simplex type 2 (which causes genital herpes infections), cytomegalovirus (a common herpes virus), chlamydia pneumoniae (a respiratory infection that can cause pneumonia) and Helicobacter pylori (a bacteria found in the stomach). These particular infections have been linked with a higher risk of stroke. Those with a higher number of these infections were said to have a higher "infection burden."

They also took a test that measured their cognitive abilities, including attention, memory and language skills.

Participants with a higher infection burden were 25 percent more likely to score below average on the cognitive test.

The link was strongest among women, those with a low socioeconomic status, and those who with low levels of physical activity, the researchers said.

However, infection burden wasn't related to participants' risk of a decline in cognitive scores over time, the researchers said.

Inflammation risk

Infections increase levels of inflammation in the body, which contribute to cognitive impairment as well as stroke, Katan said.

Because exercise can reduce inflammation, it may counteract this risk, Katan said.

Dr. Nunzio Pomara, director of the geriatric psychiatry division at the Nathan S. Kline Institute for Psychiatric Research, in Orangeburg, N.Y., who was not involved in the study said he was "quite happy to see that, at least in some instances, there could be a potentially treatable [cause of] cognitive dysfunction," referring to the fact that infections can be treated or prevented.

However, Pomara said he hoped further studies would explore the link between infections and Alzheimer's disease. The current study did not find a link between infections and the risk of cognitive decline over time, which would be expected to occur in Alzheimer's disease patients, but it could be that participants were not followed for long enough to see a change in their cognition, Pomara said.  

Given the growing evidence for the link between infections and cognitive impairment, studies that attempt to prove the link are worthwhile, Dr. Timo Strandberg of the University of Helsinki in Finland, and Allison Aiello of the University of Michigan, wrote in an editorial accompanying the new study. A first step would be a study that randomly assigns people with Alzheimer's disease to receive an antiviral medication or not, and examines the effect on disease outcome, they said.

The study and editorial are published in tomorrow's (March 26) issue of the journal Neurology.

Pass it on: Past infections are linked with an increased risk of cognitive impairment.

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Use of certain antiviral drugs during pregnancy not linked with higher risk of major birth defects, study suggests

ScienceDaily (Aug. 31, 2010) — An analysis of data from Denmark finds no associated increased risk of major birth defects for mothers who were exposed during the first trimester of pregnancy to the antiviral drugs acyclovir, valacyclovir, and famciclovir, often used to treat herpes simplex and herpes zoster infections, according to a study in the August 25 issue of JAMA.

The prevalence of herpes simplex is high, and more than 1 percent of susceptible women acquire herpes simplex during the first trimester of pregnancy, with antiviral treatment indicated for a significant number of women in pregnancy. "Although the safety of acyclovir, valacyclovir, and famciclovir in general has been well established, data on the use of these antivirals in early pregnancy are limited," the authors write.

Bjorn Pasternak, M.D., Ph.D., and Anders Hviid, M.Sc., Dr.Med.Sci., of Statens Serum Institut, Copenhagen, Denmark, conducted a registry-based study to assess associations between acyclovir, valacyclovir, and famciclovir use in the first trimester of pregnancy and major birth defects. The study included 837,795 live-born infants in Denmark from January 1996 to September 2008. Participants had no diagnoses of chromosomal aberrations, genetic syndromes, birth defect syndromes with known causes, or congenital viral infections. Nationwide registries were used to ascertain individual-level information on dispensed antiviral drugs, birth defect diagnoses and potential confounders (factors that can influence outcomes).

Among 1,804 pregnancies exposed to acyclovir, valacyclovir, or famciclovir at any time in the first trimester, 40 infants (2.2 percent) had a diagnosis of a major birth defect, compared with 19,920 of 835,991 infants (2.4 percent) among the unexposed pregnancies. Adjusting for several variables, acyclovir, valacyclovir, or famciclovir exposure at any time in the first trimester was not associated with increased risk of major birth defects. First-trimester use of acyclovir, the most commonly prescribed antiviral, was not associated with major birth defects (32 cases among 1,561 exposed [2.0 percent] vs. 2.4 percent in the unexposed). Neither valacyclovir (7 of 229 infants [3.1 percent]) nor famciclovir (1 of 26 infants [3.8 percent]) were associated with major birth defects, although use of famciclovir was uncommon.

Additional analyses revealed no associations between antiviral drug exposure and 13 different subgroups of birth defects, but the number of exposed cases in each subgroup was small.

