Recent Studies on Herpes

 

 

(Information and articles included on this page were produced by ScienceDaily.com)

 

 

Genetic Connection To Human Herpes Susceptibility Discovered

 

ScienceDaily (Jan. 31, 2008) — There's a high likelihood that people who are at risk to herpes simplex virus (HSV) outbreaks may have a genetic predisposition to the virus, researchers from University of Utah have discovered in a new study.

 

Researchers have identified an area on the long arm of human chromosome 21 with high odds--at least 1,000-to-1--of being linked to cold sore susceptibility. The researchers further report they identified six specific genes in that chromosomal region as candidates for making people susceptible to outbreaks of cold sores (or "fever blisters"). Cold sores arise when the herpes virus awakens from dormancy within the nerve, resulting in infections in the face lip, or nose.

 

Another contributor to this research study, John D. Kriesel, M.D., and research associate professor in the U School of Medicine's Division of Infectious Diseases (Primary author of this study is Maurine R. Hobbs, Ph.D., research assistant professor in the Division of Endocrinology and Metabolism.) says that this finding may lead to the production of new drugs on the market that decrease the occurrence of herpes outbreaks.

 

"…these genes might make excellent targets…to decrease … herpes outbreaks," Kriesel said.

 

The herpes simplex virus occurs in two forms. Type 1 (HSV-1) is responsible for the vast majority of cold sores—the most common recurring viral infection in humans, as well as herpes keratits, an eye infection that can lead to corneal scarring and blindness. While most of the U.S. population has the HSV-1 virus, millions go undiagnosed due to the lack of symptoms. Even still, about 40 percent of the population will have at least one cold sore during their lives.

 

The second form of the herpes virus is herpes simplex type 2 (HSV-2). This virus is the major cause of genital herpes, and infects about 17 percent of the U.S. population or approximately 50 million people. There are between 5 million and 10 million people in this group with identified cases of HSV-2.

 

To detect cold sore susceptibility genes, U researchers traced genetic markers in families to determine areas on chromosomes that harbor disease genes. This process is called linkage analysis. When genetic mutations are transmitted from parent to offspring, genetic markers near the disease gene are also transmitted. By detecting markers shared among family members, researchers can identify areas of chromosomes where genes that are responsible for disease may lie. The U of U study set a precedent because it was the first whole-genome study of the herpes simplex virus to employ linkage analysis to determine susceptibility genes.

 

Researchers used a pool of 421 people from 39 large Utah families as their test subjects in a genomic study known as the Utah Genetic Reference Project. Researchers categorized subjects according to how often they experienced cold sore outbreaks:

 

    * Frequently affected--HSV-1 infected and two or more outbreaks annually (89 participants)

    * Mildly affected--HSV-1 infected and two or less outbreaks annually (111)

    * Unaffected--HSV-1 infected but had never experienced an outbreak (85)

    * Unknown or HSV uninfected--could not be categorized (146)

 

The researchers compared the "recurrently affected" and "unaffected" groups (both proven to be HSV-1 infected) to illustrate the greatest possible distinction of outbreak occurrences. Subjects who couldn't be categorized were excluded from the study, as well as the 111 mildly affected people. Upon collection of all genetic data, a mathematical analysis concluded the probability of a relationship between cold sores and the long arm of chromosome 21 to have at least a 1000:1 ratio.

 

The likely genetic relationship is not the sole factor thought to be responsible for reactivation of HSV and cold sores. Environmental factors, i.e. fever, wind, and sunburn, also are believed to contribute to the virus. Viral factors, like strain and burden of dormant infection, are also believed to trigger HSV outbreak occurrences.

 

To be sure the study was unbiased, researchers began with no preconceived notions about which areas of the human genome may be related to cold sore susceptibility. Therefore, the relationship with the long arm of chromosome 21 was truly a new finding. "We didn't start with the thought … [which] helped ensure an unbiased study..." Kriesel said.

 

Now Kriesel, Hobbs, and other researchers are examining the six possible susceptibility genes to determine which ones are linked to cold sores. The group believes they will find that three of the genes will prove related in future studies.

 

"…a …target to reduce … cold sores would… expand our study results to include genital herpes or herpes keratitis," Kriesel said.

