Apr 23, Vaginal Herpes: What Women Should Know about Genital Herpes?

Vaginal herpes is a sexually transmitted disease that keeps affecting more and more women. It can cause a lot of pain and even death to newborn babies. However a vast majority of women seem unaware of the situation.

Why it is important to know about vaginal herpesFemale herpes symptomsHerpes and pregnancy

Herpes should be a major concern for women because studies have shown that they are four times more at risk of getting infected with herpes than men. This is because their genital surface area is bigger and often moist compared to men’s.

Women are also prone to hormonal changes during menstruation, which tends to wreak havoc in their immune responses and expose them to genital herpes.

During an outbreak, the ratio of women manifesting severe symptoms of genital herpes such as painful urination and discharge is 4 out of 5, but only 1 out of 4 in men. Also, during an initial outbreak, 7 out of 10 women suffer from flu-like symptoms along with herpes such as fever, headache, swollen glands, and painful joints.

Still another reason why you should guard yourself against herpes is that people with herpes are four times more likely to get infected with AIDS.
Condoms may partially protect against herpes, although oral sex is also another way you can get the herpes virus.

Most women manifest only minimal herpes symptoms. Red flags to watch out for are blisters on or around your genitals or rectum. When blisters dry out during the first outbreak, they leave tender ulcers or sores that usually take two weeks to a month before they heal.
Another outbreak of vaginal herpes usually appears after a few weeks or months, but this is usually less severe and with shorter duration than the first.

You may experience flu-like symptoms during the primary outbreak of genital herpes. Take note, though, that women who have herpes infection usually only notice mild signs which they usually mistake for insect bites or other skin problems. This is the reason why most people only recognize the symptoms of vaginal herpes years after the onset of infection.

The herpes virus stays in the body indefinitely, but herpes outbreaks tend to diminish over time. Those with frequent symptomatic outbreaks of genital herpes are prone to more shedding, and are at higher risk of infecting others.

Medical experts say that 20 to 25 percent of pregnant women have herpes and 2 percent acquire it during pregnancy. Women who get infected with the genital herpes virus at the later part of pregnancy have a higher risk of transmitting it to their infants.

It is also possible for women with herpes to give birth to uninfected babies, although every year, some 1,500 to 2,000 new mother-to-baby herpes infections are diagnosed. A continued rise in the number of cases has been noted, leading experts to believe that vaginal herpes among pregnant women is also on the rise.

A mother may pass on the herpes virus to her baby before, during or after delivery, although the most common is during childbirth. It is estimated that 1 to 2 percent of pregnant women with recurring herpes have asymptomatic shedding (without noticeable symptoms) during childbirth.

The transmission happens during the passage of the infant through the herpes virus infected birth canal during delivery. This is the reason why doctors usually recommend delivery via a c-section.

They may be rare, but newborns getting infected with the vaginal herpes virus suffer life-threatening and long-term complications including damage to the brain and nervous system. Some even die even after prompt medical treatment.
Early warning signs of herpes infections in babies include fever, listlessness, skin sores and lack of appetite. Seek immediate medical help and testing for your child if you notice these symptoms.

The best way to protect your baby is to remain symptom free and avoid sexual contact with your partner. If your partner is infected he should do everything he can to protect you from getting vaginal herpes.If either of you is infected you should learn how to prevent and cure herpes.

Vaginal herpes or Yeast infectionHave you ever wondered if your symptoms were caused by a virus or a fungi? Do you want to know how to make the difference?

View the original article here

Apr 2, Herpes Transmission: What You Must Know

Herpes transmission is the biggest concern for people with herpes. Often they don't mind having symptoms as much as they worry about transmitting the virus. It seems that many would consider herpes to be no more than a nasty form of eczema if the risk of giving it to someone else did not exist. I had confirmation of this when I did an online survey with people who had already bought one of my books, Herpes Wise. To understand why people with herpes are so concerned with transmitting to someone else, one has to understand how herpes is transmitted and how tricky it can be to prevent transmission.

Herpes is a highly contagious virus that can be transmitted with or without any outward signs that the virus is present. Transmission is usually through skin-on-skin contact such as kissing and sexual contact. It can also be passed on by sharing a drinking glass or lipstick.

What makes herpes transmission especially hard to avoid is that carriers may not show any outward signs of the virus, but still be “shedding” the virus from their skin. It is not possible to predict when this asymptomatic shedding occurs.

Genital herpes is usually transmitted through sexual contact. Direct contact with the virus includes kissing or caressing infected areas and vaginal, anal or oral sex. If you have a cold sore and kiss a partner’s genital area you can infect that person with genital herpes.

Cold sores are a sign of oral herpes. They are usually on the lips, but can also appear inside the mouth and even on the face or neck. Oral herpes can also be passed on by kissing, with or without tongues. If you have a cold sore, you are infectious from the first sign of it.

The herpes virus can be spread from one part of the body to another, especially to the eyes. It is important to avoid touching an infected area during an outbreak and remember to wash your hands if you do.

There is little chance of catching the herpes virus through shared towels or toilet seats because the virus cannot live for very long outside the body. It is practically impossible to transmit herpes at the swimming pool, because the chlorine in the water kills the virus.

If you are someone who has herpes, then you will definitely want to inform yourself about the virus itself and all the ways you can prevent both oral herpes and genital herpes transmission.

Further readings:

Four Top Herpes Transmission Facts You Must Know to Prevent Spreading Herpes

Genital Herpes: How is the Virus Transmitted and how you can Prevent Spreading it?

Oral Herpes Transmission and Cold Sores: Learn The Facts!

View the original article here

Novel RNA transport mechanism: Ribonucleoprotein granules exit the nucleus via a budding mechanism

ScienceDaily (May 10, 2012) — The movement of genetic materials, such as RNA and ribosomes, from the nucleus to the cytoplasm is a critical component in a cell's ability to make the proteins necessary for essential biological functions. Until now, it was believed the nuclear pore complex was the sole pathway between the cell nucleus and cytoplasm for these materials.

New evidence published in Cell by Vivian Budnik, PhD, professor of neurobiology, Melissa J. Moore, PhD, the Eleanor Eustis Farrington Chair in Cancer Research, Howard Hughes Medical Institute Investigator and professor of biochemistry & molecular pharmacology, and colleagues, reveals a novel budding mechanism, similar to the process used by some viruses, capable of exporting large ribonucleoprotein (RNP) particles from the nucleus to the cytoplasm.

"The findings in this paper fundamentally change our understanding of mRNA export from the nucleus," said Dr. Moore. "In addition to the canonical pathway of mRNA export going through the nuclear pore complex, we now know that large RNA transport granules can be assembled in the cell nucleus and exported via a budding mechanism previously thought to only be used by the herpes virus."

This study has helped to unravel how RNAs support the development of the post-synaptic apparatus, said Dr. Budnik. "It provides new evidence about communication between the nucleus and cytoplasm that has implications for diseases that affect the nuclear envelope such as muscular dystrophies and herpes-type infections such as shingles."

Found along the surface of the nuclear envelope, nuclear pores are small openings that allow certain molecules, such as messenger RNA, transfer RNA and ribosomes, to be transported across this physical barrier that separates a cell's nucleus and DNA from its cytoplasm. Once in the cytoplasm, these genetic materials are the factories and blueprints used by the cell to create proteins. In some cells, these RNAs are bound together in large clusters known as transport granules, which are carried to precise locations within a cell to synthesize specific proteins needed at that site.

"When we look at these transport granules to scale, we see that they're too large to pass through the nuclear pore complex," said Moore. "An open question has been, where are these transport granules first assembled? And if it's in the nucleus, how do they make their way to the cytoplasm?"

Working to understand how synapses develop and communicate with neighboring muscle cells, Budnik discovered a new method whereby these large granules, in the form of RNP particles, were transported across the nuclear envelope. Specifically, Budnik and colleagues were investigating how the Wnt/wingless (Wg) protein secreted by the motor neuron initiates a reaction involving the DFrizzled2 (DFz2) receptor on the nearby muscle cell. This interaction between Wg and DFz2 eventually leads a portion of the DFz2 into the muscle cell nucleus where it accumulates around large RNP granules containing messenger RNAs. Once they reach their final destination in the muscle cell cytoplasm, these RNAs are responsible for making the synaptic proteins critical to increasing the size of the junction between motor neuron and muscle cell.