"Our study, to our knowledge the largest of its kind, found no significant association between first-trimester exposure to antiherpetic antiviral drugs and major birth defects. Consequently, it has immediate clinical implications and may support informed decisions on safety when prescribing antivirals for herpes infections in early pregnancy. Acyclovir is the most extensively documented antiviral and should therefore be the drug of choice in early pregnancy, while data on valacyclovir and famciclovir are still insufficient. Future research on antiherpetic antivirals and mother-child health should include safety studies with regard to spontaneous abortion and preterm birth, and during breastfeeding," the authors conclude.

Editorial: Acyclovir Exposure and Birth Defects -- An Important Advance, But More Are Needed

In an accompanying editorial, James L. Mills, M.D., M.S., and Tonia C. Carter, Ph.D., of the National Institutes of Health, Bethesda, Md., comment on the findings of this study.

"The study by Pasternak and Hviid is helpful in demonstrating the safety of acyclovir in pregnancy, but additional strategies must be developed to resolve the remaining issues. At a time when the health care system in the United States is facing enormous financial challenges, it is important not to ignore any sources of data that could answer critical medical questions."

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Journal Reference:

Björn Pasternak, MD, PhD; Anders Hviid, MSc, DrMedSci. Use of Acyclovir, Valacyclovir, and Famciclovir in the First Trimester of Pregnancy and the Risk of Birth Defects. JAMA, 2010;304(8):859-866 DOI: 10.1001/jama.2010.1206

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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Specific gene linked to cold sore susceptibility, study finds

ScienceDaily (Oct. 28, 2011) — Investigators have identified a human chromosome containing a specific gene associated with susceptibility to herpes simplex labialis (HSL), the common cold sore. Published in The Journal of Infectious Diseases and now available online, the study looks at how several genes may affect the severity of symptoms and frequency of this common infection. The findings, if confirmed, could have implications for the development of new drugs to treat outbreaks.

HSL outbreaks, or cold sores, are skin infections that appear with the reactivation of herpes simplex virus, a virus that infects 70 percent of the U.S. population. Cold sore outbreaks vary in frequency and severity; some people may experience symptoms rarely, only once every 5 to 10 years, while others may experience them once a month or even more frequently. In addition to investigating environmental activating factors (e.g., sunlight) that may play a role in outbreaks, researchers for some time have been looking at the possible role of genetic factors in virus susceptibility and activation.

This study, led by John D. Kriesel, MD, and colleagues from the University of Utah School of Medicine in Salt Lake City and the University of Massachusetts Medical School in Worcester, follows previous studies identifying a region of chromosome 21 as a base for genes possibly linked to cold sore outbreaks. To identify which of six possible genes in this region were associated with the frequency of outbreaks, this latest study used single nucleotide polymorphism genotyping in genome-wide, family-based linkage studies of 618 people from 43 large families. The investigators found a positive link between the frequency of outbreaks, hereditability, and the presence of a specific gene, C21orf91, on chromosome 21.

"While these findings await confirmation in a larger, unrelated population," the study authors note, "these findings could have important implications for the development of new drugs that affect determinants of the cold sore phenotype."

In an accompanying editorial, Anthony L. Cunningham, MD, and David Booth, MD, of the Centre for Virus Research and the Institute of Immunology and Allergy Research at Westmead Millennium Institute and the University of Sydney in Australia, note that if the findings regarding the C21orf91 gene are confirmed, additional research may then begin to determine possible therapeutic applications and whether the same gene also plays a role in recurring genital herpes.

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The above story is reprinted from materials provided by Infectious Diseases Society of America.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal References:

J. D. Kriesel, B. B. Jones, N. Matsunami, M. K. Patel, C. A. St. Pierre, E. A. Kurt-Jones, R. W. Finberg, M. Leppert, M. R. Hobbs. C21orf91 Genotypes Correlate With Herpes Simplex Labialis (Cold Sore) Frequency: Description of a Cold Sore Susceptibility Gene. Journal of Infectious Diseases, 2011; 204 (11): 1654 DOI: 10.1093/infdis/jir633A. L. Cunningham, D. Booth. The First Common Cold Sore Susceptibility Gene. Journal of Infectious Diseases, 2011; 204 (11): 1645 DOI: 10.1093/infdis/jir635

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Herpes linked to Alzheimer's disease: 'Cold sores' connected to cognitive decline

ScienceDaily (Apr. 4, 2011) — Laboratories at the University of New Mexico (UNM), Brown University, and House Ear Institute (HEI) have developed a new technique to observe herpes simplex virus type 1 (HSV1) infections growing inside cells. HSV1, the cause of the common cold sore, persists in a latent form inside nerve cells. Re-activation and growth of HSV1 infections contribute to cognitive decline associated with Alzheimer's disease.

