Genital Herpes 101

Genital herpes is an incredibly contagious sexually transmitted diseases, one spread through skin-to-skin contact that affects one in five adults in the United States — about 45 million people in all.

Herpes infects as many as one million new patients each year. It is viral in nature, caused by the herpes simplex viruses (HSV) type 1 and type 2. Most genital herpes results from HSV type 2.

Genital Herpes Transmission and Symptoms

The herpes virus infects people by passing through a break in the skin during vaginal, oral sex, or anal sex. These tiny skin breaks are caused by typical levels of friction during sex and are not visible to the naked eye. HSV also can enter the body through the moist membranes of the sexual organs, urinary opening, cervix, or anus. The virus can be transmitted even if the infected person has no blisters, sores, or other visible signs of an outbreak. However, there is no evidence that it can be picked up through contact with a toilet seat, hot tub, or other objects.

Genital herpes can be transmitted to other parts of the body, including the lips, tongue, gums, eyes, and fingers. For example, during oral sex, herpes can pass from the genitals to the mouth, and vice versa. Infection can also occur if a person touches a herpes sore and then rubs or scratches another part of the body.

Many people who are infected with genital herpes show no symptoms most of the time, and may not even be aware they are infected. When symptoms do occur, they vary from mild to severe depending on the person.

Symptoms of a genital herpes outbreak can include:

Blisters on or around the genitals or rectum. When the blisters break, they leave behind tender ulcers that may take two to four weeks to heal.Pain, itching, and burning in the genital area.Vaginal discharge.Flu-like symptoms, including fever, headache, muscle aches, and swollen glands.

The first outbreak usually occurs within two weeks after transmission. After the first outbreak, most people will have four or five more outbreaks within the year. The outbreaks of blisters occur less frequently over time.

HPV and Cervical Cancer

Diagnosing Genital Herpes

Doctors often can diagnose genital herpes by looking for physical signs of an outbreak and using a swab to take a sample from any open sores. Blood tests designed to find herpes antibodies — released by the immune system to fight the virus — can be used to verify infection during times between outbreaks, when the virus is dormant.

Treatment for Genital Herpes

There is no cure for genital herpes. Once infected, patients will have the virus in their bodies for the rest of their lives, regardless of whether they ever experience outbreaks. Prescription drugs are available that can shorten outbreaks, decrease their severity, or keep them from happening at all.

These drugs include:

8 Ways to Prevent HPV

Preventing Genital Herpes

During a herpes outbreak, patients can stay more comfortable and prevent transmission of the virus to other parts of their body or other people by:

Keeping the sores clean and drySteering clear of any contact with the soresWashing their hands after any contact with soresAvoiding any sexual activity until the sores have completely healed

In between outbreaks, the herpes carrier should always practice safe sex to avoid transmitting the virus to other people. The person with herpes should use a condom during sex. Drugs like Valtrex also can decrease the risk of transmission, but they are no substitute for the protection provided by condoms.

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NIH launches trial of investigational genital herpes vaccine

Researchers have launched an early-stage clinical trial of an investigational vaccine designed to prevent genital herpes disease. The National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, is sponsoring the Phase I trial, which is being conducted at the NIH Clinical Center in Bethesda, Md.

Genital herpes is one of the most common sexually transmitted infections in the United States. Most genital herpes cases are caused by infection with herpes simplex virus type 2 (HSV-2); however, herpes simplex virus type 1 (HSV-1) can also cause genital herpes. An estimated 776,000 people in the United States are infected with HSV-2 or HSV-1 each year. There is no vaccine to prevent genital herpes.

“Although genital herpes is treatable, it is a lifelong infection that can exact a substantial psychological and physical toll on infected individuals and places them at higher risk of acquiring HIV,” said NIAID Director Anthony S. Fauci, M.D. “Furthermore, mothers with active genital herpes infection at time of delivery can transmit the virus to their newborns, which can lead to severe illness and death.”

“A protective vaccine would help to reduce significantly the spread of this all-too- common sexually transmitted infection,” Fauci added.

Led by principal investigator Lesia K. Dropulic, M.D., of NIAID’s Laboratory of Infectious Diseases, the trial will test an investigational HSV-2 vaccine candidate, called HSV529, for safety and the ability to generate an immune system response. The investigational vaccine manufactured by Sanofi Pasteur was developed by David Knipe, Ph.D., professor of microbiology and immunobiology at Harvard Medical School, Boston.

Preclinical testing of the candidate vaccine involved a 10-year collaborative effort between Dr. Knipe and Jeffrey Cohen, M.D., chief of NIAID’s Laboratory of Infectious Diseases.  The experimental product is a replication-defective vaccine, meaning that scientists have removed two key proteins from the vaccine virus so that it cannot multiply to cause genital herpes.

The clinical trial is expected to enroll 60 adults ages 18 to 40, who will be divided into three groups of 20 participants each. The first group will be of people who have been previously infected with HSV-2 and HSV-1 or solely with HSV-2; the second will have individuals who had been infected with HSV-1 only; and the third will consist of those who have not been  infected with HSV-1 or HSV-2. The investigational vaccine is being tested among study participants who have previously been infected with HSV to determine if it may pose any safety issues.

Within each of the three groups, researchers will randomly assign participants to receive three doses (0.5 milliliters each) of the investigational HSV529 vaccine (15 participants) or a saline-based placebo vaccine (five participants). The three vaccinations will occur at study enrollment and again one month and six months later. Participant safety will be monitored throughout the course of the trial, and researchers will follow participants for six months after they have received their last dose of vaccine. Blood samples will be used to evaluate the candidate vaccine’s ability to stimulate immune system responses to HSV-2, including production of virus-specific antibodies and T-cell responses. The study is expected to be completed by October 2016.

HSV-2 is generally transmitted through sexual contact and can spread even when the infected individual shows no symptoms. Although HSV-1 commonly infects the mouth and lips, it can also cause genital herpes. Once in the body, HSV migrates to nerve cells and remains there permanently, where it can reactivate to cause painful sores and blisters.

For more information about this clinical trial, see http://www.ClinicalTrials.gov using the identifier NCT01915212.

NIAID conducts and supports research—at NIH, throughout the United States, and worldwide—to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIH...Turning Discovery Into Health®

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Genital Herpes May Never Go Dormant

By Jennifer Thomas
HealthDay Reporter

WEDNESDAY, Nov. 18 (HealthDay News) -- Herpes, the sexually transmitted disease that causes genital lesions, never truly goes into a dormant state, new research suggests.