It was while investigating this process that Budnik and colleagues witnessed these large granules exiting the muscle cell's nucleus in an unusual manner. "What was so surprising," said Sean D. Speese, PhD, former postdoctoral fellow in the Budnik lab and currently research assistant professor at Oregon Health and Sciences University, "was that the nuclear DFz2-large-RNPs utilized a novel mechanism for exiting the nucleus, which appeared independent of the nuclear pores and resembled the egress of herpes-type viruses from the nuclear envelope."

During infection, herpes virus particles are assembled in the nucleus. But they are much too large to exit through the nuclear pores. Instead, they bud through the double membranes of the nuclear envelope. To exit the nucleus, the protein shell surrounding the virus disrupts the lamina, a fibrous component located beneath the inner nuclear membrane which, among other properties, anchors the nuclear pore complexes to the nuclear membranes. This allows the virus to bud into the space between the inner and the outer nuclear membrane, becoming enveloped by the inner nuclear membrane. Fusion of this coat with the outer nuclear membrane then allows the virus to be released into the cytoplasm.

"Similarly, we found that DFz2C-RNPs used the same mechanism and viral machinery to reach the cytoplasm," said Dr. Speese. Once inside the muscle cell nucleus, the DFz2C RNPs recruit proteins, such as kinase C, to disrupt the lamins, which allows them to bud into the inner nuclear membrane. "In both cases, this process was dependent on an A-type lamina protein, which in humans is associated with a number of muscular dystrophies and early aging syndromes when mutated," said Speese.

Collectively, these discoveries have significant ramifications for our understanding of multiple biological questions including RNA transport, synapse development and the herpes virus, which causes chicken pox and shingles as well as Epstein-Barr virus, which causes mononucleosis.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by University of Massachusetts Medical School. The original article was written by Jim Fessenden.

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

Journal Reference:

Sean D. Speese, James Ashley, Vahbiz Jokhi, John Nunnari, Romina Barria, Yihang Li, Bulent Ataman, Alex Koon, Young-Tae Chang, Qian Li, Melissa J. Moore, Vivian Budnik. Nuclear Envelope Budding Enables Large Ribonucleoprotein Particle Export during Synaptic Wnt Signaling. Cell, 2012; 149 (4): 832 DOI: 10.1016/j.cell.2012.03.032

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

Shingles vaccine is safe, according to new study

ScienceDaily (Apr. 23, 2012) — The herpes zoster vaccine, also known as the shingles vaccine, is generally safe and well tolerated according to a Vaccine Safety Datalink study of 193,083 adults published online in the Journal of Internal Medicine.

More than 1 million people develop shingles every year in the United States. Shingles is a painful contagious rash caused by the dormant chickenpox virus which can reactivate and replicate, damaging the nerve system. The elderly are especially vulnerable because immunity against the virus that causes shingles declines with age.

The VSD project is a collaborative effort between the Centers for Disease Control and Prevention and integrated care organizations, including Kaiser Permanente. The VSD project monitors immunization safety and addresses the gaps in scientific knowledge about any rare and serious events that occur following immunization.

This study examined adverse events after the zoster vaccine was administered to 193,083 adults aged 50 and older from Jan. 1, 2007, to Dec. 31, 2008. Vaccination data were retrieved from electronic health records and collected from eight managed care organizations participating in the VSD project.

Researchers found a small increased risk of local reactions from one to seven days after vaccination. These findings corroborate clinical trials of the vaccine in which there was evidence of a minor local reaction at the injection site in the form of redness and pain.

The study found no increased risk for cerebrovascular diseases; cardiovascular diseases; meningitis, encephalitis, and encephalopathy; Ramsay-Hunt syndrome; or Bell's palsy.

"It's good to know there is no serious adverse reaction to the zoster vaccine. The study supports the CDC's Advisory Committee on Immunization Practices' recommendation and reassures the general public that the vaccine is safe," said study lead author Hung Fu Tseng, PhD, MPH, a research scientist with the Kaiser Permanente Southern California Department of Research & Evaluation in Pasadena, Calif.

The herpes zoster vaccine was licensed in 2006, but few people have been vaccinated, national data shows. The ACIP recommends the vaccine for healthy people age 60 years and older. In 2011, the U.S. Food and Drug Administration approved the use of the herpes zoster vaccine in individuals 50 to 59 years of age. The study results provide important safety data for people in this age group as well as adults 60 and older.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Kaiser Permanente.

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

Journal Reference:

H. F. Tseng, A. Liu, L. Sy, S. M. Marcy, B. Fireman, E. Weintraub, J. Baggs, S. Weinmann, R. Baxter, J. Nordin, M. F. Daley, L. Jackson, S. J. Jacobsen. Safety of zoster vaccine in adults from a large managed-care cohort: a Vaccine Safety Datalink study. Journal of Internal Medicine, 2012; 271 (5): 510 DOI: 10.1111/j.1365-2796.2011.02474.x

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

Possible origin of chronic lymphatic leukemia identified

ScienceDaily (Apr. 11, 2012) — Up until now the causes of the development of chronic lymphatic leukemia, the most common form of cancer of the blood in Europe, have been unknown. At present a cure is not possible. A research group at the MedUni Vienna led by Christoph Steininger of the University Department of Internal Medicine I has now however discovered a lead on the origin of this disease. Says Steiniger: "This could influence the therapy approach taken in treating chronic lymphatic leukemia."

For approximately 20 years it has been suspected that chronic lymphatic leukemia occurs through the stimulation of B cells with other factors also playing a part. In the current research study, which has been published in the journal "Blood," the scientists were looking for an antigen that attaches itself to the leukemia cell receptors and they were able to identify the protein pUL32 of the human cytomegalovirus.

Virus "conceals" itself in cells

The cytomegalovirus, a member of the herpes family of viruses, is carried by approximately 60 to 70 percent of the Austrian population without them getting ill from it and without them even noticing that they are carrying the virus. In most cases people are infected with the virus during childhood. After being infected, the virus goes on to survive in the cells of the immune system their whole life long. The virus conceals itself within the cells and in addition it confuses the immune system with its own chemical messengers.

Only when the immune system in an infected person is weakened, for example by medical suppression as part of an organ transplant or in an HIV-illness, can the virus make someone ill. Whether this virus infection can trigger leukemia, or whether the connection observed between leukemia and the cytomegalovirus points to another mechanism, independent of the virus, in the origin of the cancer is now the subject of several follow-up studies.

One of the follow-up studies is looking at whether an antiviral treatment against the cytomegalovirus can prevent the leukemia cells from being stimulated and so prevent the further advance of the disease.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Medical University of Vienna, via AlphaGalileo.

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

Journal Reference:

C. Steininger, G. F. Widhopf, E. M. Ghia, C. S. Morello, K. Vanura, R. Sanders, D. Spector, D. Guiney, U. Jager, T. J. Kipps. Recombinant antibodies encoded by IGHV1-69 react with pUL32, a phosphoprotein of cytomegalovirus and B-cell superantigen. Blood, 2012; 119 (10): 2293 DOI: 10.1182/blood-2011-08-374058

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

Study challenges concerns on effectiveness of administering pneumococcal, shingles vaccines together

ScienceDaily (May 11, 2011) — Administering both the pneumococcal and the herpes zoster vaccines to patients during the same visit is beneficial and does not appear to compromise the protective effect of the zoster vaccine, according to a Kaiser Permanente study published in the journal Vaccine.

The study's findings challenge information in the zoster vaccine manufacturer's package insert. This new information is important to patients who find it more convenient and less costly to receive both vaccines from their health care providers during the same visit.

A revision to the zoster vaccine package insert, approved in 2009, stated that the zoster vaccine and the pneumococcal vaccine should not be given together because such concurrent use reduced the ability of the zoster vaccine to generate an immune response.

"Our study found no evidence that receiving the zoster vaccine and pneumococcal vaccine on the same day would compromise the immune response necessary to protect against herpes zoster, also known as shingles," noted study lead author Hung Fu Tseng, PhD, MPH, a research scientist with the Kaiser Permanente Department of Research & Evaluation in Pasadena, Calif.

The study was conducted from Jan. 1, 2007, to June 30, 2010, starting from the date of receipt of the zoster vaccine for two groups of Kaiser Permanente Southern California members, 60 years of age and older. The incidence of herpes zoster after vaccination with a zoster vaccine in the population receiving both vaccines on the same day was compared to that in the population receiving a pneumococcal vaccine from one year to 30 days before the zoster vaccine. Vaccinations and the incidence of herpes zoster cases were identified by electronic health records.