Details are published in the March 31 issue of PLoS ONE.

"Herpes infects mucous membranes, such as the lip or eye, and generates viral particles," submits study Principal Investigator Elaine Bearer, M.D., Ph.D., Harvey Family Professor and Vice Chair for Research, Department of Pathology, UNM School of Medicine. "These viral particles burst out of the cells of the mucous membrane and enter sensory nerve cells where they travel inside the nerve toward the brain. We now can see this cellular transportation system and watch how the newly formed virus engages cellular APP on its journey out of the cell."

Tagging herpes virus inside cells with green fluorescent protein, scientists used live confocal imaging to watch HSV1 particles emerge from infected cells. Newly produced viral particles exit the cell nucleus and then bud into cellular membranes containing amyloid precursor protein (APP). Electron microscopy at HEI detailed the ultrastructural relationship between HSV1 particles and APP.

This dance between viral particles and cellular APP results in changes in cellular architecture and the distribution of APP, the major component of senile plaques found in the brains of Alzheimer's disease patients. Results from this study indicate that most intracellular HSV1 particles undergo frequent, dynamic interplay with APP, which facilitates viral transport while interfering with normal APP transport and distribution. This dynamic interaction reveals a mechanism by which HSV1 infection leads to Alzheimer's disease.

In developed countries such as the U.S., approximately 20 percent of children are infected with HSV1 prior to the age of five. By the second and third decades of life, as much as 60 percent of the population is infected, and late-in-life infection rate reaches 85 percent.

Symptoms of primary HSV1 infection include painful blisters of the mouth, lips or eyes. After infection, HSV1 persists in nerve cells by becoming latent. Upon re-awakening, new viral particles are made in the neuron and then travel back out its pathways to re-infect the mucous membrane. Many infected people experience sporadic episodes of viral outbreaks as the well-known recurrent cold sore.

"Clinicians have seen a link between HSV1 infection and Alzheimer's disease in patients, so we wanted to investigate what might be going on in the body that would account for this," adds Dr. Shi-Bin Cheng, post-doctoral associate, Department of Pathology and Laboratory Medicine, Alpert Medical School, Brown University. "What we were able to see in the lab strongly suggests a causal link between HSV1 and Alzheimer's Disease."

"It's no longer a matter of determining whether HSV1 is involved in cognitive decline, but rather how significant this involvement is," Bearer asserts. "We'll need to investigate anti-viral drugs used for acute herpes treatment to determine their ability to slow or prevent cognitive decline."

Researchers recommend people treat a cold sore as quickly as possible to minimize the amount of time the virus is actively traveling through a person's nervous system. The faster a cold sore is treated, the faster the HSV1 returns to a dormant stage.

Additional Authors include: Paulette Ferland, senior research assistant, UNM; Paul Webster, House Ear Institute, Los Angeles, CA; participation of Kathleen Kilpatrck, UNM; and many undergraduate students at Brown who contributed to this project are acknowledged.

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Story Source:

The above story is reprinted from materials provided by Brown University, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Shi-Bin Cheng, Paulette Ferland, Paul Webster, Elaine L. Bearer. Herpes Simplex Virus Dances with Amyloid Precursor Protein while Exiting the Cell. PLoS ONE, 2011; 6 (3): e17966 DOI: 10.1371/journal.pone.0017966

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Gene is first linked to herpes-related cold sores

ScienceDaily (Nov. 29, 2011) — A team of researchers from the University of Utah and the University of Massachusetts has identified the first gene associated with frequent herpes-related cold sores.

The findings were published in the Dec. 1, 2011, issue of the Journal of Infectious Diseases.

Herpes simplex labialis (HSL) is an infection caused by herpes simplex virus type 1 (HSV-1) that affects more than 70 percent of the U.S. population. Once HSV-1 has infected the body, it is never removed by the immune system. Instead, it is transported to nerve cell bodies, where it lies dormant until it is reactivated. The most common visible symptom of HSV-1 reactivation is a cold sore on or around the mouth. Although a majority people are infected by HSV-1, the frequency of cold sore outbreaks is extremely variable and the causes of reactivation are uncertain.