As a matter of fact, even when it's not causing an outbreak, the virus is shedding tiny bits of itself in the genital tract.

While the study did not specifically address whether or not the very small amounts of virus being continually shed are enough to infect someone else, the findings have the potential to change the way in which scientists view the life cycle of the disease.

The herpes virus is believed to hide out in the neurons around the spine during latent periods, then periodically travel down neurons that end in the genital tract, where it infects the skin cells, causing a lesion.

The accepted view is that the virus was largely inactive during latent periods, said study author Dr. Joshua Schiffer, a senior fellow at the University of Washington in Seattle.

"We've known for many years that herpes maintains a latent state in the nerves around the spinal cord. In effect, it hibernates there," Schiffer said. "The older idea was that it didn't do much while it was there ... But what our model suggests is the virus is continually being released from the neurons."

The study appears in the Nov. 18 issue of Science Translational Medicine.

The study looked at herpes simplex 2 virus, not herpes simplex 1 virus, which causes cold sores or fever blisters, though it can also cause genital lesions. Schiffer said he suspected the findings would hold true for herpes simplex 1 as well, though previous studies suggest herpes simplex 1 may shed less often.

Schiffer and his colleagues used data from two previous studies. In the first, participants swabbed their genitals every day during an outbreak and until their lesions went away. In the second, patients swabbed their genitals four times a day for 60 days, even when they were asymptomatic.

The data was then put into a mathematical model to determine the probable rate of shedding. According to the study, 85% of shedding episodes were asymptomatic, or did not cause a lesion. About 60% lasted less than 12 hours.

About 45 million Americans, or one in five over the age of 12, are infected with the genital herpes virus in the United States, according to the U.S. Centers for Disease Control and Prevention. But many of them aren't aware they are infected because they've never had, or have never been aware of, their lesions. "Within their skin there is this constant battle going on within the virus and the immune system," Schiffer explained.

Typically, patients are counseled to avoid having sex during an outbreak and to use a condom to prevent transmission when they are not having symptoms.

Antiviral drugs available, including acyclovir, valacyclovir and famciclovir, can control many, but not all, outbreaks, Schiffer said.

Nancy Sawtell, a researcher in the division of infectious diseases at Cincinnati Children's Hospital Medical Center, said the study opens up new avenues for research. But it's too soon to suggest that low levels of viral DNA necessarily mean a person can still infect another.

She noted that the researchers tested for viral DNA, which is only a portion of the virus and doesn't in and of itself mean a person is infectious. "The presence of viral DNA does mean you are infected, but it doesn't necessarily mean you have an infectious particle there," Sawtell said.

Secondly, because the neurons themselves were not examined, it's possible the viral DNA that's present could have originated from somewhere else in the body. Previous animal studies have shown herpes does indeed go into an inactive state.

"It would be really nice to be able to look at the neurons in this human model to determine that the virus is coming from the spine, and wasn't just present in the genitalia and missed by an earlier swab," Sawtell said.

Couples trying to avoid infecting one partner should continue to take the same precautions they did prior to the study, including using condoms even when asymptomatic.

"I wouldn't panic over it," Sawtell said. "We have a lot to learn about how infectious these low levels of viral DNA actually are."

Copyright © 2009 ScoutNews, LLC. All rights reserved. SOURCES: Joshua Schiffer, M.D., research associate, Fred Hutchinson Cancer Research Center, and senior fellow, University of Washington, Seattle; Nancy Sawtell, Ph.D., researcher, division of infectious diseases, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Nov. 18, 2009, Science Translational Medicine

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Agenus genital herpes vaccine succeeds in mid-stage trial

n">(Reuters) - Agenus Inc said a trial of its experimental genital herpes vaccine reduced the rate at which patients released the virus, reducing the likelihood of infecting others, sending its shares up 32 percent in premarket trading.

The 15 percent reduction in the release of the virus by patients receiving the vaccine in a mid-stage trial compared to those on a placebo, who showed no reduction.

The vaccine, HerpV, also reduced the severity of the infection by 34 percent.

The mid-stage trial had 80 patients with a history of 1-9 herpes recurrences within the prior 12 months. Of them, 70 received the vaccine and 10 received placebo, Agenus said in a statement.

HerpV, being developed as an "off-the-shelf" vaccine, contains Agenus's QS-21 Stimulon adjuvant that boosts specific immune responses.

The trial tested the efficacy of the vaccine by measuring the release of the virus by patients 45 days before and after three injections of HerpV. A majority of the patients also received a booster injection, given 6 months after the first vaccination.

Genital herpes, a highly contagious sexually transmitted infection, is usually caused by the herpes simplex virus (HSV). There are two types of HSV and Agenus's vaccine targets HSV type 2, which most often causes genital herpes.

According to the U.S. Centers for Disease Control and Prevention, 776,000 people in the United States get new herpes infections annually and one out of six people aged 14 to 49 years has genital HSV-2 infection.

Agenus said it expected more data in the first half of 2014, showing how the patients fared after the booster shots.

The company's partners are also testing the QS-21 Stimulon adjuvant in combination with other vaccines.

Agenus shares were up at $3.16 in trading before the bell. The stock closed at $2.40 on Wednesday on the Nasdaq.

(Reporting by Esha Dey in Bangalore; Editing by Saumyadeb Chakrabarty and Kirti Pandey)

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HerpV: Genital Herpes Vaccine Shows Promise

Nov 7 (Reuters) - Agenus Inc said a trial of its experimental genital herpes vaccine reduced the rate at which patients released the virus, reducing the likelihood of infecting others, sending its shares up 32 percent in premarket trading.

The 15 percent reduction in the release of the virus by patients receiving the vaccine in a mid-stage trial compared to those on a placebo, who showed no reduction.

The vaccine, HerpV, also reduced the severity of the infection by 34 percent.

The mid-stage trial had 80 patients with a history of 1-9 herpes recurrences within the prior 12 months. Of them, 70 received the vaccine and 10 received placebo, Agenus said in a statement.

HerpV, being developed as an "off-the-shelf" vaccine, contains Agenus's QS-21 Stimulon adjuvant that boosts specific immune responses.

The trial tested the efficacy of the vaccine by measuring the release of the virus by patients 45 days before and after three injections of HerpV. A majority of the patients also received a booster injection, given 6 months after the first vaccination.