Included in the study were two groups or cohorts: 7,187 people who received both vaccines at the same time and 7,179 people who received the two vaccines at different times (nonconcurrently). There were 114 herpes zoster cases identified in the study: 56 cases in the concurrent group, and 58 cases in the nonconcurrent vaccination group. The study found no statistically significant difference in incidence of shingles between the two groups.

Dr. Tseng adds, "Ideally, when a new vaccine is introduced to the public, one should consider giving it at the same time as other vaccines to increase coverage levels and minimize administration costs, if there are no immune response issues or safety concerns."

According to the Centers for Disease Control and Prevention, pneumococcal polysaccharide vaccine protects against 23 types of pneumococcal bacteria, including those most likely to cause serious disease. Pneumococcal disease can result in long-term problems such as like brain damage, hearing loss and limb loss, and in some cases can be fatal. Most healthy adults who get the vaccine develop protection to most or all of these types within two to three weeks of getting the shot.

The risk of developing shingles during a lifetime is about 30 percent, and there are more than 1 million episodes of shingles every year in the United States. Shingles is a painful condition that can last months or years and can seriously impact quality of life. Less than 7 percent of the eligible U.S. population was vaccinated for herpes zoster by the end of 2008.

The CDC continues to recommend that the zoster vaccine and pneumococcal vaccine be administered at the same visit if the person is eligible for both vaccines.

The FDA approved the package label change in 2009 based on a research study by Merck that found antibody levels to the herpes zoster virus were lowered if the vaccine was administered concomitantly with pneumonia vaccine. However that study used the antibody level as the marker of protection, but it is the cell-mediated immunity against the herpes virus, instead of the antibody level that protects against the disease explained Dr. Tseng.

"This new study provides even stronger data because it relies on the measurement of the occurrence of disease rather than intermediate markers of immunity," Tseng said.

This study is the latest in a series of published Kaiser Permanente studies undertaken to better understand vaccine effectiveness and safety:

A study of 300,000 people published in JAMA earlier this year by Dr. Tseng found that receiving the herpes zoster vaccine was associated with a 55 percent reduced risk of developing shingles.Another Tseng study published in JAMA last year found the pneumococcal pneumonia vaccination is not associated with a reduced risk of heart attacks or strokes.Another Kaiser Permanente study found the combination vaccine for measles, mumps, rubella and chickenpox (MMRV) is associated with double the risk of febrile seizures for 1- to 2-year-old children compared to same-day administration of the separate vaccine for MMR (measles, mumps, rubella) and the varicella (V) vaccine for chickenpox.Other recent published Kaiser Permanente studies found children of parents who refuse vaccines are nine times more likely to get chickenpox and 23 times more likely to get whooping cough compared to fully immunized children. A study published last year found that herpes zoster, also known as shingles, is very rare among children who have been vaccinated against chickenpox.

Co-authors of the paper include Hung Fu Tseng, PhD, MPH, Ning Smith, PhD, Lina S. Sy, MPH, and Steven J. Jacobsen, MD, PhD, with Kaiser Permanente Department of Research & Evaluation.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Kaiser Permanente, 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:

Hung Fu Tseng, Ning Smith, Lina S. Sy, Steven J. Jacobsen. Evaluation of the incidence of herpes zoster after concomitant administration of zoster vaccine and polysaccharide pneumococcal vaccine. Vaccine, 2011; 29 (20): 3628 DOI: 10.1016/j.vaccine.2011.03.018

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

Multiple sclerosis-like disease discovered in monkeys

ScienceDaily (June 28, 2011) — Researchers at Oregon Health & Science University have discovered a naturally occurring disease in monkeys that is very much like multiple sclerosis in humans -- a discovery that could have a major impact on efforts to understand the cause of multiple sclerosis.

The disease that the researchers discovered in monkeys at OHSU's Oregon National Primate Research Center is associated with a herpes virus that could give significant clues into how multiple sclerosis develops in humans. MS researchers have long believed that a type of herpes virus may trigger multiple sclerosis in people who are genetically susceptible to the disease.

The OHSU researchers' findings were published online in the Annals of Neurology.

"These findings could have a huge impact on our understanding of MS and could be a landmark in someday developing more effective treatments for the disease, or even methods to prevent the onset of MS," said Scott Wong, Ph.D., senior author of the study and a scientist at the Vaccine and Gene Therapy Institute and the Oregon National Primate Research Center.

Both elements of the OHSU discovery are important for MS researchers.

Before the OHSU findings, researchers had been able to study MS-like diseases in nonhuman primates only after the disease had been artificially induced. A naturally occurring disease, such as the one discovered at OHSU, can give researchers many more clues into the causes and development of the disease.

"Now, we may be able to tease apart what's triggering the onset of the disease," Wong said.

And the fact that the disease, found in a small percentage of the Japanese macaques at OHSU each year, came from a herpes virus could prove hugely important to MS researchers worldwide. Researchers can now search for a similar virus in MS patients.

The cause of MS, which affects about 400,000 people in the United States, is unknown. But researchers have long believed that a virus, possibly a herpes virus, might trigger the disease in people who are genetically susceptible.

"Understanding how this herpes virus causes the MS-like disease in the monkeys will give us important new knowledge -- and drive new research that could lead to significant advancements in finding and preventing the virus that might cause MS," said Dennis Bourdette, M.D., a co-author of the study, director of the Multiple Sclerosis Center of Oregon and professor and chairman of the OHSU Department of Neurology.

From 1986 through 2010, 56 of the Japanese macaque monkeys at the Oregon National Primate Research Center at OHSU spontaneously developed paralysis in their hind limbs, along with other symptoms. The monkeys were humanely euthanized because they could not have been returned to the monkey colony safely. Researchers later did necropsies on the their bodies and performed MRI scans on eight of the animals.

That work and other testing allowed researchers to discover that an MS-like disease called Japanese macaque encephalomyelitis was causing the paralysis. While the disease typically afflicted young adult animals, it also was present in juveniles and older animals, and was present in both males and females.

About 1 to 3 percent of the more than 300 Japanese macaques at the primate center develop the disease each year, according to the researchers.

With this discovery, MS researchers now will be able to move toward trying to prevent or treat the virus in monkeys, which might help scientists make progress in treating MS in humans.

In addition to Wong and Bourdette, co-authors of the study include Michael Axthelm, D.V.M., Ph.D., of the Vaccine and Gene Therapy Institute; William Rooney, Ph.D., of OHSU's Advanced Imaging Research Center; and Larry Sherman, Ph.D., of the Oregon National Primate Research Center.

The research was supported by the National Institutes of Health, the Research Enrichment Award Program of the Department of Veterans Affairs Biomedical Laboratory Research and Development, the OHSU Multiple Sclerosis Center, and the United States Department of Defense. The study is titled "Japanese macaque encephalomyelitis: a spontaneous multiple sclerosis-like disease."

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Oregon Health & Science University.

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

Journal Reference:

Michael K. Axthelm, Dennis N. Bourdette, Gail H. Marracci, Weiping Su, Elizabeth T. Mullaney, Minsha Manoharan, Steven G. Kohama, Jim Pollaro, Ellen Witkowski, Paul Wang, William D. Rooney, Lawrence S. Sherman, Scott W. Wong. Japanese macaque encephalomyelitis: A spontaneous multiple sclerosis-like disease in a nonhuman primate. Annals of Neurology, 2011; DOI: 10.1002/ana.22449

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

Study Evaluates Use Of Corticosteroids And Antiviral Agents For Treatment Of Bell Palsy

ScienceDaily (Sep. 1, 2009) — Among patients with Bell Palsy, a facial paralysis with unknown cause, treatment with corticosteroids is associated with a reduced risk of an unsatisfactory recovery, and treatment with a combination of corticosteroids and antiviral agents may be associated with additional benefit, according to a systematic review and meta-analysis of previously published studies, reported in the September 2 issue of JAMA.

In background information provided by the authors, they note that Bell Palsy "is an acute weakness or paralysis of the facial nerve," and has an annual incidence of 20 to 30 per 100,000 population. "While 71 percent of untreated patients will completely recover and 84 percent will have complete or near normal recovery, the remainder will have persistent to moderate to severe weakness, facial contracture, or synkinesis [involuntary movement]." The authors explain that a herpes infection likely causes the disorder. DNA samples from patients have yielded herpes simplex virus type 1 (HSV-1). Varicella zoster virus (VZV) reactivation is also associated with Bell Palsy.