"Researchers believe that three factors contribute to HSV-1 reactivation -- the virus itself, exposure to environmental factors, and genetic susceptibility," says John D. Kriesel, M.D., research associate professor of infectious diseases at the University of Utah School of Medicine and first author on the study. "The goal of our investigation was to define genes linked to cold sore frequency."

Kriesel and his colleagues previously had identified a region of chromosome 21 containing six genes significantly linked to HSL disease using DNA collected from 43 large families to map the human genome. In the current study, Kriesel and his colleagues performed intensive analysis of this chromosome region using single nucleotide polymorphism (SNP) genotyping, a test which identifies differences in genetic make-up between individuals.

"Using SNP genotyping, we were able to identify 45 DNA sequence variations among 618 study participants, 355 of whom were known to be infected with HSV-1," says Kriesel. "We then used two methods called linkage analysis and transmission disequilibrium testing to determine if there was a genetic association between particular DNA sequence variations and the likelihood of having frequent cold sore outbreaks."

Kriesel and his colleagues discovered that an obscure gene called C21orf91 was associated with susceptibility to HSL. They identified five major variations of C21orf91, two of which seemed to protect against HSV-1 reactivation and two of which seemed to increase the likelihood of having frequent cold sore outbreaks.

"There is no cure for HSV-1 and, at this time, there is no way for us to predict or prevent cold sore outbreaks," says Kriesel. "The C21orf91 gene seems to play a role in cold sore susceptibility, and if this data is confirmed among a larger, unrelated population, this discovery could have important implications for the development of drugs that affect cold sore frequency."

Kriesel's University of Utah collaborators include Maurine R. Hobbs, Ph.D., research assistant professor of internal medicine and adjunct assistant professor of human genetics, and Mark F. Leppert, Ph.D., distinguished professor and former chair of human genetics.

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Story Source:

The above story is reprinted from materials provided by University of Utah Health Sciences.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

J. D. Kriesel, B. B. Jones, N. Matsunami, M. K. Patel, C. A. St. Pierre, E. A. Kurt-Jones, R. W. Finberg, M. Leppert, M. R. Hobbs. C21orf91 Genotypes Correlate With Herpes Simplex Labialis (Cold Sore) Frequency: Description of a Cold Sore Susceptibility Gene. Journal of Infectious Diseases, 2011; 204 (11): 1654 DOI: 10.1093/infdis/jir633

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Herpes linked to Alzheimer's disease: 'Cold sores' connected to cognitive decline

ScienceDaily (Apr. 4, 2011) — Laboratories at the University of New Mexico (UNM), Brown University, and House Ear Institute (HEI) have developed a new technique to observe herpes simplex virus type 1 (HSV1) infections growing inside cells. HSV1, the cause of the common cold sore, persists in a latent form inside nerve cells. Re-activation and growth of HSV1 infections contribute to cognitive decline associated with Alzheimer's disease.

Details are published in the March 31 issue of PLoS ONE.

"Herpes infects mucous membranes, such as the lip or eye, and generates viral particles," submits study Principal Investigator Elaine Bearer, M.D., Ph.D., Harvey Family Professor and Vice Chair for Research, Department of Pathology, UNM School of Medicine. "These viral particles burst out of the cells of the mucous membrane and enter sensory nerve cells where they travel inside the nerve toward the brain. We now can see this cellular transportation system and watch how the newly formed virus engages cellular APP on its journey out of the cell."

Tagging herpes virus inside cells with green fluorescent protein, scientists used live confocal imaging to watch HSV1 particles emerge from infected cells. Newly produced viral particles exit the cell nucleus and then bud into cellular membranes containing amyloid precursor protein (APP). Electron microscopy at HEI detailed the ultrastructural relationship between HSV1 particles and APP.

This dance between viral particles and cellular APP results in changes in cellular architecture and the distribution of APP, the major component of senile plaques found in the brains of Alzheimer's disease patients. Results from this study indicate that most intracellular HSV1 particles undergo frequent, dynamic interplay with APP, which facilitates viral transport while interfering with normal APP transport and distribution. This dynamic interaction reveals a mechanism by which HSV1 infection leads to Alzheimer's disease.

In developed countries such as the U.S., approximately 20 percent of children are infected with HSV1 prior to the age of five. By the second and third decades of life, as much as 60 percent of the population is infected, and late-in-life infection rate reaches 85 percent.