Genital herpes, a highly contagious sexually transmitted infection, is usually caused by the herpes simplex virus (HSV). There are two types of HSV and Agenus's vaccine targets HSV type 2, which most often causes genital herpes.

According to the U.S. Centers for Disease Control and Prevention, 776,000 people in the United States get new herpes infections annually and one out of six people aged 14 to 49 years has genital HSV-2 infection.

Agenus said it expected more data in the first half of 2014, showing how the patients fared after the booster shots.

The company's partners are also testing the QS-21 Stimulon adjuvant in combination with other vaccines.

Agenus shares were up at $3.16 in trading before the bell. The stock closed at $2.40 on Wednesday on the Nasdaq. (Reporting by Esha Dey in Bangalore; Editing by Saumyadeb Chakrabarty and Kirti Pandey)

View the original article here

[Video] Doctor answers questions about genital herpes (HSV) and HPV

Dr. Peter Leone (who has appeared in the New York Times and NPR’s Talk of the Nation) stopped by our monthly herpes support group on April 8, 2013, in Raleigh, NC, to give herpes facts and update us on the latest herpes statistics. He gave so much clarity around all the horribly misunderstood herpes information out there!

Topics covered:

View the original article here

[Video] Doctor answers questions about genital herpes (HSV) and HPV

Dr. Peter Leone (who has appeared in the New York Times and NPR’s Talk of the Nation) stopped by our monthly herpes support group on April 8, 2013, in Raleigh, NC, to give herpes facts and update us on the latest herpes statistics. He gave so much clarity around all the horribly misunderstood herpes information out there!

Topics covered:

View the original article here

Spreading genital herpes (HSV-2) from oral sex?

Can I spread genital herpes to my partners mouth if s/he gives me oral sex?
The exciting and resounding answer to this question is a (slightly qualified) NO! Genital HSV-2 will most likely not be passed to the mouth! It’s 99% impossible (hence the slight qualification). If you use incredibly basic precautionary measures (avoiding oral sex during a herpes outbreak), you’re home free when it comes to receiving oral sex. Ain’t that the best news you’ve heard in a while? I thought so. Go enjoy yourself. Get down on it.

“98-99% of all oral herpes cases are caused by the HSV-1 virus, NOT HSV-2.”

98-99% of the cases of oral herpes (cold sores) are caused by HSV-1, not HSV-2. (Download the helpful handouts here for more helpful herpes statistics.) According to Dr. Peter Leone, there should be no reason you should avoid receiving oral sex from your partner just because you have genital HSV-2 (of course, avoid oral sex during herpes outbreaks). Even without using dental dams or condoms during oral sex, you run only a 1-2% risk of your partner getting HSV-2 in their mouth because HSV-2 has an overwhelmingly huge preference for the genitals.

What about if I have genital HSV-1? Read this article for more on oral sex and HSV-1 »

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How to Prevent Genital Herpes? polyDNA’s Monthly Survey Shows an Ignorant Public

polyDNA recommends using Gene-Eden-VIR to protect against genital herpes.

Rochester, NY (PRWEB) April 17, 2013

polyDNA’s monthly survey shows that many in the public are unaware of the recommended ways of preventing genital herpes.

In the open comments section of the survey, a typical response was offered by Shari C. from Raleigh, N.C. “I have been dating a really great guy who recently told me he has herpes (got it from his ex-wife). I don't have herpes and I don't a lot about STDs. It’s scary because I have no clue how to protect myself from herpes except for what you always hear. You know, have your man wear a condom.”

This ignorance is an important issue since, “Nationwide, 16.2%, or about one out of six, people aged 14 to 49 years have genital HSV-2 infection.” (1) Moreover, “Most individuals infected with HSV-1 or HSV-2 experience either no symptoms or have very mild symptoms that go unnoticed or are mistaken for another skin condition.”(1) Yet, these people can still infect their partners.

According to the CDC, there are three methods of herpes prevention. (1) These methods include the use of condoms, abstention from sexual contact, and having sex only within a committed, monogamous relationship.

polyDNA would like to recommend a fourth way of genital herpes prevention, which has unique advantages. This method reduces the risk of having sex with an infected individual. In addition, it provides protection against other viruses such as HPV.

That method is taking the antiviral, dietary supplement, Gene-Eden-VIR.

“The key to your health is to reduce the level of the latent viruses in your body to harmless levels.” – Dr. Hanan Polansky

A recent post marketing clinical study showed that Gene-Eden-VIR is effective against the latent herpes virus. By helping the body's immune system target the latent herpes virus, people also lower their risk of developing genital herpes symptoms. (2)

Gene-Eden-VIR is highly effective against the latent herpes virus. Each ingredient was chosen through a scientific approach. Scientists scanned thousands of scientific and medical papers published in various medical and scientific journals around the world to identify the safest, most effective natural ingredients that target the latent forms of both HSV-1 and HSV-2. (3)

To learn more about Gene-Eden-VIR, visit http://www.gene-eden-kill-virus.com.

References:

(1) http://www.cdc.gov/std/herpes/stdfact-herpes.htm

(2) http://www.cbcd.net/Gene-Eden-VIR-Clinical-Study.php

(3) http://www.gene-eden-kill-virus.com/studies.php

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polyDNA is a biotechnology company that develops dietary supplements using the unique scientific method developed by Dr. Hanan Polansky, which is based on Computer Intuition.

In addition to his unique scientific method, Dr. Polansky published the highly acclaimed scientific discovery, called Microcompetition with Foreign DNA. The discovery explains how foreign DNA fragments, and specifically, DNA of latent viruses, cause most major diseases.

polyDNA developed Gene-Eden-VIR , an antiviral natural remedy that helps the immune system kill latent viruses.

View the original article here

Study: Scientists Discover How Genital Herpes Infects Cells; polyDNA Recommends Natural Herpes Remedy

In a new study, prevention of cellular calcium responses blocked viral entry, and inhibited plaque formation by 90%.

Rochester, NY (PRWEB) April 07, 2013

polyDNA has learned that a new paper underlines the status of recent research into the mechanism that allows the herpes virus to invade human cells. (1) The research showed that “calcium release occurs because the viruses activate a critical cell-signaling molecule called Akt at the cell membrane.” (2)

Professor Herold said “We’ve essentially identified the molecular ‘key’ that herpes viruses use to penetrate cell membranes and infect cells of the human body.”(2)

polyDNA points out that the discovery of how the herpes virus enters human cells is an important step forward in understanding the pathology of the herpes virus. However, an effective therapy that uses this new knowledge could be years away.