John R. de Almeida, M.D., from Sunnybrook Hospital and the University of Toronto, Canada, and colleagues conducted a search of the medical literature for randomized controlled trials comparing treatment with either corticosteroids or antiviral agents with a control measuring unsatisfactory facial recovery (four months or more), unsatisfactory short-term recovery (six weeks to less than four months), synkinesis and autonomic dysfunction, or adverse effects. The authors identified 854 studies, of which 18 were eligible for inclusion for evaluation. The 18 studies included 2,786 patients and were conducted in 12 countries and five continents.

"… high-quality evidence suggests that corticosteroids alone reduce the risk of unsatisfactory recovery by 9 percent in absolute terms, with a NNTB (number of patients needed to treat for one patient to experience benefit) of 11," the authors report. "Corticosteroid therapy combined with antiviral agents reduced the risk of unsatisfactory recovery compared with antiviral agents alone. Corticosteroids were also associated with a 14 percent absolute risk reduction of synkinesis and autonomic dysfunction (NNTB, 7; moderate quality of evidence). Corticosteroids were not associated with an increased risk of adverse effects."

"Our results suggest a possible incremental benefit of antiviral agents in addition to corticosteroids, with an absolute risk reduction of 5 percent compared with corticosteroids alone. This effect, however, is not definitive and did not quite reach statistical significance," the authors write. "Further primary studies are needed to definitively establish – or refute – an incremental benefit of combined therapy compared with corticosteroid mono therapy," the authors conclude.

Editorial: Treatment of Bell Palsy – Translating Uncertainty Into Practice

"The systematic review by de Almeida et al of medications for treatment of Bell palsy helps resolve lingering doubt about the benefits of corticosteroids, but raises questions about the adjunctive role of antiviral medications," John F. Steiner, M.D., M.P.H., of Kaiser Permanente Colorado, Denver, writes in an accompanying editorial.

"Until the next generation of clinical trials is completed, clinicians and patients will have to deal with substantial uncertainty in deciding whether to add antiviral drugs to corticosteroids for Bell palsy. By assessing how clinicians alter their prescribing patterns and how treatment guidelines are revised in response to this new evidence, it will be possible to learn more about how clinical uncertainty is translated into practice."

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

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:

John R. de Almeida; Murtadha Al Khabori; Gordon H. Guyatt; Ian J. Witterick; Vincent Y. W. Lin; Julian M. Nedzelski; Joseph M. Chen. Combined Corticosteroid and Antiviral Treatment for Bell Palsy: A Systematic Review and Meta-analysis. JAMA, 2009; 302 (9): 985-993 [link]

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 virus' tactical maneuver visualized in 3-D

ScienceDaily (Jan. 6, 2011) — For the first time, researchers have developed a 3-D picture of a herpes virus protein interacting with a key part of the human cellular machinery, enhancing our understanding of how it hijacks human cells to spread infection and opening up new possibilities for stepping in to prevent or treat infection. This discovery uncovers one of the many tactical maneuvres employed by the virus.

The Biotechnology and Biological Sciences Research Council (BBSRC)-funded team, led by The University of Manchester, have used NMR -- a technique related to the one used in MRI body scanners and capable of visualizing molecules at the smallest scales -- to produce images of a herpes virus protein interacting with a mouse cellular protein. These images were then used to develop a 3-D model of this herpes virus protein interacting with human protein. The research is published in PLoS Pathogens.

Lead researcher Dr. Alexander Golovanov from Manchester's Interdisciplinary Biocentre and Faculty of Life Sciences said: "There are quite a few types of herpes viruses that cause problems as mild as cold sores through to some quite serious illnesses, such as shingles or even cancer. Viruses cannot survive or replicate on their own -- they need the resources and apparatus within a human cell to do so. To prevent or treat diseases caused by viruses we need to know as much as possible about how they do this so that we can spot weak points or take out key tactical maneuvres."

The 3-D model shows how the viral protein piggybacks onto the molecular machinery components inside human cells, promoting virus replication and spread of infection through the body.

"When you look at the image, it's like a backpack on an elephant: the small compact fragment of viral protein fits nicely on the back of the human protein," said Dr. Golovanov.

By studying the images along with biochemical experiments using the human version of the cellular protein, the team has uncovered the mechanism by which the viral and cellular proteins work together to guide the viral genetic material out of the cell's nucleus. Once there, the genetic material can be utilized to make proteins that are used as building blocks for new viruses. The researchers have also confirmed that this relationship between the two proteins exists for related herpes viruses that infect monkeys.

Dr. Golovanov continued: "Our discovery gives us a whole step more detail on how herpes viruses use the human cell to survive and replicate. This opens up the possibilities for asking new questions about how to prevent or treat the diseases they cause."

Professor Janet Allen, BBSRC Director of Research said: "This new research gives us an important piece of the jigsaw for how a particular viral infection works on a molecular level, which is great news. Understanding the relationship between a human, animal or plant -- the host -- and the organisms that cause disease -- pathogens -- is a fundamental step toward successful strategies to minimize the impact of infection. To study host-pathogen relationships we have to look in detail at the smallest scale of molecules -- as this study does -- and also right through to the largest scale of how diseases work in whole systems -- a crop disease in the context of a whole area of agricultural land, for example. BBSRC's broad portfolio of research into host-pathogen relationships facilitates this well."

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Biotechnology and Biological Sciences Research Council, 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:

Richard B. Tunnicliffe, Guillaume M. Hautbergue, Priti Kalra, Brian R. Jackson, Adrian Whitehouse, Stuart A. Wilson, Alexander P. Golovanov. Structural Basis for the Recognition of Cellular mRNA Export Factor REF by Herpes Viral Proteins HSV-1 ICP27 and HVS ORF57. PLoS Pathogens, 2011; 7 (1): e1001244 DOI: 10.1371/journal.ppat.1001244

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

Type Of Rheumatoid Arthritis Medication May Be Associated With Increased Risk For Shingles

ScienceDaily (Feb. 17, 2009) — Use of certain medications known as monoclonal anti– tumor necrosis factor a (TNF-a) antibodies for the treatment of rheumatoid arthritis appears to be associated with an increased risk for herpes zoster (shingles), the painful infection characterized by blisters, according to a new study.

There has been evidence from some studies that patients treated with anti–TNF-a agents are at an increased risk of bacterial infections, but little is known about the risk of viral infections, such as herpes zoster, in patients with rheumatoid arthritis receiving these types of medications. Herpes zoster is one of the most common adverse events reported in clinical trials of anti–TNF-a agents, according to background information in the article. Patients with rheumatoid arthritis are at increased risk of herpes zoster compared with the general population.

Anja Strangfeld, M.D., of the German Rheumatism Research Center, Berlin, and colleagues investigated the association of various rheumatoid arthritis treatments, including anti–TNF-a therapy, with the risk of herpes zoster. The researchers analyzed data from patients who began treatment with adalimumab or infliximab (monoclonal anti–TNF-a antibodies), etanercept (a fusion protein), the monotherapeutic agent anakinra, or when patients changed conventional disease-modifying anti-rheumatic drug (DMARD). Treatment, clinical status and adverse events were assessed by rheumatologists at fixed points during follow-up (of up to three years). A total of 5,040 patients were included in the analysis.

There were 86 cases of herpes zoster among 82 patients. Thirty-nine occurrences could be attributed to treatment with anti–TNF-a antibodies (23 to etanercept, 24 to conventional DMARDs). The researchers found a significant association between herpes zoster and treatment with the monoclonal anti–TNF-a antibodies infliximab and adalimumab, although this risk was lower than the threshold for clinical significance. There was no significant association between herpes zoster and treatment with etanercept, or anti–TNF-a treatment as a class.

A significantly higher risk of developing herpes zoster was found for patients of older age and for treatment with glucocorticoids (steroid hormones that are widely used as anti-inflammatory medications).

"Based on our data, we recommend careful monitoring of patients treated with monoclonal anti–TNF-a antibodies for early signs and symptoms of herpes zoster," the authors conclude.

Editorial: Herpes Zoster in the Age of Focused Immunosuppressive Therapy

In an accompanying editorial, Richard J. Whitley, M.D., and John W. Gnann Jr., M.D., of the University of Alabama at Birmingham, comment on the findings of this study.