 

The full report of this research is now available on the Journal of Infectious Diseases web site and will be published in the Feb 1 print edition.

 

In addition to Kriesel and Hobbs, co-authors of this research project are Mark F. Leppert, Ph.D., distinguished professor and co-chair of the Department of Human Genetics; Brandt B. Jones (B.S., senior research scientist), Division of Infectious Diseases; and Brith E.M. Otterud (B.S., computer professional), Department of Human Genetics.

 

 

(Adapted by ScienceDaily.com from materials provided by University of Utah Health Sciences)

 

 

Anti-viral medicines can decrease Ceasarian sections for women who have herpes virus

 

ScienceDaily (Jul. 10, 2006) — Administering anti-viral medication to pregnant women who have genital herpes significantly decreases the necessity of Caesarean sections—which are often needed to protect the infant from contracting the virus, a recent UT Southwestern Medical Center study found.

 

The UT Southwestern study, which appears in this month's issue of the journal Obstetrics and Gynecology, is the first large-scale proof that the drug valacyclovir hydrochloride (Valtrex) is effective in the final month of pregnancy.

 

"…this will help…in [providing] stronger evidence in using this treatment," said Dr. Jeanne Sheffield, who is the chief author of this study and assistant professor of obstetrics and gynecology at UT Southwestern. "[IN addition to] reducing…herpes outbreaks at birth…numbers of women without symptoms who were shedding the virus into the birth canal [were also deacresed]."

 

Herpes is characterized by an initial outbreak of genital sores, followed by months or years of inactivity and is recognized as one of the most common sexually transmitted infections. While it is incurable, the frequency and intensity of outbreaks can be decreased through use of proper medication. Due to periods of outbreak inactivity and lack of symptoms, many people, including women who are in the reproductive age, may not know they are infected with the herpes virus.

 

In some rare documented cases, infants have been found to contract the herpes simplex virus from the mother’s birth canal or genital area during birth, even when the mother is asymptomatic—or not currently experiencing an outbreak. Medical protocol for these instances is to recommend C-sections to women with active genital herpes lesions at the time of delivery. However, researchers found that 70 percent of neonatal herpes cases occur in newborns of women who shed the virus near delivery during a latent outbreak period.

 

"This study [attempted to] reduce … genital herpes lesions…to [prohibit] neonatal herpes," Dr. Sheffield said.

 

To conduct this study, The UT Southwestern research team used 338 pregnant women who had a history of genital herpes, in a randomized, double-blind trial—where both the doctors and women being studied were unaware of who was receiving medication.

 

Because of active herpes lesions, 28 of the women in this study underwent C-sections. Seven of the 170 women in the valacyclovir group (or 4 percent) had C-sections, while 21 of the 168 women in the placebo group (13 percent) had C-sections. The 69 percent decrease in the occurrence of the clinical herpes simplex virus at the time of birth was statistically noteworthy, the researchers reported.

 

No infants in either group contracted herpes at birth. Nor were there any variations in delivery complications between either group found in this study.

 

"This… [is] a well-designed study … to help [increase] confidence in the efficacy and safety of anti-viral suppression in late pregnancy," said Dr. George Wendel, professor of obstetrics and gynecology and senior research contributor.

 

In addition to Dr. Wendel, other UT Southwestern researchers who helped in facilitating this study were Dr. Vanessa Laibl, assistant professor of obstetrics and gynecology; Dr. Scott Roberts, associate professor of obstetrics and gynecology; and Dr. Pablo Sanchez, professor of pediatrics.

 

This research study was supported in part by GlaxoSmithKline.

 

Adapted by ScienceDaily.com from materials provided by UT Southwestern Medical Center, via EurekAlert!, a service of AAAS.

 

 

In Last 20 Years, Herpes Instances Increased 30%

 

(March 1, 1998) - The frequency of genital herpes in the U.S. over the last 20 years has increased according to The Centers for Disease Control and Prevention. This means that roughly 45 million people in the U.S. are seropositive for the most common cause of genital herpes, herpes simplex virus HSV-2, which amounts to about one in five people over the age of 12 who are infected with HSV-2.