Moreover, there are few drugs currently on the market that help prevent genital herpes outbreaks. In addition, one can transmit the herpes virus to one’s partner even while taking one of the few drugs that do exist.

The CDC notes that “Antiviral medications can, however, prevent or shorten outbreaks during the period of time the person takes the medication. In addition, daily suppressive therapy (i.e., daily use of antiviral medication) for herpes can reduce the likelihood of transmission to partners.” (3)

Reducing the likelihood and eliminating the likelihood of transmitting the herpes virus to ones partner are not the same thing.

As WebMD notes, “University of Washington researcher Christine Johnston, MD, and colleagues show that people with no herpes symptoms often shed infectious genital herpes virus -- even while taking very high doses of anti-herpes drugs.” (4)

Thus, polyDNA recommends that people educate themselves about natural alternatives to such chemically manufactured drugs and for which, 73% of users reported a significant decrease in symptoms. (5)

One such natural alternative is Gene-Eden-VIR.

This all-natural product was scientifically designed to help the human body maintain low concentrations of the dormant or latent herpes virus.

Gene-Eden-VIR is highly effective against the latent herpes virus, each ingredient was chosen through a scientific approach. Scientists scanned thousands of scientific and medical papers published in various medical and scientific journals around the world to identify the safest, most effective natural ingredients that target the latent forms of both HSV-1 and HSV-2. (6)

In addition Gene-Eden-VIR recently underwent a post marketing clinical study in which this all natural herpes remedy was found to be extremely safe. In over 3 years on the market, there have been no reported side effects. (5]

To learn more about Gene-Eden-VIR, the only product on the market today that helps the body target the latent herpes virus and that is scientifically backed by published material, visit http://www.gene-eden-kill-virus.com.

References:

(1) http://www.ncbi.nlm.nih.gov/pubmed/?term=HSV+activates+Akt+to+trigger+calcium+release+and+promote+viral+entry%3A+novel+candidate+target+for+treatment+and+suppression.

(2) http://www.sci-news.com/medicine/article00981.html

(3) http://www.cdc.gov/std/herpes/stdfact-herpes.htm

(4) http://www.webmd.com/genital-herpes/news/20120112/herpes-drugs-dont-stop-herpes-spread

(5) http://www.cbcd.net/Gene-Eden-VIR-Clinical-Study.php

(6) http://www.gene-eden-kill-virus.com/studies.php

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polyDNA is a biotechnology company that develops dietary supplements using the unique scientific method developed by Dr. Hanan Polansky, which is based on Computer Intuition.

In addition to his unique scientific method, Dr. Polansky published the highly acclaimed scientific discovery, called Microcompetition with Foreign DNA.The discovery explains how foreign DNA fragments, and specifically, DNA of latent viruses, cause most major diseases.

polyDNA developed Gene-Eden-VIR (), an antiviral natural remedy that helps the immune system kill latent viruses.

Mike Davis
PolyDNA
5852509999
Email Information

View the original article here

Genital Herpes Makes it Easier to Contract HIV; polyDNA Monthly Survey Results Show Public isn't Aware of Facts

During one particular study, having prior genital-herpes infection increased the risk of acquiring HIV by 80%.

Rochester, NY (PRWEB) March 25, 2013

With results of a monthly survey in, polyDNA has learned that individuals are not aware that a genital herpes infection can make it easier to become infected with HIV.

In fact, the CDC notes on its website that “Genital herpes can cause sores or breaks in the skin or mucous membranes (lining of the mouth, vagina, and rectum). The genital sores caused by herpes can bleed easily. When the sores come into contact with the mouth, vagina, or rectum during sex, they increase the risk of HIV transmission if either partner is HIV-infected.”[1]

During one particular study, having prior genital-herpes infection increased the risk of acquiring HIV by 80%. [2]

Conversely, those with HIV and genital herpes are more infectious than those with HIV alone. In a new paper published this year in PLoS One, researchers said “Clinical herpes was associated with higher levels of genital HIV shedding….” [3]

The authors of the study noted that their findings were “consistent with results from a study carried out in Bangui, Central African Republic, where …(the study found) a significant correlation between genital HIV RNA shedding and genital shedding of HSV.” [4]

They concluded that their “study adds to the accumulating evidence that HSV-2 infection increases genital shedding of HIV, and may therefore increase the infectivity of HIV….”

What does this mean?

In simple terms, the authors of these studies say that genital herpes increases the risk of contracting HIV. They also suggest that those with HIV and genital herpes shed the virus more, and infect others more easily.

The public should be aware of the relationship between genital herpes and HIV and should take precautions to prevent an HSV infection. polyDNA recommends boosting the immune system against a latent herpes infection through the use of a scientific, all natural remedy. That remedy is Gene-Eden-VIR. A recent post marketing clinical study showed that Gene-Eden-VIR is effective against the latent herpes virus. [5]

This all-natural product was scientifically designed to help the human body maintain low concentrations of the dormant or latent herpes virus.

By helping the body’s immune system target the latent herpes virus, people also lower their risk of developing fever blisters, cold sores, or genital herpes symptoms.

Gene-Eden-VIR is highly effective against the latent herpes virus, each ingredient was chosen through a scientific approach. Scientists scanned thousands of scientific and medical papers published in various medical and scientific journals around the world to identify the safest, most effective natural ingredients that target the latent forms of both HSV-1 and HSV-2. [6]

In addition, each bottle is GMP Certified.

To learn more about Gene-Eden-VIR, visit http://www.gene-eden-kill-virus.com.

References:

1: Genital Herpes - CDC Fact Sheet

2: Herpes Simplex Virus Type 2 Infection as a Risk Factor for Human Immunodeficiency Virus Acquisition in Men Who Have Sex with Men

3:Effect of Genital Herpes on Cervicovaginal HIV Shedding in Women Co-Infected with HIV AND HSV-2 in Tanzania

4: Mbopi-Keou FX, Gresenguet G, Mayaud P, Weiss HA, Gopal R, et al. (2000) Interactions between herpes simplex virus type 2 and human immunodeficiency virus type 1 infection in African women: opportunities for intervention. J Infect Dis 182: 1090–1096. doi: 10.1086/315836.