"The TNF-a inhibitors provide tremendous benefit to a broad spectrum of patients with systemic inflammatory diseases. As with any therapy, time is required for all of the safety concerns related to these potent medications to become apparent. TNF-a inhibitors have revolutionized the management of a number of difficult diseases, especially inflammatory arthritis, but clinicians must continue to remain aware of the potential for serious infectious complications, which now include herpes zoster."

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

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:

Anja Strangfeld; Joachim Listing; Peter Herzer; Anke Liebhaber; Karin Rockwitz; Constanze Richter; Angela Zink. Risk of Herpes Zoster in Patients With Rheumatoid Arthritis Treated With Anti%u2013TNF-{alpha} Agents. JAMA, 2009;301(7):737-744 [link]

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

Transcriptional Coactivators Not Useful As Herpes Antiviral Drug Targets

ScienceDaily (Mar. 25, 2009) — Researchers at Van Andel Research Institute (VARI) have determined that the herpes simplex virus type 1 (HSV-1) does not require transcriptional coactivators for viral gene expression early in the infection process. The finding is significant in determining that, in contradiction to earlier models, chemical inhibitors of these cellular proteins are not likely to serve as useful antiviral drugs.

Researchers sought to determine how herpes simplex virus “turns on” its viral genes during the first stages of infection. Specifically, they tested whether the expression of the viral genes would be similar to how cellular genes are turned on, and specifically whether the viral genes would depend on a set of cellular proteins called “coactivators.”

“Based on an earlier model we expected that expression of the viral genes would depend on a set of transcriptional coactivators,” said Scientific Investigator Steve Triezenberg, Ph.D., head of the VARI Laboratory of Transcriptional Regulation and co-author of the study published in a recent issue of the Journal of Virology. “As it turns out, we got an unexpected answer.  Using several different approaches, we consistently saw that the coactivator proteins are not required for viral gene expression.”

Researchers have understood that virion protein 16 (VP16) of herpes simplex virus type 1 is a potent transcriptional activator of viral immediate early (IE) genes. However, the role of transcriptional coactivators had not been fully understood.

“This is a significant finding because it tells us that chemical inhibitors of these coactivators are not likely to be good antiviral drugs, despite our earlier model,” said Triezenberg.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Van Andel Research Institute.

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

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 Medication Does Not Reduce Risk Of HIV Transmission

ScienceDaily (May 8, 2009) — A recently completed international multi-center clinical trial has found that acyclovir, a drug widely used as a safe and effective treatment to suppress herpes simplex virus-2 (HSV-2), which is the most common cause of genital herpes, does not reduce the risk of HIV transmission when taken by people infected with both HIV and HSV-2.

The majority of people with HIV infection also have HSV-2 infection. Multiple studies have shown that frequent genital herpes recurrences increase the amount of HIV in the blood and genital tract. The HIV virus is also shed from genital herpes ulcers and individuals with such ulcers transmit HIV to others more efficiently. Five preliminary studies showed that it is possible to decrease the amount of HIV in the blood and genital tract through treatment to suppress HSV-2, but these studies did not measure whether this translated into a reduction in HIV transmission. Researchers had hoped that acyclovir's ability to suppress the herpes virus, which causes symptomatic genital sores and breaks in the skin but also frequently is active without symptoms, could reduce the likelihood of sexual transmission of HIV from a person with HIV and HSV-2. The study being reported today is the first to determine whether twice daily use of acyclovir by individuals who are infected with both HSV-2 and HIV reduced the transmission of HIV to their sexual partners.

Led by the University of Washington in Seattle and funded by the Bill & Melinda Gates Foundation, the Partners in Prevention HSV/HIV Transmission Study was conducted among 3,408 African HIV discordant couples, in which one partner had HIV and the other did not. In all the couples, the partner who had HIV also had HSV-2 infection. The study took place at 14 sites in seven countries in eastern and southern Africa (Botswana, Kenya, Rwanda, South Africa, Tanzania, Uganda and Zambia). In sub-Saharan Africa, the majority of new HIV infections occur among heterosexual HIV discordant couples, many of whom are in stable partnerships and unaware that one partner has HIV and the other does not. Genital herpes is thought to be a factor in a substantial proportion of new HIV infections in Africa.

In the primary analysis of HIV transmissions determined by laboratory testing to have occurred within the couple and not acquired from an outside partner, there were 41 infections in the acyclovir arm and 43 in the placebo arm – not a significant difference. Acyclovir suppressive treatment reduced the frequency of genital ulcers by 73% and the average amount of HIV in the blood (by 0.25 log10 copies/milliliter, a reduction of 40%), compared to the placebo arm.

"The Partners in Prevention Study is a direct assessment of the impact of herpes suppression on HIV transmission," explained Dr. Connie Celum, the leader of the study and a UW professor of Global Health and Medicine in the Division of Allergy and Infectious Diseases. "A clinical trial of genital herpes suppression in HIV discordant couples is the most direct way to see if we can make a person less infectious and less likely to transmit HIV to their partner. The study did find that acyclovir significantly reduced genital ulcers due to HSV-2 and modestly reduced HIV levels in the blood, consistent with what the preliminary studies of HSV-2 suppressive treatment had shown. However, it appears that these effects were not sufficient to reduce the risk of HIV transmission."

The study also determined whether acyclovir can slow HIV disease progression among individuals with HIV and HSV-2 who also have CD4 T-cell counts that are too high for HIV antiretroviral treatment under current national guidelines. Specifically, the investigators studied the number of participants in the acyclovir and placebo arms whose CD4 T-cell counts declined to below 200, who started HIV medications, or who died. In this analysis, HIV disease progression was slowed by 17% by acyclovir, an effect that was statistically significant. Given that low-cost, safe ways to delay progression of HIV disease are needed for individuals who are not yet taking HIV medications, this result is encouraging, but the modest effect observed in this study may not be sufficient to promote use of this dose of acyclovir for slowing HIV disease.

"Although the primary outcome of reducing HIV transmission was not observed, the study yielded important information that will inform HIV prevention research in a number of ways," Celum said. "Most importantly, we have demonstrated that interventions must achieve a bigger reduction in HIV levels in order to reduce HIV transmission, especially among persons with high HIV levels. This was an ambitious study, which required testing of an estimated 50,000 couples of unknown HIV status in Africa to recruit the 3,408 HIV discordant couples who volunteered to enroll in the study. This was an important and courageous study to undertake, and I applaud our collaborators at the University of Washington, the investigators and study teams in Africa, the study participants, and the communities where the study was done, for their dedication over the past five years. The findings will bear fruit for both the HIV prevention and the vaccine fields for years to come."

HSV-2 is one of the most common sexually transmitted infections worldwide and is especially prevalent in areas with high rates of HIV infection, with up to 90% of individuals who have HIV also being infected with HSV-2. Most people who are infected with HSV-2 do not know they have the virus because symptoms can be mild or absent. HSV-2 infection can cause recurrent sores and breaks in the skin of the genital region, which can be mild and often go unnoticed. HSV-2 infection also attracts immune cells called CD4 T-cells to the genital region, which HIV uses to establish or pass infection.

The Partners in Prevention HSV/HIV Transmission Study is the first clinical trial to directly test whether suppressing HSV-2 infection could reduce rates of HIV transmission and HIV disease progression. The study, which began recruitment at the 14 African sites in November 2004, ended follow-up of participants in October 2008. The study was randomized, placebo-controlled and double-blinded, meaning that both participants and care providers did not know which treatment the participants were receiving. Both the placebo and treatment groups received standard HIV prevention services, which included being supplied with condoms, treated for other sexually transmitted infections, and provided care for HIV infection. All participants received extensive counseling, both individually and as a couple, throughout the study period, on how to reduce the risk of HIV infection.

"Based on the findings from this study, we now better understand the relationship between HIV levels and HIV transmission. This shows us that the 'bar' is higher than we anticipated for the amount of reduction in HIV levels needed in order to reduce HIV infectiousness and transmission. This is relevant for other interventions," Celum said, "such as anti-retroviral drugs to treat HIV, treatment of co-infections such as malaria, and therapeutic HIV vaccines. This understanding is a major contribution to HIV research that will help guide our search for new HIV prevention and treatment strategies."

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by University of Washington.

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

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

Sleeping Beauty hooks up with herpes to fight brain disease

ScienceDaily (Jan. 8, 2010) — Neuroscientists have forged an unlikely molecular union as part of their fight against diseases of the brain and nervous system.