 

The only 10% effective way to avoid contracting HSV-2 is abstinence. Many people who have genital herpes say that they abstain from sex during outbreaks because the genital ulcers that signal an outbreak can be painful, thus resulting in painful sex. Other couples abstain from sex to avoid transmitting herpes to their mates.

 

"[It’s common to believe that] since there is more virus present on the genitalia during an outbreak than between outbreaks. Yet, if …genital herpes was really a reliable method to prevent transmission, then why do so many people have genital herpes?" This query was posed today at the American Academy of Dermatology's 56th Annual Meeting in Orlando, by Stephen K. Tyring, MD, PhD, Professor of Dermatology, University of Texas Medical Branch, Galveston.

 

Herpes simplex virus (HSV) can be found on the genitalia even when no indicators are present.

 

Even the most careful couples may transmit HSV when there is no sign of an outbreak. This is known as asymptomatic viral shedding, which has been proven to be the cause of at least 80% of HSV transmissions.

 

Using condoms is another way people may try to prevent herpes transmission. But according to Dr. Tyring, "…condoms do reduce the risk of transmission of genital herpes…However…condoms can slip and/or break. In addition, condoms can only protect the skin that they cover. Many cases of herpes…can be transmitted to/from skin not covered..."

 

Most people who are seropositive for genital herpes never have a clinically identified outbreak. However, these people may still occasionally shed the virus and thus, transmit the disease. Even with condom use and abstaining from sex, the possibility of passing genital herpes to an uninfected partner has been estimated at 10% per year. The chance of a male passing HSV-2 to his female partner is much greater than vice versa. Actually, per year, a female’s likelihood of transmitting HSV-2 is about 30%.

 

Why is it necessary to study developments in the prevention and treatment of HSV-2 if there are little to no signs of it? "…the person who acquires [it]… suffers more severe and more frequent outbreaks than did the persons from whom they acquired genital herpes… If he passes it to his wife, she may suffer painful genital ulcers...The worst scenario [occurs] if she were to acquire HSV-2 during pregnancy... Another reason … is that genital ulcers facilitate … HIV…" Dr. Tyring said.

 

Two new techniques are being evaluated to determine their viability in decreasing instances of HSV-2: vaccinating the person at risk; or using antiviral medicines to decrease outbreaks and asymptomatic viral shedding in the person who already has HSV-2.

 

Studies are still being performed to verify viability of the vaccination method. Today there are vaccines for prevention of 14 viral diseases. Vaccines to prevent genital herpes are not produced from the herpes virus; they are copies of proteins on the surface of the virus. Therefore, it is not possible for a person to become infected if given the vaccination. "In fact,” Dr. Tyring said, “more than 10,000 people have received the vaccine... What remains unknown is whether [it] actually protects a person from being infected...”

 

People who have been vaccinated must undergo periodic blood tests for two years to find out if the amount of antibodies to HSV-2 remains high. Perhaps the best benefit to receiving the vaccine is that patients who receive it aid physicians in comparing their whether their rate of transmission against the rate of transmission of those who didn’t receive the HSV-2 vaccination.

 

Research is underway to determine if HSV-2 patients who receive daily treatments of antiviral medicine can lower the chance of giving HSV-2 to partners who do not have the virus. Three antiviral drugs are on the market to treat or decrease instances of outbreaks of genital herpes: acyclovir, famciclovir and valacyclovir. Taking one of these drugs daily has been shown to prevent outbreaks. Also, a daily treatment of the drug acyclovir has a 95% success rate of decreasing asymptomatic viral shedding.

 

As for valacyclovir and famciclovir, they are believed to also aid in decreased asymptomatic viral shedding. Since one daily dose of valacyclovir prevents clinical outbreaks in most HSV-2 patients and is assumed to have a significant effect on decreasing asymptomatic viral shedding, it may also aid in the prevention of transmission to the uninfected people. In addition to these three drugs, researchers are also seeking other methods of prevention.

 

Boasting more than 10,000 members worldwide, The American Academy of Dermatology is the world's biggest physicians’ organization.

 

Information in this report has been adapted by ScienceDaily.com from information supplied by American Academy Of Dermatology.