5: Gene-Eden-VIR is Antiviral: Results of a Post Marketing Clinical Study

6: Gene-Eden-VIR: Laboratory and Clinical Studies

###

polyDNA is a biotechnology company that develops dietary supplements using the unique scientific method developed by Dr. Hanan Polansky, which is based on Computer Intuition.

In addition to his unique scientific method, Dr. Polansky published the highly acclaimed scientific discovery, called Microcompetition with Foreign DNA. The discovery explains how foreign DNA fragments, and specifically, DNA of latent viruses, cause most major diseases.

polyDNA developed Gene-Eden-VIR , an antiviral natural remedy that helps the immune system kill latent viruses.

Mike Davis
PolyDNA
5852509999
Email Information

View the original article here

Can Genital Herpes Spread in the Body? polyDNA Surveys the Public Knowledge

polyDNA answers new questions on herpes, HSV, herpes virus, genital sores, etc. collected from the public in its March, 2013 survey.

Rochester, NY (PRWEB) March 13, 2013

Genital herpes can spread from one area in the body to another via touching active lesions, as well as through oral sex.

One survey respondent commented, “I mean I don’t know…can herpes really travel from one spot on your genitals to say, your legs or someplace else on your body? Sometimes I get sores and they’re not always in the same spot.” – Maria from Queens, NY

polyDNA would like to point out that several health authorities have shown that genital herpes can spread from the genital region elsewhere.

Dr. Thomas Nesbitt said, “Herpetic auto-inoculation from one part of the body to another is always possible but not always predictable. Herpetic infections can spread from one portion of the body to another, for example, from an active genital lesion to the eyes by one’s own hands.” (1) Dr. Nesbitt served as Clinical Microbiology Consultant to St. Joseph Mercy Hospital, Ann Arbor. He is currently self-employed as a Microbiologist Consultant.

This means that it is normal for herpes outbreaks to sometimes jump around the general area, even by several inches, and that a person can potentially spread herpes from their genitals to other body parts.

However, this is rare.

In a study using a central Kentucky medical center population over a six year period, “HSV-2 was isolated from only 9.4% of patients with nongenital HSV for the entire 6-year period.” (2)

Thus, while spreading HSV-2 to multiple body locations is rare, it can happen.

Mike Evans, from the Center for the Biology of Chronic Disease (CBCD) said, “Many people are completely horrified when they get a diagnosis of herpes infection. That’s despite the fact that the CDC says that most people with a herpes infection don’t even know they have an infection. Do outbreaks jump around on a person? Lots of people are ignorant of the facts and they need these facts to help them cope with their fears.”

After an initial period of activity where there can be up to five major outbreaks in a year, herpes establishes what scientists call a latent infection. When a virus is latent, it acts as if it is asleep or dormant. The moment the immune system is weakened, however, the herpes virus can “wake up” and become active again.

The best defense against a latent herpes infection is a healthy immune system.

polyDNA would like to point out a herpes remedy that boosts the immune system and helps target the dormant (latent) HSV virus.

“The key to your health is to reduce the level of the chronic viruses in your body to harmless levels.” – Dr. Hanan Polansky

The name of that herpes remedy is Gene-Eden-VIR. This all-natural product was scientifically designed to help the human body maintain low concentrations of the dormant or latent herpes virus.

By helping the body’s immune system target the latent herpes virus, people also lower their risk of developing fever blisters, cold sores, or genital herpes symptoms. This is just one reason polyDNA believes Gene-Eden-VIR is an important product.

Gene-Eden-VIR is highly effective against the latent herpes virus; each ingredient was chosen through a scientific approach. Scientists scanned thousands of scientific and medical papers published in various medical and scientific journals around the world to identify the safest, most effective natural ingredients that target the latent forms of both HSV-1 and HSV-2. (3)

Gene-Eden-VIR is extremely safe. It has been on the market for over three years, and in that time, no side effects were reported. Each capsule contains a patented formula of five all natural ingredients including selenium, camellia sinesis extract, quercetin, cinnamomum extract, and licorice extract. In addition, each bottle is GMP Certified.

Gene-Eden-VIR is sold online through the Gene-Eden website. Each bottle of Gene-Eden-VIR (a one month’s supply) costs just $37.99.

To learn more about Gene-Eden-VIR, the only product on the market today that helps the body target the latent herpes virus and that is scientifically backed by published material, visit http://www.gene-eden-kill-virus.com.

References:

(1) http://www.herpes.com/showAskTom3.shtml

(2) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC88338/

(3) http://www.gene-eden-kill-virus.com/studies.php

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Genital herpes stigma as an opportunity to help

Guest author from our community: Shannon (SingBlueSilver)

Something fascinating is happening to me … There’s a small seed inside of me. It’s pushing for more attention daily. Changing, growing, morphing. It’s always been there, really, but never nurtured. I’ve been in therapy most of my life trying to coax the seed to gain roots and prosper. In the end, I think I was afraid to make real changes in my life to love myself and be happy because being a victim and sad all the time was easier. Real growth takes work and dedication. So the seed of my inner strength lay stagnant …

And then it started to sink in. The seed within me started to grow … I realize now that I am lovable, worthy and, actually, strong.

Five months ago, my world was rocked to the core, every vestige of progress and mental growth I had ever gained was shattered. I got genital herpes. Devastation and utter despair were the only words I could fathom. I cried. I felt shame. Guilt. Disgust … Hopelessness. The same emotions that most all of us share when diagnosed.

I spent most of my time blaming myself for bad choices and blaming society for creating and buying into a shameful herpes stigma. I even felt like I deserved to get herpes because I had sex out of marriage; my Christian upbringing came back to slam in me in the gut, telling me God was punishing me for my wanton behavior.

I think all of us with this condition have similar experiences: shame, depression, wanting to talk about it, but fearing who you can trust. But eventually, that seed of inner strength started to speak to me. I felt like I had two choices: 1) find a way to accept my new reality or 2) live in a pit of despair.

The pit of despair was something I felt pretty comfortable with as I’ve always struggled with depression and never felt good enough. But then I started talking to friends and all of them were very supportive and kept saying the same thing, “Herpes does not define you. You are still the same person.” And then I found the Herpes Opportunity website with so many others who were struggling just like me. And I found Adrial Dale who started to frame this condition in a healthy manner. And I kept reading and talking and thinking. I saw my therapist and then a new age hypnotherapist. The message was consistent, “You’re still you and this is a hardship, but it’s not the end of your life. You are lovable.”