The team has brought together the herpes virus and a molecule known as Sleeping Beauty to improve a technology known as gene therapy, which aims to manipulate genes to correct for molecular flaws that cause disease.

The work, detailed in a paper published online in Gene Therapy, has allowed scientists at the University of Rochester Medical Center to reach a long-sought goal: Shuttling into brain cells a relatively large gene that can remain on for an extended period of time.

"We've broken what is in effect a size barrier -- a limit to how much genetic material we can put into the nucleus of a cell and keep functioning for a long period of time," said neuroscientist William Bowers, Ph.D., a scientist in the Center for Neural Development and Disease and the leader of the team. "That opens up more diseases to possible treatment with gene therapy."

The first author of the paper is Biochemistry graduate student Suresh de Silva, who defends his doctoral thesis later this month.

The molecular rendezvous of Sleeping Beauty and herpes in human brain cells could spell good news in the search for treatments for horrific brain diseases known as pediatric leukodystrophies, or a group of diseases known as lysosomal storage disorders. In many of these diseases, even though just a single gene or protein is defective, the effects are devastating -- the diseases slowly rob children of their brain cells and are often fatal after years of severe symptoms.

The findings bolster the tools that researchers have when approaching certain diseases, said Bowers, including Usher syndrome, which results in deafness and vision loss; Niemann-Pick disease Type C, a fatal childhood lysosomal storage disorder; and von Willebrand disease, an inherited disease that causes extensive, chronic bleeding.

"The field of gene therapy is just beginning to yield some successes for patients. Improvements like this are crucial for increasing the number of patients who might benefit from such an approach," said Bowers, who is an associate professor of Neurology, Microbiology and Immunology, and of Pharmacology and Physiology.

The research is part of a decades-long endeavor by scientists trying to get the right genes into the right cells at the right time to improve human health.

In the new work, scientists dramatically increased the size of the "genetic payload" they can deliver to brain cells compared to some conventional techniques, nearly tripling the amount of genetic material by some measures. They hope to deliver even bigger genes in the future.

The team did this by bringing together in a new way two molecular players, herpes and Sleeping Beauty, which are commonly used in molecular technology.

For years Bowers' team has been using the herpes virus -- HSV-1, the type that causes cold sores -- to shuttle genes into cells. Viruses like herpes are adept at infecting human cells, and scientists like Bowers use such viruses to carry into cells genes that would help people who are sick. Bowers and colleagues modify the viruses extensively, removing the portions that could make a person sick and using the portions that the virus uses to gain access to human cells.

Many scientists use other viruses, such as lentiviruses or a cold-related virus known as adeno-associated virus (AAV), to do a similar job. Each virus has its strengths and weaknesses when it comes to gene therapy. Herpes, for instance, readily infects cells, and it can carry a huge amount of genetic material, typically 15 to 30 times the amount of DNA that other viruses can carry into a cell.

But herpes as a genetic tool has a couple of big weaknesses. While the virus can deliver DNA into the nucleus of a cell, the genetic payload it carries does not become part of the package of genes that cells pass from one to another. Simply put, herpes cannot integrate the new DNA into the host genome. Instead, the DNA is adrift in the nucleus, where it's silenced within a few weeks. The short time span spells trouble when scientists are trying to treat a disease that requires the genes to be active for months or years.

That's where Sleeping Beauty comes in.

In molecular biology, Sleeping Beauty is a mobile genetic element that jumps into and out of longer segments of DNA. It's normally silent, but years ago a team of scientists was able to activate or "awaken" the snippet -- hence, Sleeping Beauty. Since Sleeping Beauty actually integrates segments of DNA into mammalian genomes, it sidesteps the main difficulties that herpes encounters inside a cell: Genes integrated within the cell's chromosomes by Sleeping Beauty operate for much longer periods of time. The drawback: The molecule can insert only small snippets of DNA.

So the Rochester team brought herpes and Sleeping Beauty together in an attempt to get the best of both worlds: Delivery of the bigger genetic package made possible by herpes, and the integration of the DNA into the host genome made possible by Sleeping Beauty.

And that's exactly what happened. In the tag-team approach funded by the National Institute of Neurological Disorders and Stroke, herpes gets the genetic package into the right neighborhood, the cell's nucleus, and then Sleeping Beauty delivers the package precisely where it needs to go to be most effective -- into the cellular genome.

In the current experiments, the herpes virus carried into cell nuclei the gene for green fluorescent protein, which allows scientists to track where the gene is active. The team also outfitted the herpes package with special molecular signals that Sleeping Beauty would recognize. Separately, the team introduced Sleeping Beauty into the cells. When the two met, Sleeping Beauty transferred the gene for GFP from the herpes package to the genome of the human cells, where the gene was stably expressed.

The team has previously shown that the Sleeping Beauty/herpes combination works efficiently in brain cells known as neural progenitor cells, which go on to form brain cells known as neurons. Modifying these cells -- perhaps by adding a gene that creates a protein crucial for health -- is one technique scientists are experimenting with to try to treat several brain diseases that are currently untreatable.

The gene segment used in the experiment described in Gene Therapy was about 12 kilobases long, which is larger than the limit of either AAV (4.5 kb) or lentiviruses (9 kb). Those few kilobases matter, a lot. The ability to transfer bigger genes gives scientists room to try to address more diseases with a gene therapy approach. The added space also makes it possible to include more regulatory elements -- instructions that help determine how and when genes are turned on or off. This allows scientists to package additional safety directives, in the form of more DNA, along with the gene designed to treat the disease.

In addition to de Silva and Bowers, authors include technical associates Michael Mastrangelo, Louis T. Lotta Jr., and Clark Burris, as well as Howard J. Federoff, M.D., Ph.D., a former Rochester faculty member who is now executive vice president for health sciences at Georgetown University.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by University of Rochester Medical Center.

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

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

No More Cold Sores? Scientists Find Cellular Process That Fights Herpes Virus

ScienceDaily (Mar. 23, 2009) — Scientists have discovered a new way for our immune system to combat the elusive virus responsible for cold sores: Type 1 herpes simplex (HSV-1). As reported in the advance online edition of Nature Immunology, a group of virus hunters from the Université de Montréal, in collaboration with American colleagues, have identified a cellular process that seeks out and fights herpes.

The five-year study, partially supported by the Canadian Institutes of Health Research, was a joint project with Washington University and Pennsylvania State University.

"Once human cells are infected with Type 1 herpes simplex, the virus comes back because it hides and blocks protection from our immune system," says Luc English, the study's lead author and a doctoral student at the Université de Montréal's Department of Pathology and Cell Biology. "For the first time, our research team has identified a combative cellular mechanism in this game of hide-and-seek."

"We've found that the nuclear membrane of an infected cell can unmask Type 1 herpes simplex and stimulate the immune system to disintegrate the virus," says English.

The team made its discovery while conducting various tests in HSV-1 infected mice cells. They replicated environments when Type 1 herpes simplex thrives, namely periods of low-grade fever between 38.5 to 39 degrees, and found that herpes-fighting mechanisms were unleashed.

The research team now plans to study how activation of the herpes-combating cellular process could be applied to other illnesses. The outcome could hasten the development of therapies to prevent other immune-evading bacteria, parasites and viruses. "Our goal is to further study the molecules implicated in this mechanism to eventually develop therapies against diseases such as HIV or even cancer," says English.

According to Dr. Michel Desjardins, senior author and a professor in the Department of Pathology and Cell Biology at the Université de Montréal, treatment options might be imaginable in a decade.

"Now that we've identified the novel mechanism in cells that activate immune response to Type 1 herpes simplex, scientists are one step closer to creating new treatments that can activate the defence against this and other viruses," says Dr. Desjardins. "While it may not be possible to completely eradicate Type 1 herpes simplex in people who are already infected, at the very least, future therapies may be able to keep the virus in its dormant state."

This study was funded by the Canadian Institutes of Health Research, the Natural Science and Engineering Research Council of Canada, the Fonds de la Recherche en Santé du Québec, the U.S. National Institutes of Health and the foundation Research to Prevent Blindness.

About Herpes

There are two types of herpes viruses: Type 1 herpes simplex causes facial cold sores and Type 2 causes genital herpes. Both types of herpes affect an estimated 80 million people in America alone and there is currently no cure for the condition.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by University of Montreal.