 

New information about HSV-2 Vaccinations

 

Research done by Montana State University poses a new possibility in the development of a vaccination for HSV-2 and other diseases that are related to the herpes simplex virus.

 

 

MSU virologist William Halford found that mice vaccinated with a live, genetically-altered strain of HSV-1 showed no signs of disease 30 days after being subjected to a lethal "wild-type" strain of the virus. His findings were published earlier this year in the Virology Journal.

 

However, Halford found that, a second group of mice to whom he administered a more common vaccine died within six days of being subjected to the identical lethal "wild-type" strain as the first group.

 

Halford, who works in MSU's Department of Veterinary Molecular Biology, said, "[There is] a clear roadmap for a live vaccine … my studies were performed with HSV-1, [but] the implications for HSV-2-induced genital herpes are clear. Overall the …viruses are…[genetic equivalents]."

 

About 55 million people in the U.S. have HSV-2. Genital herpes is incurable, which means that the infection is life-long. Roughly 5% of those with genital herpes – 2 to 3 million people in the U.S. – experience genital herpes outbreaks one to four times a year. There is no vaccine that provides life-long protection from genital herpes.

 

The foundation of Halford's research was a deep knowledge of how the herpes simplex virus attacks the body's natural defenses against the virus.

 

A herpes simplex infected cell alerts neighboring cells in the body in a process called an interferon response, which triggers neighboring cells to go into "an anti-viral state" which is the equivalent of putting on a suit of armor to defend themselves from herpes.

 

However, the herpes virus makes a protein known as, ICP0 that essentially “fools” each herpes-infected cell into destroying its own defenses. With the cells’ armor destroyed, the virus can multiply and begin attacking neighboring cells and this cycle continues throughout the cells of the body.

 

In his experiment, Halford made a vaccine that interrupted the genetic instructions that create the ICP0 protein. When these instructions were inhibited, the virus could still infect the mice, but the spread of the herpes virus to other cells is prohibited before disease has a chance to be spread.

 

Halford shows that "…we can disarm the virus [and make it] unable to cause disease, [while being a viable] …a vaccine.”

 

In humans, we would take out the genetic instructions for ICP0 just like in Halford’s mouse experiment, which would create an "attenuated," or weakened virus. The remainder of the herpes simplex virus' genetic code would remain intact. Other vaccines that are produced from weakened viruses include measles, mumps, rubella, polio and yellow fever.

 

The latest research in this area, however, has focused primarily on subunit vaccines--vaccines created from one part of a virus. Subunit vaccines carry less risk than attenuated virus vaccines because it is impossible for a subunit to replicate or cause disease. But, unfortunately, subunit vaccines do not protect against chronic viruses like genital herpes and AIDS, Halford said.

 

"[Theoretically] subunit vaccines are poor … natural virus infection," Halford said. "There's not enough… to build a protective response..."

 

Halford, who is 38, knows that critics view his stance on the herpes virus as controversial.

 

"… I'm young .. I don't know how long it can take to [influence] scientists and clinicians," he said. "I …hope that … the scientific community would …consider these proposals."

 

To perform further research on a human herpes vaccination, Halford is seeking a commercial partner or secure government funding. "I'd like to take this concept … to the clinics," he said.

 

Montana State University (2006, October 16). Research Holds Promise For Herpes Vaccine. ScienceDaily. Retrieved March 20, 2008, from http://www.sciencedaily.com– /releases/2006/10/061013201826.htm

 

Herb Fights Herpes: Introducing Prunella Vulgaris

 

ScienceDaily (May 20, 2003) — WASHINGTON, DC – May 19, 2003 – A new anti-herpes agent derived from a common herb has proven successful in treatment and prevention of herpes in animals. Dalhousie University (Nova Scotia) researchers will reveal their findings at the 103rd General Meeting of the American Society for Microbiology.