And then it started to sink in. The seed started to grow.

I started to think that maybe I was given this “opportunity” to finally grow into the person I need to be. It’s a hard lesson to learn, but lessons are never easy. I had spend 38 years of my life feeling sorry for myself, playing a victim, never really being happy with what I have. And when I got herpes, it was my wake up call. My inner strength (that was there all along) was forced to reveal itself because my only other choice was death (figuratively). I could lay down and give up on life or I could pull the strength from my core and finally embrace it.

Other thoughts also quickly appeared: “Maybe I’m meant to help others. Maybe I have the courage to help change society’s perception. Maybe I could speak out.” Ideas rapidly came about visiting schools and talking about my experience. Part of my anger over this experience is that I was truly ignorant about how to get and spread herpes; I didn’t know that condoms don’t protect you; I didn’t know that so many people have no herpes symptoms; and I didn’t know that STD tests don’t include an actual herpes test.

I was also one of the people who thought being careful was good enough. I was part of the society who created this stigma. I have now started thinking that I can be part of the change. It has only been a short five months since my herpes diagnosis, so these are still just thoughts. But these ideas have turned my harsh reality into something I can do to help myself and others. Starting to give others support brings a joy that I was lacking.

I realize now that I am lovable, worthy and, actually, strong.

It’s not the ideal way to realize this but it has become my opportunity. Accepting that I have herpes has somehow translated into an acceptance of me as a valuable woman. I write this in hopes to inspire you to find your inner strength and realize that herpes isn’t a death sentence socially or emotionally. I’m not saying that every day is easy. I’ve struggled my entire life to feel lovable, good enough and happy, but instead of herpes being the final straw in my life struggle, it’s provided a way for me to see clearly who I really am.

I am a beautiful, worthy, amazing and awesome woman.

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Why Even Treated Genital Herpes Sores Boost The Risk Of HIV Infection

ScienceDaily (Aug. 7, 2009) — New research helps explain why infection with herpes simplex virus-2 (HSV-2), which causes genital herpes, increases the risk for HIV infection even after successful treatment heals the genital skin sores and breaks that often result from HSV-2.

Scientists have uncovered details of an immune-cell environment conducive to HIV infection that persists at the location of HSV-2 genital skin lesions long after they have been treated with oral doses of the drug acyclovir and have healed and the skin appears normal. These findings are published in the advance online edition of Nature Medicine on Aug. 2.

Led by Lawrence Corey, M.D., and Jia Zhu, Ph.D., of the Fred Hutchinson Cancer Research Center and Anna Wald, M.D., M.P.H., of the University of Washington, both in Seattle, the study was funded mainly by the National Institute of Allergy and Infectious Diseases (NIAID) with support from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, both part of the National Institutes of Health.

"The findings of this study mark an important step toward understanding why HSV-2 infection increases the risk of acquiring HIV and why acyclovir treatment does not reduce that risk," says NIAID Director Anthony S. Fauci, M.D. "Understanding that even treated HSV-2 infections provide a cellular environment conducive to HIV infection suggests new directions for HIV prevention research, including more powerful anti-HSV therapies and ideally an HSV-2 vaccine."

One of the most common sexually transmitted infections worldwide, HSV-2 is associated with a two- to three-fold increased risk for HIV infection. Some HSV-2-infected people have recurring sores and breaks in genital skin, and it has been hypothesized that these lesions account for the higher risk of HIV acquisition. However, recent clinical trials, including an NIAID-funded study completed last year, demonstrated that successful treatment of such genital herpes lesions with the drug acyclovir does not reduce the risk of HIV infection posed by HSV-2 . The current study sought to understand why this is so and to test an alternative theory.

"We hypothesized that sores and breaks in the skin from HSV-2 are associated with a long-lasting immune response at those locations, and that the response consists of an influx of cells that are a perfect storm for HIV infection," says Dr. Corey, co-director of the Vaccine and Infectious Diseases Institute at The Hutchinson Center and head of the Virology Division in the Department of Laboratory Medicine at the University of Washington. "We believe HIV gains access to these cells mainly through microscopic breaks in the skin that occur during sex."

The research team took biopsies of genital skin tissue from eight HIV-negative men and women who were infected with HSV-2. These biopsies were taken at multiple time points: when the patients had genital herpes sores and breaks in the skin, when these lesions had healed, and at two, four and eight weeks after healing. The researchers also took biopsies from four of the patients when herpes lesions reappeared and the patients underwent treatment with oral acyclovir. The scientists continued to take biopsies at regular intervals for 20 weeks after the lesions had healed. For comparison, the investigators also took biopsies from genital tissue that did not have herpes lesions from the same patients.

Previous research has demonstrated that immune cells involved in the body's response to infection remain at the site of genital herpes lesions even after they have healed. The scientists conducting the current study made several important findings about the nature of these immune cells. First, they found that CD4+ T cells—the cells that HIV primarily infects—populate tissue at the sites of healed genital HSV-2 lesions at concentrations 2 to 37 times greater than in unaffected genital skin. Treatment with acyclovir did not reduce this long-lasting, high concentration of HSV-2-specific CD4+ T cells at the sites of healed herpes lesions.

Second, the scientists discovered that a significant proportion of these CD4+ T cells carried CCR5 or CXCR4, the cell-surface proteins that HIV uses (in addition to CD4) to enter cells. The percentage of CD4+ T cells expressing CCR5 during acute HSV-2 infection and after healing of genital sores was twice as high in biopsies from the sites of these sores as from unaffected control skin. Moreover, the level of CCR5 expression in CD4+ T cells at the sites of healed genital herpes lesions was similar for patients who had been treated with acyclovir as for those who had not.

Third, the scientists found a significantly higher concentration of immune cells called dendritic cells with the surface protein called DC-SIGN at the sites of healed genital herpes lesions than in control tissue, whether or not the patient was treated with acyclovir. Dendritic cells with DC-SIGN ferry HIV particles to CD4+ T cells, which the virus infects. The DC-SIGN cells often were near CD4+ T cells at the sites of healed lesions—an ideal scenario for the rapid spread of HIV infection.