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

Journal Reference:

Luc English, Magali Chemali, Johanne Duron, Christiane Rondeau, Annie Laplante, Diane Gingras, Diane Alexander, David Leib, Christopher Norbury, Roger Lippé & Michel Desjardins. Autophagy enhances the presentation of endogenous viral antigens on MHC class I molecules during HSV-1 infection. Nature Immunology, 2009; DOI: 10.1038/ni.1720

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

Genital herpes more virulent in Africa than in US, report finds

ScienceDaily (Apr. 15, 2011) — Strains of genital herpes in Africa are far more virulent than those in the United States, researchers at Harvard Medical School report, a striking insight into a common disease with important implications for preventing HIV transmission in a region staggered by the HIV/AIDS epidemic. The researchers arrived at this finding by testing mouse model strains of the disease against vaccine candidates. All vaccines were far more efficacious in abating the U.S. strain.

The researchers say identification of the properties of the African viruses would open the door to developing a more potent vaccine against an infection now rampant in sub-Saharan Africa. This is important, they say, because genital herpes patients are more vulnerable to HIV/AIDS infection, as the open sores symptomatic of herpes contain a high concentration of immune cells that are targeted by HIV.

The challenge lies in formulating either a single vaccine that protects against both types of strains of the genital herpes virus or two different vaccines. The vaccine farthest along in development -- it is headed for clinical trials in about a year -- works best against the U.S. isolates of herpes simplex 2, but it also protects laboratory animals from the African viral strains if given in five-fold-higher doses.

This research, which appears online on April 15 in The Journal of Infectious Diseases, is led by David M. Knipe, the Higgins Professor of Microbiology and Molecular Genetics and vice chair of that department at Harvard Medical School, and Clyde Crumpacker, professor of medicine at Harvard Medical School and a physician in division of infectious disease at Beth Israel Deaconnes Medical Center. Their collaborators are former Knipe lab members Timothy E. Dudek, currently of the Ragon Institute of Massachusetts General Hospital, and Ernesto Torres-Lopez, now of the Universidad Autonoma in Monterrey, Mexico.

Live-virus vaccine

In southern Africa, infection rates among adults for genital herpes are exceedingly high -- from 80 percent to 90 percent in some groups compared to slightly less than 20 percent in the United States.

In evolutionary terms, the herpes viruses are very old. They have honed their talents to become efficient parasites in humans, often persisting for decades while causing limited or no disease symptoms -- although they can be deadly in immunocompromised persons and in newborns.

The herpes virus that causes ordinary cold sores, herpes simplex 1, is present in about 70 percent of the U.S. population. These stealthy viruses hide in nerve cells but can emerge over and over again, prompting repeated cold sore outbreaks.

Despite decades of research, there is no commercially available vaccine for herpes. But Knipe says their prototype vaccines are being tested in animals, and one such vaccine has been licensed to the French pharmaceutical firm Sanofi Pasteur.

According to Knipe, animal tests demonstrate clearly that the strains of herpes virus seen in sub-Saharan Africa are more virulent than the herpes simplex 2 virus strains seen in the United States. That difference suggests that an effective vaccine will probably have to be given to people in Africa in larger or more frequent doses. So far, says Knipe, results of animal tests are heartening.

Part of the promise in this work lies in the strong chance that a vaccine against herpes simplex 2 can help reduce the impact of HIV/AIDS in southern Africa. Epidemiological studies have shown that genital herpes infection is associated with a three-fold increase in the risk of HIV infection.

"If the rate of herpes infection can be reduced, it's conceivable the rate of HIV/AIDS infection will also come down, perhaps reducing the death rate," says Knipe.

Knipe's approach to vaccine development is based on using abnormal, live, mutant viruses to stimulate protective immune responses. These disabled viruses cannot multiply inside cells or cause symptomatic disease, but they do contain enough of the right proteins and molecules needed to arouse detection by a healthy immune system. Knipe's strategy is to trigger a strong immune response without causing disease.

"The candidate vaccine, ACAM529, is under development by Sanofi Pasteur, and under the current plan will enter phase I clinical testing in 2012," said Jim Tartaglia, a company respresentative. Phase I testing involves giving vaccine to a few human volunteers and watching for signs of toxicity. Trials for efficacy come later.

Although it has been difficult to create a vaccine for genital herpes, vaccines against a closely related herpes virus -- varicella zoster virus, the cause of chicken pox and shingles -- proved successful and are now widely used. This gives reason for optimism about a genital herpes vaccine.

The researchers do caution that, previously, two well-executed trials of Acyclovir, an effective, safe, antiviral drug for herpes, did decease the occurrence of genital herpes infections but failed to prevent transmission of HIV-1 in African study participants.

This research was funded by the National Institutes of Health.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Harvard Medical School.

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

Journal Reference:

T. E. Dudek, E. Torres-Lopez, C. Crumpacker, D. M. Knipe. Evidence for Differences in Immunologic and Pathogenesis Properties of Herpes Simplex Virus 2 Strains From the United States and South Africa. Journal of Infectious Diseases, 2011; 203 (10): 1434 DOI: 10.1093/infdis/jir047

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.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

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

Childhood Chicken Pox Can Lead To Shingles Later In Life

ScienceDaily (Feb. 18, 2009) — You may recall as a child catching the itchy red rash, chicken pox. The unsightly infection was caused by the varicella zoster virus and was responsible for nearly 4 million cases each year, according to the Centers for Disease Control (CDC), until a vaccine introduced in 1995 reduced that number by 83 percent.

Yet, if you were among those that suffered from chicken pox, the varicella zoster virus may still be present in your body and could lead to serious (and irreversible) oral health problems such as herpes-type lesions and severe bone damage to the jaws.

 Varicella zoster can lie dormant in the body for decades, and if activated can lead to herpes zoster (HZ), more commonly referred to as shingles, according to a study that appeared in General Dentistry, the Academy of General Dentistry’s (AGD) clinical, peer-reviewed journal.

Affecting nearly 1 million Americans each year, 50 percent of all new cases of herpes zoster occur in individuals over the age of 60.

“Herpes zoster manifests as painful blisters that erupt along the sensory nerves usually on one side of the body or face,” according to co-author of the study, M.A. Pogrel, DDS, MD. “It can be a debilitating disease that can lead to osteonecrosis of the jaw and vision loss in addition to a prolonged painful syndrome.”

Osteonecrosis is a condition in which bone in the lower or upper jaw becomes exposed. As a result, the jaw bone suffers severe damage and/or death, eventually leading to tooth loss.

While the exact reason for tooth loss is unknown, it has been noted that restricted blood flow and inflammation may be a cause.

However, AGD spokesperson, Laura Murcko, DMD, notes that, “Your dentist can help detect early signs of osteonecrosis of the jaw by checking for loose teeth, detached gums as well as taking dental x-rays.”

Dr. Murcko encourages patients who may have signs of or are suffering from osteonecrosis to visit their dentist regularly and practice good oral hygiene. She recommends that patients consume 1,000 to 1,200 milligrams of calcium a day, add vitamin D to their diet, exercise and weight train, quit smoking and decrease caffeine and alcohol intake.

Symptoms of osteonecrosis:

Pain, swelling or infection of the gumsLoosening of teethPoor healing of the gumsNumbness or the feeling of heaviness in the jawShare this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Academy of General Dentistry.

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

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

Eczema Patients Most At Risk For Dangerous Viral Infections

ScienceDaily (June 25, 2009) — Eczema patients at risk for serious viral infections have more severe disease, are more likely to be allergic to food and other allergens, and have a frequent history of staph infections, according to researchers at National Jewish Health and other institutions in the NIH-funded Atopic Dermatitis Vaccinia Network.

The findings, published June 22 in the online version of The Journal of Allergy and Clinical Immunology, could help identify people at risk for serious complications of smallpox vaccinations, and point to defects in the skin barrier and antimicrobial-protein production as possible causes for the increased susceptibility.

"Previous studies have suggested that eczema is not only becoming more prevalent, but that patients have increased susceptibility to disseminated viral infections," said senior author Donald Leung, MD, PhD, Edelstein Family Chair of Pediatric Allergy and Clinical Immunology at National Jewish Health. "Our study is the largest and first in the United States to carefully characterize eczema patients who have suffered widespread herpes simplex viral infections of their skin. It is also the first to report that these patients are more susceptible to staphylococcus and other infections of the skin and eye."