 

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According to researcher, Song Lee, "Prunella vulgaris…a perennial plant commonly found in China, the British Isles, Europe, and North America … described as a hot water infusion to treat sores in the mouth and throat, an astringent for internal and external purposes, as a crude anti-cancer drug, and as an herbal remedy…”

 

Lee and his team took a lignin-carbohydrate compound from the prunella vulgaris plant, and incorporated it into a topical cream. This cream was tested on mice and guinea pigs that carried experimental HSV-1 and HSV-2. Guinea pigs that received the lignin-carbohydrate complex cream treatment showed a significant decrease in skin lesions compared to those that received no treatment with the cream. These mice also displayed a noticeable increase in survival rate in comparison to the animals that did not undergo treatment with the cream.

 

"The anti-HSV compound from P. vulgaris is a…complex with potent activity against HSV-1 and HSV-2 ...different…than acyclovir, the current… drug," says Lee. "Given … the emergence of acyclovir-resistant strains of herpes viruses, the Prunella … may … be a… new anti-herpes [treatment]."

 

Adapted by ScienceDaily.com from information gathered from the American Society For Microbiology.

 

American Society For Microbiology (2003, May 20). New Herpes Treatment From Common Herb. ScienceDaily. Retrieved March 20, 2008, from http://www.sciencedaily.com– /releases/2003/05/030520083354.htm

 

The Latest on Herpes Vaccination

 

ScienceDaily (Jan. 6, 2005) — Researchers from the National Institutes of Health and Harvard Medical School believe that an effective herpes vaccine may be ready to be tested in human trials. Futher details of their research will be published in the Journal of Virology’s January 2005 edition.

 

HSV-2 infects about 22% of adults in the U.S. It carries with it physical, psychological, and social effects for people who contract it, and can create an even more serious risk for immuno-compromised patients which fuels the necessity to develop a vaccine.

 

Researchers acknowledge, “… the burden of …herpes has made development of more effective prevention strategies a …priority.”

 

In this study, 3 vaccines were observed, a DNA vaccine, an antigenic vaccine and a live mutant strain of HSV-2, d15-29, in mice and guinea pigs. The live mutant strain, d15-29, indicated little risk of triggering disease due to the fact that it lacks two of the genes necessary for it to multiply and it triggered a more powerful immune response in both animals.

 

“Given … its defectiveness for latency, and…ability to induce rapid … cell responses, … dl5-29 ..may be good …for early-phase human trials,” it’s believed.

 

(Y. Hoshino, S.K. Dalai, K. Wang, L. Pesnicak, T.Y. Lau, D.M. Knipe, J.I. Cohen, S.E. Straus. 2004. Comparative efficacy and immunogenicity of replication-defective, recombinant glycoprotein, and DNA vaccines for herpes simplex virus 2 infections in mice and guinea pigs. Journal of Virology, 79. 1: 410-418.)

 

Adapted by ScienceDaily from information gathered from American Society For Microbiology.

American Society For Microbiology (2005, January 6). New Herpes Vaccine May Be Ready For Human Trials. ScienceDaily. Retrieved March 20, 2008, from http://www.sciencedaily.com– /releases/2005/01/050104112342.htm

 

New Evidence Suggests Possible Link Between Herpes And Alzheimer’s

 

ScienceDaily (May 12, 2000) — Could Lead to New Treatments Targeting the Herpes Virus

 

Researchers have long believed that there was a relationship between herpes and Alzheimer’s. Now, a new study may shed new light on this belief and lead to production of a vaccine to prevent the disease or new medication to treat it.  Biochemistry, a peer-reviewed publication of the American Chemical Society and the world’s largest scientific society will publish the findings in its May 16 edition.

 

Researchers at the University of California, Irvine, indicated that an artificial protein that is comparable to HSV-1 mimics the makeup and behavior of a protein called beta-amyloid, a toxic agent that has been found to settle in the brains of people who suffer from Alzheimer’s.

 

Genetic sequencing determined that two-thirds of a portion of the viral protein is an exact replica of the beta-amyloid protein. The research found that, like beta-amyloid, it could destroy brain neurons, a main factor in the development of Alzheimer’s. In fact, in laboratory tests, the viral protein produced abnormal twisted fibers similar to those we see in the brains of people who suffer from Alzheimer’s — the trademark of the Alzheimer’s disease.

 

There are two main forms of herpes. Most people contract HSV-1, which causes cold sores, during childhood from non-sexual contacts. While HSV-2, commonly called genital herpes, is contracted through sexual activities.