Symptoms of primary HSV1 infection include painful blisters of the mouth, lips or eyes. After infection, HSV1 persists in nerve cells by becoming latent. Upon re-awakening, new viral particles are made in the neuron and then travel back out its pathways to re-infect the mucous membrane. Many infected people experience sporadic episodes of viral outbreaks as the well-known recurrent cold sore.

"Clinicians have seen a link between HSV1 infection and Alzheimer's disease in patients, so we wanted to investigate what might be going on in the body that would account for this," adds Dr. Shi-Bin Cheng, post-doctoral associate, Department of Pathology and Laboratory Medicine, Alpert Medical School, Brown University. "What we were able to see in the lab strongly suggests a causal link between HSV1 and Alzheimer's Disease."

"It's no longer a matter of determining whether HSV1 is involved in cognitive decline, but rather how significant this involvement is," Bearer asserts. "We'll need to investigate anti-viral drugs used for acute herpes treatment to determine their ability to slow or prevent cognitive decline."

Researchers recommend people treat a cold sore as quickly as possible to minimize the amount of time the virus is actively traveling through a person's nervous system. The faster a cold sore is treated, the faster the HSV1 returns to a dormant stage.

Additional Authors include: Paulette Ferland, senior research assistant, UNM; Paul Webster, House Ear Institute, Los Angeles, CA; participation of Kathleen Kilpatrck, UNM; and many undergraduate students at Brown who contributed to this project are acknowledged.

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Story Source:

The above story is reprinted from materials provided by Brown University, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Shi-Bin Cheng, Paulette Ferland, Paul Webster, Elaine L. Bearer. Herpes Simplex Virus Dances with Amyloid Precursor Protein while Exiting the Cell. PLoS ONE, 2011; 6 (3): e17966 DOI: 10.1371/journal.pone.0017966

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Use of certain antiviral drugs during pregnancy not linked with higher risk of major birth defects, study suggests

ScienceDaily (Aug. 24, 2010) — An analysis of data from Denmark finds no associated increased risk of major birth defects for mothers who were exposed during the first trimester of pregnancy to the antiviral drugs acyclovir, valacyclovir, and famciclovir, often used to treat herpes simplex and herpes zoster infections, according to a study in the August 25 issue of JAMA.

The prevalence of herpes simplex is high, and more than 1 percent of susceptible women acquire herpes simplex during the first trimester of pregnancy, with antiviral treatment indicated for a significant number of women in pregnancy. "Although the safety of acyclovir, valacyclovir, and famciclovir in general has been well established, data on the use of these antivirals in early pregnancy are limited," the authors write.

Bjorn Pasternak, M.D., Ph.D., and Anders Hviid, M.Sc., Dr.Med.Sci., of Statens Serum Institut, Copenhagen, Denmark, conducted a registry-based study to assess associations between acyclovir, valacyclovir, and famciclovir use in the first trimester of pregnancy and major birth defects. The study included 837,795 live-born infants in Denmark from January 1996 to September 2008. Participants had no diagnoses of chromosomal aberrations, genetic syndromes, birth defect syndromes with known causes, or congenital viral infections. Nationwide registries were used to ascertain individual-level information on dispensed antiviral drugs, birth defect diagnoses and potential confounders (factors that can influence outcomes).

Among 1,804 pregnancies exposed to acyclovir, valacyclovir, or famciclovir at any time in the first trimester, 40 infants (2.2 percent) had a diagnosis of a major birth defect, compared with 19,920 of 835,991 infants (2.4 percent) among the unexposed pregnancies. Adjusting for several variables, acyclovir, valacyclovir, or famciclovir exposure at any time in the first trimester was not associated with increased risk of major birth defects. First-trimester use of acyclovir, the most commonly prescribed antiviral, was not associated with major birth defects (32 cases among 1,561 exposed [2.0 percent] vs. 2.4 percent in the unexposed). Neither valacyclovir (7 of 229 infants [3.1 percent]) nor famciclovir (1 of 26 infants [3.8 percent]) were associated with major birth defects, although use of famciclovir was uncommon.

Additional analyses revealed no associations between antiviral drug exposure and 13 different subgroups of birth defects, but the number of exposed cases in each subgroup was small.

"Our study, to our knowledge the largest of its kind, found no significant association between first-trimester exposure to antiherpetic antiviral drugs and major birth defects. Consequently, it has immediate clinical implications and may support informed decisions on safety when prescribing antivirals for herpes infections in early pregnancy. Acyclovir is the most extensively documented antiviral and should therefore be the drug of choice in early pregnancy, while data on valacyclovir and famciclovir are still insufficient. Future research on antiherpetic antivirals and mother-child health should include safety studies with regard to spontaneous abortion and preterm birth, and during breastfeeding," the authors conclude.