Finally, using biopsies from two study participants, the scientists found laboratory evidence that HIV replicates three to five times as quickly in cultured tissue from the sites of healed HSV-2 lesions than in cultured tissue from control sites.

All four of these findings help explain why people infected with HSV-2 are at greater risk of acquiring HIV than people who are not infected with HSV-2, even after successful acyclovir treatment of genital lesions.

"HSV-2 infection provides a wide surface area and long duration of time for allowing HIV access to more target cells, providing a greater chance for the initial 'spark' of infection," the authors write. This spark likely ignites once HIV penetrates tiny breaks in genital skin that commonly occur during sex. "Additionally," the authors continue, "the close proximity to DC-SIGN-expressing DCs [dendritic cells] is likely to fuel these embers and provide a mechanism for more efficient localized spread of initial infection." The investigators conclude that reducing the HSV-2-associated risk of HIV infection will require diminishing or eliminating the long-lived immune-cell environment created by HSV-2 infection in the genital tract, ideally through an HSV vaccine. Further, they hypothesize that other sexually transmitted infections (STIs) may create similar cellular environments conducive to HIV infection, explaining why STIs in general are a risk factor for acquiring HIV.

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Journal References:

J Zhu et al. Persistence of HIV-1 receptor-positive cells after HSV-2 reactivation is a potential mechanism for increased HIV-1 acquisition. Nature Medicine, DOI: 10.1038/nm2006 (2009)Celum et al. Effect of aciclovir on HIV-1 acquisition in herpes simplex virus 2 seropositive women and men who have sex with men: a randomised, double-blind, placebo-controlled trial. The Lancet, 2008; 371 (9630): 2109 DOI: 10.1016/S0140-6736(08)60920-4

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

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Genital herpes virus reactivates widely throughout genital tract

ScienceDaily (Jan. 30, 2010) — Genital herpes caused by a reactivation of herpes simplex virus type 2 (HSV-2) is generally treated as a lesion in one specific area of the genital region. A new study, however, finds that the virus can frequently reactivate throughout the genital tract, an important new concept that could help guide both HSV-2 treatment and prevention. Now available online, the study appears in the Feb. 15 issue of The Journal of Infectious Diseases.

In the study, Christine Johnston, MD, MPH, and colleagues at the University of Washington and the Fred Hutchinson Cancer Research Center in Seattle collected daily samples during a 30-day period from seven separate genital sites in four women infected with HSV-2. HSV-2 was detected from more than one anatomic site on 56 percent of days when there was viral shedding -- and on genital surfaces on both sides of the participants' bodies on most days when virus was detected at more than one site.

Using a detailed sampling method and a sensitive assay, the authors showed that both symptomatic and asymptomatic HSV-2 reactivations often occurred at widely spaced regions throughout the genital tract. These reactivations were often on both sides of the body, even though clinical lesions typically emanate from one anatomic spot. The study's findings illustrate an important new concept in HSV-2 pathogenesis, the authors wrote, and may help in developing comprehensive treatment that both suppresses and limits the transmission of HSV-2 infection.

The authors also noted limitations of their study, including a small sample size and the unique features of the study's subjects. For example, all participants had a history of symptomatic genital herpes, and three of the four had acquired HSV-2 infection within the past year, increasing the chances of high viral reactivation and lesion rates. Additionally, although there were a high proportion of days with lesions during the study period, two of the participants who had recently acquired genital herpes contributed the majority of lesion days.

In an accompanying editorial, Edward W. Hook III, MD, of the University of Alabama at Birmingham, called the study's findings "of great potential importance, as they further challenge widely held beliefs regarding genital herpes and, by extension, its management." Many clinicians treat patients with newly diagnosed herpes episodically, managing the signs and symptoms of periodic symptomatic recurrences, Dr. Hook wrote. "From a personal and public health perspective, the biology of the infection suggests that a national campaign for serological testing of those at risk would provide the foundation for more effective efforts to control HSV transmission to others, and that for most sexually active persons with HSV-2 whose sex partners are not known to also be infected, suppressive therapy should be the preferred approach."

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Progress made toward a genital herpes vaccine

ScienceDaily (Jan. 6, 2012) — An investigational vaccine protected some women against infection from one of the two types of herpes simplex viruses that cause genital herpes, according to findings in the New England Journal of Medicine.

The vaccine was partially effective at preventing herpes simplex virus type 1 (HSV-1), but did not protect women from herpes simplex virus type 2 (HSV-2). There were less than half of the cases of genital herpes caused by HSV-1 -- 58 percent fewer -- in women who received the investigational vaccine compared to women who received the control vaccine.

"There is some very good news in our findings. We were partially successful against half of the equation -- protecting women from genital disease caused by HSV-1," said Robert Belshe, M.D., director of the Saint Louis University Center for Vaccine Development and lead author of the study.

"It's a big step along the path to creating an effective vaccine that protects against genital disease caused by herpes infection. It points us in the direction to work toward making a vaccine that works on both herpes simplex viruses."

Both HSV-1 and HSV-2 are members of the herpesvirus family. Typically, HSV-2 causes lesions and blisters in the genital area. HSV-1 generally causes sores in the mouth and lips, although it increasingly has been found to cause genital disease.

There currently is no cure or approved vaccine to prevent genital herpes infection, which affects about 25 percent of women in the United States and is one of the most common communicable diseases. Once inside the body, HSV remains there permanently. The virus can cause severe neurological disease and even death in infants born to women who are infected with HSV and the virus is a risk factor for sexual transmission of HIV.

The clinical trial of an investigational genital herpes vaccine was funded by the National Institute of Allergy and Infectious Diseases (NIAID), which is part of the National Institutes of Health, along with GlaxoSmithKline (GSK), and conducted at 50 sites in the U.S. and Canada.

The study enrolled 8,323 women between ages 18 and 30 who did not have HSV-1 or HSV-2 infection at the start of the study. They were randomly assigned to receive either three doses of the investigational HSV vaccine that was developed by GSK or a hepatitis A vaccine, which was the control.

Participants were followed for 20 months and evaluated carefully for occurrence of genital herpes disease. In addition, all study participants were given blood tests to determine if asymptomatic infection with HSV-1 or HSV-2 occurred during the trial. Researchers found that two or three doses of the investigational vaccine offered significant protection against genital herpes disease caused by HSV-1. However the vaccine did not protect women from genital disease caused by HSV-2.