A subset of the estimated 6 million eczema patients in the United States are susceptible to widespread infections of their skin by herpes simplex and vaccinia viruses. The herpes simplex virus is common but only rarely causes disseminated skin infections that can spread to the eye and bloodstream sometimes leading to encephalitis and meningitis. The widespread herpes simplex skin infection is known as eczema herpeticum.

Vaccinia virus, which is used in smallpox vaccinations, can also cause a serious and life-threatening skin infections in a smaller subset of patients. People who have eczema or had it in the past are susceptible to this infection when they receive a smallpox vaccination. This situation could limit the ability of those people to safely receive vaccinations in case of a smallpox bioterrorism event.

The Atopic Dermatitis Vaccinia Network (ADVN) is an NIH-funded multi-center network charged with better understanding the susceptibility of eczema patients to the vaccinia infection and to search for ways to protect against it. Atopic dermatitis is another name for eczema, an allergic skin condition that causes itchy, inflamed and cracked skin.

The ADVN researchers believed that they might be able to identify eczema patients at high risk for these infections and to obtain clues about the mechanisms of susceptibility by studying a large cohort of patients who had suffered eczema herpeticum, the herpes simplex viral skin infections. They examined a wide variety of demographic, pathologic and biologic characteristics  in 901 subjects, 138 of whom had suffered eczema herpeticum.

They found that eczema patients susceptible to herpes simplex infections had more severe disease, earlier age of disease onset, more frequent history of other allergic diseases such as food allergy, asthma and hay fever, more allergic biomarkers, and more frequent skin infections with other microbes.

"These characteristics associated with eczema herpeticum should help us identify young patients at greater risk for eczema herpeticum so that we can be more vigilant with them and better equipped to prevent this serious complication of eczema," said Dr. Leung.

The greater allergic disease and sensitization, as well as infection by other microbes,  point to a potential mechanism for the increased susceptibility to viral skin infections. An emerging model of eczema highlights the importance of skin-barrier defects and a lack of antimicrobial proteins among eczema patients. The skin-barrier defect is believed to result in the greater allergic sensitization among eczema patients in general. The even higher allergic sensitization among EH patients suggests the skin-barrier defect is particularly acute in those patients.

The higher levels of infections with staphylococcus and other microbes suggests that EH patients may be particularly lacking in antimicrobial proteins.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by National Jewish Medical and Research Center.

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

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

Persons with herpes simplex virus type 2, but without symptoms, still shed virus

ScienceDaily (Apr. 12, 2011) — Persons who have tested positive for herpes simplex virus type 2 (HSV-2) but do not have symptoms or genital lesions still experience virus shedding during subclinical (without clinical manifestations) episodes, suggesting a high risk of transmission from persons with unrecognized HSV-2 infection, according to a study in the April 13 issue of JAMA, a theme issue on infectious disease and immunology.

Anna Wald, M.D., M.P.H., of the University of Washington and Fred Hutchinson Cancer Research Center, Seattle, presented the findings of the study at a JAMA media briefing at the National Press Club in Washington, D.C.

"Herpes simplex virus type 2 is one of the most frequent sexually transmitted infections worldwide, with global estimates of 536 million infected persons and an annual incidence of 23.6 million cases among persons aged 15 to 49 years. In the United States, 16 percent of adults are HSV-2 seropositive, but only 10 percent to 25 percent of persons with HSV-2 infection have recognized genital herpes. Moreover, most HSV-2 infections are acquired from persons without a clinical history of genital herpes," according to background information in the article. Thus, the risk of sexual transmission does not correlate with the recognition of clinical signs and symptoms of HSV-2 but most likely correlates with the activity of the virus on the genital skin or mucosa (viral shedding).

Dr. Wald and colleagues compared the rates and patterns of genital HSV shedding in 498 immunocompetent HSV-2-seropositive persons between March 1992 and April 2008. Each participant obtained daily self-collected swabs of genital secretions for at least 30 days. The rate of viral shedding (the presence of virus that is actively replicating, and can thereby be transmitted to another person) was measured by polymerase chain reaction (testing method for viral DNA) from the swabs.

Among the findings of the researchers, HSV-2 was detected on 4,753 of 23,683 days (20.1 percent) in 410 persons with symptomatic genital HSV-2 infection compared with 519 of 5,070 days (10.2 percent) in 88 persons with asymptomatic infection. Genital HSV was detected at least once in 342 of 410 persons (83.4 percent) with symptomatic HSV-2 infection and in 60 of 88 (68.2 percent) persons with asymptomatic HSV-2 infection during the 2 month study.

Subclinical genital shedding rates were higher in persons with symptomatic infection compared with asymptomatic infection (2,708 of 20,735 [13.1 percent] vs. 434 of 4,929 [8.8 percent]). "However, the median [midpoint] amount of HSV detected during subclinical genital shedding episodes was similar in persons with symptomatic and asymptomatic infection," the authors write.

Persons with symptomatic infection had more frequent genital shedding episodes compared with persons with asymptomatic infection (median 17.9 vs. 12.5 episodes per year). Days with lesions accounted for 2,045 of 4,753 days (43.0 percent) with genital viral shedding among persons with symptomatic genital HSV-2 infection compared with 85 of 519 days (16.4 percent) among persons with asymptomatic infection. This indicates that the bulk of days of shedding in persons with asymptomatic HSV-2 is unrecognized, and people may engage in sexual activity not knowing that they are at risk for transmitting the virus to sexual partners.

"Our findings suggest that 'best practices' management of HSV-2-infected persons who learn that they are infected from serologic testing should include anticipatory guidance with regard to genital symptoms, as well as counseling about the potential for transmission. The issue of infectivity is both a patient management and a public health concern. The primary concern of many HSV-2-seropositive persons is the risk of transmission to sexual partners; in our experience this is the main source of angst in patients with genital herpes."

The researchers note that several methods have been identified that partly reduce the risk of HSV-2 transmission to sexual partners. "Condom use, daily valacyclovir therapy, and disclosure of HSV-2 serostatus each approximately halve the risk of HSV-2 transmission. However, these approaches reach a small portion of the population and have not had an influence on HSV-2 seroprevalence in the last decade. One of the reasons for such a limited effect is that few people are aware of their genital HSV-2 infection, and routine serologic testing, although available commercially, is recommended only in limited settings. We hope that these data will result in further discussions regarding control programs for HSV-2 in the United States."

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

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:

E. Tronstein, C. Johnston, M.-L. Huang, S. Selke, A. Magaret, T. Warren, L. Corey, A. Wald. Genital Shedding of Herpes Simplex Virus Among Symptomatic and Asymptomatic Persons With HSV-2 Infection. JAMA: The Journal of the American Medical Association, 2011; 305 (14): 1441 DOI: 10.1001/jama.2011.420

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

'Stealth' Herpes Simplex Inflammation Impacts Corneal Transplants

ScienceDaily (July 1, 2009) — The herpes simplex virus (HSV) can infect the eye and sometimes causes so much damage that the person's cornea must be replaced with a transplant. (The cornea is the clear covering of the front of the eye that helps focus light for vision.) Doctors knew transplants were more likely to fail in people with HSV than in patients with other disorders, such as keratoconus, an abnormal steepening of the cornea.

This higher failure rate occurred even when HSV infection did not appear to be active in patients. Researchers at the Kellogg Eye Center, University of Michigan, theorized that such patients might have corneal inflammation that could not be detected upon clinical examination but might increase the risk of transplant rejection.

To test this theory, a study led by Victor M. Elner, MD, PhD, examined the corneal tissue, removed during surgery, of 62 Kellogg Eye Center patients (between 1990 and 2000) to identify inflammation biomarkers that might be linked to rejection of transplants. Unlike organ transplants, in corneal procedures the new tissue is placed on a bed of existing tissue. Though HSV had been inactive for six months before surgery in 81 percent of patients, microscopic evidence of inflammation was found in 74 percent, and the transplant failure rate did indeed correlate with the presence of this biomarker. Testing for inflammatory biomarkers will help Eye M.D.s (ophthalmologists) predict whether an HSV patient is likely to reject a transplant.

"It is also possible that treating inflammation intensively before corneal transplant surgery would reduce the risk of rejection," said Dr. Roni M. Shtein, MD, MS, cornea specialist and lead author of the report.

This research is published in The July issue of Ophthalmology.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by American Academy of Ophthalmology, via EurekAlert!, a service of AAAS.

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

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