 

“What’s unique … is that it [shows] a way … herpes can act,” says Frank M. LaFerla, Ph.D., chief investigator of this research and an assistant professor in the university’s Department of Neurobiology and Behavior. LaFerla is also associate director of the university's Institute for Brain Aging and Dementia.

 

Having HSV-1 is not a guaranteed indicator that a person will develop Alzheimer’s. LaFerla expounds on this apparent inconsistency by calling our attention to recent studies that indicate that people with a family history of Alzheimer’s are more susceptible to it if they are exposed to HSV-1.

 

Herpes is one of a growing number of indicators believed to increase risk of Alzheimer’s— a form of dementia that primarily affects the elderly that has no cure and whose scope has not been fully understood by the medical community. In roughly 10% of Alzheimer’s cases there is a genetic history of the disease. President Reagan, whose mother had Alzheimer’s, also had the disease.

 

Research suggests that there are various factors that contribute to most instances of Alzheimer’s. While genetic predisposition has been proven, stress, prior head injury, and an abnormal concentration of metals in the brain are also potential indicators.

 

“..Researchers will … find new factors associated with Alzheimer’s…” predicts LaFerla.

 

The study was created with the support of the National Institute on Aging, the Alzheimer's Association, and the state of California.

 

Adapted by ScienceDaily.com from information gathered from American Chemical Society.

American Chemical Society (2000, May 12). New Evidence Found Linking Herpes And Alzheimer’s. ScienceDaily. Retrieved March 20, 2008, from http://www.sciencedaily.com– /releases/2000/05/000512083302.htm

 

THC Found to be Prohibitive to Cancer-Causing Herpes Viruses

 

ScienceDaily (Sep. 24, 2004) — Tampa, FL (Sept. 22, 2004) -- Delta-9 tetrahydrocannbinol more commonly known as THC found in marijuana, may prohibit the spread of several types of cancer-causing herpes viruses, University of South Florida College of Medicine research suggests. This research, published Sept. 15 in the BMC Medicine online journal, could lead to the development of antiviral medicine created from non-psychoactive derivatives of THC.

 

The gamma herpes viruses include Kaposi's Sarcoma Associated Herpes virus, which is associated with an increased risk of cancer that is particularly prevalent in AIDS sufferers. Another is Epstein-Barr virus, which predisposes infected individuals to cancers such as Burkitt's lymphoma and Hodgkin's disease.

 

Once someone is infected, these viruses can lie in a state of dormancy inside white blood cells for long periods of time before they are released and begin multiplying. This reactivation increases the amount of infected cells, which in turn increases the risk that the cells will become cancerous.

 

Virologist Peter Medveczky, MD who led the study, found that if infected cells were grown with THC present, this reactivation did not occur. While cells that had a mouse gamma herpes virus normally died when the virus was reactivated, they survived when cultured in the lab alongside the cannabinoid compound – which further supports the suggestion that THC may prevent viral outbreaks.

 

Also, the research found that THC reacts only on gamma herpes viruses. THC did not affect HSV-1, which causes cold sores and genital herpes.

 

“… THC [was] found to be stronger and [more] selective…than … acyclovir, gancicyclovir and foscamet,” said Dr. Medveczky, a professor in the Department of Medical Microbiology and Immunology.

 

USF researchers propose that THC reduces the spread of gamma herpes viruses by targeting ORF50, a common gene on these viruses.

 

Dr. Medveczky stressed that more studies must be conducted to verify findings. "We have not evaluated … THC in an animal model … we do not recommend [its use to humans]."

 

“Moreover,” Dr. Meveczky said, “THC has also been known to suppress the immune system so smoking marijuana could "do more harm than good" to patients whose immune systems are often already weakened.”

 

Adapted by ScienceDaily.com from information gathered by University Of South Florida Health Sciences Center.