Editorial: Acyclovir Exposure and Birth Defects -- An Important Advance, But More Are Needed

In an accompanying editorial, James L. Mills, M.D., M.S., and Tonia C. Carter, Ph.D., of the National Institutes of Health, Bethesda, Md., comment on the findings of this study.

"The study by Pasternak and Hviid is helpful in demonstrating the safety of acyclovir in pregnancy, but additional strategies must be developed to resolve the remaining issues. At a time when the health care system in the United States is facing enormous financial challenges, it is important not to ignore any sources of data that could answer critical medical questions."

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Story Source:

The above story is reprinted from materials provided by JAMA and Archives Journals.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Björn Pasternak, MD, PhD; Anders Hviid, MSc, DrMedSci. Use of Acyclovir, Valacyclovir, and Famciclovir in the First Trimester of Pregnancy and the Risk of Birth Defects. JAMA, 2010;304(8):859-866 DOI: 10.1001/jama.2010.1206

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Gene is first linked to herpes-related cold sores

ScienceDaily (Nov. 30, 2011) — A team of researchers from the University of Utah and the University of Massachusetts has identified the first gene associated with frequent herpes-related cold sores.

The findings were published in the Dec. 1, 2011, issue of the Journal of Infectious Diseases.

Herpes simplex labialis (HSL) is an infection caused by herpes simplex virus type 1 (HSV-1) that affects more than 70 percent of the U.S. population. Once HSV-1 has infected the body, it is never removed by the immune system. Instead, it is transported to nerve cell bodies, where it lies dormant until it is reactivated. The most common visible symptom of HSV-1 reactivation is a cold sore on or around the mouth. Although a majority people are infected by HSV-1, the frequency of cold sore outbreaks is extremely variable and the causes of reactivation are uncertain.

"Researchers believe that three factors contribute to HSV-1 reactivation -- the virus itself, exposure to environmental factors, and genetic susceptibility," says John D. Kriesel, M.D., research associate professor of infectious diseases at the University of Utah School of Medicine and first author on the study. "The goal of our investigation was to define genes linked to cold sore frequency."

Kriesel and his colleagues previously had identified a region of chromosome 21 containing six genes significantly linked to HSL disease using DNA collected from 43 large families to map the human genome. In the current study, Kriesel and his colleagues performed intensive analysis of this chromosome region using single nucleotide polymorphism (SNP) genotyping, a test which identifies differences in genetic make-up between individuals.

"Using SNP genotyping, we were able to identify 45 DNA sequence variations among 618 study participants, 355 of whom were known to be infected with HSV-1," says Kriesel. "We then used two methods called linkage analysis and transmission disequilibrium testing to determine if there was a genetic association between particular DNA sequence variations and the likelihood of having frequent cold sore outbreaks."

Kriesel and his colleagues discovered that an obscure gene called C21orf91 was associated with susceptibility to HSL. They identified five major variations of C21orf91, two of which seemed to protect against HSV-1 reactivation and two of which seemed to increase the likelihood of having frequent cold sore outbreaks.

"There is no cure for HSV-1 and, at this time, there is no way for us to predict or prevent cold sore outbreaks," says Kriesel. "The C21orf91 gene seems to play a role in cold sore susceptibility, and if this data is confirmed among a larger, unrelated population, this discovery could have important implications for the development of drugs that affect cold sore frequency."

Kriesel's University of Utah collaborators include Maurine R. Hobbs, Ph.D., research assistant professor of internal medicine and adjunct assistant professor of human genetics, and Mark F. Leppert, Ph.D., distinguished professor and former chair of human genetics.

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Story Source:

The above story is reprinted from materials provided by University of Utah Health Sciences.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

J. D. Kriesel, B. B. Jones, N. Matsunami, M. K. Patel, C. A. St. Pierre, E. A. Kurt-Jones, R. W. Finberg, M. Leppert, M. R. Hobbs. C21orf91 Genotypes Correlate With Herpes Simplex Labialis (Cold Sore) Frequency: Description of a Cold Sore Susceptibility Gene. Journal of Infectious Diseases, 2011; 204 (11): 1654 DOI: 10.1093/infdis/jir633

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Specific gene linked to cold sore susceptibility, study finds

ScienceDaily (Oct. 28, 2011) — Investigators have identified a human chromosome containing a specific gene associated with susceptibility to herpes simplex labialis (HSL), the common cold sore. Published in The Journal of Infectious Diseases and now available online, the study looks at how several genes may affect the severity of symptoms and frequency of this common infection. The findings, if confirmed, could have implications for the development of new drugs to treat outbreaks.