 

University Of South Florida Health Sciences Center (2004, September 24). Cannabis May Help Combat Cancer-causing Herpes Viruses. ScienceDaily. Retrieved March 20, 2008, from http://www.sciencedaily.com– /releases/2004/09/040923092627.htm

 

Oral and Vaginal Sex Indicate Higher Herpes Infection Rates, Recent Research Reveals

 

ScienceDaily (Mar. 12, 2005) — PITTSBURGH, Feb. 28 – The first clinical research conducted to determine the likelihood of contracting HSV-1 based on studying sexual activity has found a connection between oral sex and vaginal intercourse with an evidently higher infection rate, especially in young women, University of Pittsburgh researchers reported in the February edition of Sexually Transmitted Diseases, the journal of the American Sexually Transmitted Diseases Association.

 

HSV-2 is one of the most common STDs in America. Across the nation, at least 45 million people over the age of 12  (one out of five adolescents and adults) have genital herpes. Between the late 1970s and the early 1990s, the amount of people in the U.S. who had HSV-2 increased by 30%, the U.S. Centers for Disease Control and Prevention reported. There is no cure, but antiviral drugs have been proven to decrease and prevent outbreaks. Also, daily practice of suppressive therapy can decrease, but not remove, the chance of passing the virus to sexual partners who do not have it.

 

It is protocol to teach medical students that HSV-1 is most common above the waist, while HSV-2 occurs below the waist. There is new evidence, however, that HSV-1 also is a key pathogen in genital herpes, especially in younger women. HSV-1 is traditionally known to infect the mouth and lips, as evident by fever blisters or cold sores. Viral shedding and contracting the virus can occur even when there is no sign of an outbreak.

 

"[Oral and vaginal sex] were … significant risk factors for ... HSV-1," said Thomas Cherpes, M.D., an infectious diseases fellow at the University of Pittsburgh School of Medicine and the study's first author. "… HSV-1 infections are less frequent in childhood and adolescence, future prevention strategies [must] consider increased susceptibility for HSV-1 among young adults … to the growing genital herpes epidemic."

 

Between 1998 and 2000, 1207 non-pregnant women from the ages of 18 to 30 were admitted to three Pittsburgh health clinics. Participants were instructed to return for three follow-up visits at four-month intervals. During each study visit, blood samples were tested for HSV-1 and HSV-2-specific antibodies.  Researchers also administered sexual behavior surveys and collected demographic information from participants.

 

At first, HSV-1 was detected in 38% of women aged 20 or younger. During the follow-up period, however, analysis found that females who participated in vaginal intercourse had more than six times higher risk of transmitting HSV-1 than women who did not engage in sexual activity, or 6.8 compared to 1.2 cases. For women who only engaged in receptive oral sex and abstained from vaginal intercourse, the study revealed the risk was even greater – 9.8 compared to 1.2 cases.

 

"[This] …is consistent with other research indicating a reduction in HSV-1 [in] younger people," said Sharon Hillier, Ph.D., professor in the departments of obstetrics, gynecology and reproductive sciences and molecular genetics and biochemistry at the University of Pittsburgh School of Medicine and the study's chief author. "… a significant number of young adults are [vulnerable] to oral or genital HSV-1..."

 

This is significant because most of the new studies being conducted on vaccine development for genital herpes only researches HSV-2, Dr. Hillier said. Dr. Hillier is also is a chief investigator at the Magee-Women’s Research Institute.

 

The evident decrease in childhood HSV-1 cases confounds the situation because it leaves more young people at risk of contracting a genital infection of HSV-1, Dr. Cherpes believes, especially with surveys indicating higher rates sexual activities, which increases the risk.

 

"[Recurrence]…among sexually active women is 75 percent," he said. "In our group, more than 90 percent of …participants reported a history...."

 

Both Dr. Cherpes and Dr. Hillier believe that subsequent vaccine development initiative must deal with HSV-1 targets in order to decrease occurrences.

 

###

 

In addition to Drs. Cherpes and Hillier, Leslie A. Meyn, M.S., Magee-Womens Research Institute, contributed to the study, which was funded by the National Institutes of Health.

 

Adapted by ScienceDaily.com from materials gathered from  University Of Pittsburgh Medical Center.

 

University Of Pittsburgh Medical Center (2005, March 12). Risk Of Herpes Infection Rises With Oral Sex. ScienceDaily. Retrieved March 20, 2008, from http://www.sciencedaily.com– /releases/2005/03/050308100931.htm

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