HSL outbreaks, or cold sores, are skin infections that appear with the reactivation of herpes simplex virus, a virus that infects 70 percent of the U.S. population. Cold sore outbreaks vary in frequency and severity; some people may experience symptoms rarely, only once every 5 to 10 years, while others may experience them once a month or even more frequently. In addition to investigating environmental activating factors (e.g., sunlight) that may play a role in outbreaks, researchers for some time have been looking at the possible role of genetic factors in virus susceptibility and activation.

This study, led by John D. Kriesel, MD, and colleagues from the University of Utah School of Medicine in Salt Lake City and the University of Massachusetts Medical School in Worcester, follows previous studies identifying a region of chromosome 21 as a base for genes possibly linked to cold sore outbreaks. To identify which of six possible genes in this region were associated with the frequency of outbreaks, this latest study used single nucleotide polymorphism genotyping in genome-wide, family-based linkage studies of 618 people from 43 large families. The investigators found a positive link between the frequency of outbreaks, hereditability, and the presence of a specific gene, C21orf91, on chromosome 21.

"While these findings await confirmation in a larger, unrelated population," the study authors note, "these findings could have important implications for the development of new drugs that affect determinants of the cold sore phenotype."

In an accompanying editorial, Anthony L. Cunningham, MD, and David Booth, MD, of the Centre for Virus Research and the Institute of Immunology and Allergy Research at Westmead Millennium Institute and the University of Sydney in Australia, note that if the findings regarding the C21orf91 gene are confirmed, additional research may then begin to determine possible therapeutic applications and whether the same gene also plays a role in recurring genital herpes.

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The above story is reprinted from materials provided by Infectious Diseases Society of America.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal References:

J. D. Kriesel, B. B. Jones, N. Matsunami, M. K. Patel, C. A. St. Pierre, E. A. Kurt-Jones, R. W. Finberg, M. Leppert, M. R. Hobbs. C21orf91 Genotypes Correlate With Herpes Simplex Labialis (Cold Sore) Frequency: Description of a Cold Sore Susceptibility Gene. Journal of Infectious Diseases, 2011; 204 (11): 1654 DOI: 10.1093/infdis/jir633A. L. Cunningham, D. Booth. The First Common Cold Sore Susceptibility Gene. Journal of Infectious Diseases, 2011; 204 (11): 1645 DOI: 10.1093/infdis/jir635

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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Gene May Be Linked to Frequent Cold Sores - WebMD

Study Suggests Some People May Have a Genetic Predisposition to Repeated Cold Sores

Nov. 18, 2011 -- Most of us have had an occasional cold sore, but some people get the painful, unsightly sores over and over again. These cold sores, which tend to appear on or around the lips, are caused by herpes simplex virus type 1 (HSV-1).

Exactly why they occur more frequently in some people was not known, but now new research suggests some of us may have a genetic predisposition to frequent, severe cold sores.

The study is published in the Journal of Infectious Disease.

If the new findings are validated in other groups of people and researchers can zero in on exactly how a gene increases cold sore risk, new treatments won't be far behind, says study researcher John D. Kriesel, MD. He is an infectious disease specialist at the University of Utah School of Medicine in Salt Lake City.

Kriesel and colleagues narrowed down their search to one specific gene called C21orf91, which the researchers also call the cold sore susceptibility gene 1.

But "genes only account for 21% of susceptibility to cold sores, the rest of the risk is environmental," Kriesel says. Outbreak triggers may include sun, wind, trauma, or stress.

As of now, many people who get frequent cold sores are treated with antiviral medication that targets HSV-1. These can be taken to prevent an outbreak or to shorten an existing one. Oral antiviral medications include acyclovir (Zovirax), famciclovir (Famvir), and valacyclovir (Valtrex).

"This research may help us predict who is vulnerable to getting cold sores frequently. And the hope is that it will lead directly to new therapies," says infectious disease specialist Bruce Hirsch, MD.

"Anywhere from 50% to 100% of us have this virus and only a third get cold sores frequently. That is intriguing," he says. Hirsch is an attending physician at North Shore University Hospital in Manhasset, N.Y.

"If we can identify a gene that can be modulated, it could go a long way to help these folks," says Richard J. Whitley, MD. He is a professor of pediatrics, microbiology, medicine, and neurosurgery at the University of Alabama at Birmingham.

Until new drugs are available, a little prevention goes a long way for people at risk of cold sores, he says.

"If you are out in the sun, put zinc oxide on the border where your lip and the skin of your face meet," Whitley says. Cold sores often develop along this area, which is called the vermilion border.

Dermatologist Michele Green, MD, looks forward to the day when there are new treatments she can offer people with frequent, severe cold sores. She works at Lenox Hill Hospital in New York City, and sees quite a few people who fit this bill.

"It can be really debilitating," she says. "Avoiding triggers such as sun and wind can also help prevent an outbreak."

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Zoster Virus, MS Possibly Linked - MedPage Today

Adults with a history of chicken pox or shingles infections had a fourfold increased risk for developing multiple sclerosis, researchers said.

In a population-wide epidemiological study conducted in Taiwan, the hazard ratio for MS diagnosis within a year of such infections, relative to those without such a history, was 3.96 (95% CI 2.22 to 7.07), reported Herng-Ching Lin, PhD, of Taipei Medical University.

Moreover, the mean time between the acute infection and MS diagnosis was just 104 days.

"Our findings suggest that the occurrence of MS could be associated with herpes zoster attack," Lin and colleagues wrote online in the Journal of Infectious Diseases.

It's the first large-scale study to support previous suggestions that MS may be triggered or exacerbated by herpes zoster (also known as varicella zoster) virus, the agent responsible for chicken pox and shingles.

The virus infects the central nervous system. Typically, after the initial chicken pox attack, the virus becomes latent in the dorsal root ganglion. Years later, what Lin and colleagues called "immunological derangement" or other triggers can reactivate the virus to cause skin eruptions with severe pain.

Herpes zoster has long been suspected of playing some type of causative role in MS -- for example, demyelination has occasionally been seen in conjunction with severe herpes zoster attacks -- but the rarity of MS in the population has made epidemiological studies difficult.

Lin and colleagues drew on records from the Taiwan National Health Insurance Research Database, which covered some 22.6 million people as of 2007 -- more than 98% of the entire Taiwanese population. It includes monthly claims summaries and care orders for participants, including ambulatory and inpatient care.

The researchers identified about 317,000 adults who had a principal diagnosis of herpes zoster infection from 2003 to 2005. Among them, 29 developed MS during the year after this diagnosis was recorded.

For comparison, Lin and colleagues also examined records of 946,650 other randomly selected adults who had ambulatory care visits during this same period, matched 3:1 for age, sex, and year of visit to the individuals with herpes zoster attacks.

In the control group, 24 individuals were diagnosed with MS during the year after the index ambulatory care visit.

The researchers found that those with herpes zoster had slightly but significantly higher monthly income and were more likely to live in the northern part of the country than the control group. These factors were taken into account in the statistical analysis that led to the hazard ratio of 3.96 for MS diagnosis following herpes zoster attacks.

The analysis did not include counting everyone with a diagnosis of MS and checking for a history of herpes zoster infection.

Nevertheless, in an accompanying editorial, two Mexican researchers agreed that the findings significantly bolster the case for a connection between the virus and MS.

"The evidence provided in this study ... allows us to better understand the role of these viral factors as an MS risk among certain genetically susceptible individuals," wrote Teresa Corona, MD, and José Flores, MD, of the National Institute of Neurology and Neurosurgery in Mexico City.

Lin and colleagues said the mechanisms by which the virus may cause or worsen MS remain unknown, although speculation centers on alterations in immune functioning that lead to autoimmunity against myelin.

Corona and Flores offered one specific possibility: "reactivation of latent herpes viruses by other infectious agents, and cross-recognition of common viral antigens with antigens found in the myelin sheath, which thereby induces molecular mimicry or superantigens," they wrote.

Lin and colleagues noted some limitations to their study, including its reliance on potentially flawed administrative data, lack of information on potential confounders such as smoking status, and the possibility that some people with herpes zoster attacks did not seek treatment.

Also, they stressed that it was restricted almost exclusively to people of Han Chinese ancestry living in Taiwan.

Corona and Flores recommended that similar studies be undertaken elsewhere in the world to confirm the association in other ethnic groups.

The database used in the study is managed by the Taiwan Department of Health.

Study authors declared they had no relevant financial interests.

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