"We were surprised by these findings," said Belshe, who also is a professor of infectious diseases and immunology at Saint Louis University School of Medicine. "We didn't expect the herpes vaccine to protect against one type of herpes simplex virus and not another. We also found it surprising that HSV-1 was a more common cause of genital disease than was HSV-2."

HSV-1 infection has become an increasingly common cause of genital disease, likely because more couples are engaging in oral sex. HSV-1 and HSV-2 are spread by direct contact -- mouth to mouth, mouth to genitals and genitals to genitals -- even when the infected person shows no symptoms, Belshe added.

Researchers are conducting laboratory tests on serum obtained from study participants as they continue to study why the vaccine protected women from genital disease caused by HSV-1 and not HSV-2.

One hypothesis, Belshe said, is HSV-1 is more easily killed by antibodies than is HSV-2. This means that the vaccine antibodies might work better against HSV-1 and result in protection from HSV-1 but not HSV-2.

Earlier studies of the investigational herpes vaccines showed it protected against genital herpes disease in women who were not infected with HSV-1 or HSV-2, but whose sexual partners were known to have genital herpes. Researchers believe the reason for the different outcome in the most recent clinical trial could be related to the fact that different populations were studied. The women in the earlier studies may have been protected due to immunologic or behavioral factors not present in the later study.

"It's always important to confirm scientific findings in repeated studies, which is why we investigated the vaccine in a large, placebo controlled trial," Belshe said. "Our findings confirmed the validity of the scientific process. You've got to have good scientific evidence that something actually works."

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Journal Reference:

Robert B. Belshe et al. Efficacy Results of a Trial of a Herpes Simplex Vaccine. New England Journal of Medicine, Jan 5, 2012 DOI: 10.1056/NEJMoa1103151

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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.

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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

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Genital herpes vaccine ineffective in women, study suggests

ScienceDaily (Sep. 30, 2010) — An experimental vaccine intended to prevent genital herpes disease in women, although generally safe and well-tolerated, proved ineffective when tested in the recently concluded clinical study known as the Herpevac Trial for Women.

The Phase 3 trial, sponsored by GlaxoSmithKline (GSK) Biologicals, based in Belgium, with support from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, began in 2002. A total of 8,323 women aged 18-30 years participated in the trial at 50 sites in the United States and Canada. At the time of their enrollment, the study participants were free of the two types of herpes simplex viruses (HSV), HSV-1 and HSV-2.

Participants in the Herpevac trial were randomly divided into two groups. One group received the candidate vaccine, containing HSV protein along with an adjuvant intended to boost immune responses. The second, control group received a version of Havrix, a licensed vaccine against hepatitis A. This study design gave all participants the potential opportunity to be protected against either genital herpes or hepatitis A. GSK developed the candidate vaccine and also manufactures Havrix.

Each volunteer was vaccinated at the beginning of the study and again one and six months later. The participants were followed for 20 months after the initial injection and evaluated at each visit for HSV infection and genital herpes disease.

In two earlier studies involving men and women who did not have genital herpes but whose sexual partners were known to be infected, the candidate vaccine prevented genital herpes disease in more than 70 percent of the female volunteers who were free of HSV-1 and HSV-2 but had no clear effect in men. These studies formed the basis to conduct the larger Herpevac study in women only.

In the Herpevac study, however, the investigational vaccine was ineffective in protecting against genital herpes disease. The estimate of vaccine effectiveness was 20 percent, but all estimates have statistical uncertainty, and this effect was not substantially different from zero.

It is not known at this time why the vaccine proved ineffective, but the study collaborators continue to evaluate the trial data and intend to provide a more detailed analysis at a later date.

All the study investigators have been informed of the results. Study participants are being notified as to which vaccine they received, and those volunteers who received the candidate herpes vaccine are being offered Havrix.

HSV-1 and HSV-2, which cause cold sores and genital herpes disease, may be transmitted through sexual or other skin-to-skin contact, and can be spread even when the infected individual shows no symptoms. HSV can cause severe illness in infants born to HSV-infected women, and the virus has been identified as a risk factor for HIV transmission in adults. An estimated 1 in 4 women in the United States has genital herpes.

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Recurring genital problems could be herpes, Swedish study suggests

ScienceDaily (Apr. 11, 2011) — A study of patients attending sexual health clinics in Gothenburg found that just four out of ten patients with genital herpes actually knew that they had the disorder. However, a third of those who did not realise that they had been infected reported typical symptoms at a follow-up visit, reveals a thesis from the University of Gothenburg, Sweden.

In her thesis Matilda Berntsson, a specialist in skin and sexually transmitted infections at the Frölunda Specialist Hospital's skin clinic and researcher at the Sahlgrenska Academy, investigated the prevalence of genital herpes type 2 among patients attending sexual health clinics in Gothenburg. Her investigation included more than 1,000 patients, both male and female.

Genital herpes caused by herpes simplex virus type 2 infects the genital membranes before moving to the nerve ganglia alongside the spinal cord, where it remains for the rest of a patient's life. Although many people who have been infected do not experience any discomfort, the virus can be activated and spread further through sexual contact. The disorder can also result in recurring genital problems.

"1,014 patients who attended sexual health clinics, the Sahlgrenska University Hospital skin clinic and the Sesam sexual health clinic were tested for herpes simplex virus type 2," says Matilda Berntsson. "The presence of antibodies in the blood shows that a person is infected with the virus."

The test results revealed that more than one in five women and one in ten men were infected with genital herpes type 2. Just four out of ten patients with herpes type 2 antibodies actually knew that they were infected. However, a third of those patients who did not know that they were infected reported typical symptoms in the form of recurring genital blisters and sores at a follow-up visit.

"The study reinforces our perception that genital herpes is common and that most people carrying it are unaware that they have it," says Berntsson. "Non-specific recurring genital symptoms could be undiagnosed herpes, which can be detected with a simple test at the doctor's."

She therefore suggests that people with non-specific genital symptoms who are worried about genital herpes should see a doctor for an examination.

"If the symptoms and/or findings suggest herpes, there are good methods for testing for the disorder," says Berntsson. "Pronounced symptoms can be treated with medicines that alleviate discomfort, and a daily preventative treatment can be given for longer periods where recurrences are frequent."

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Mar 21, Genital Herpes Transmission: How is the Virus Transmitted and how you can Preven

Knowledge of the herpes virus, how it is transmitted and how genital herpes transmission can be prevented, is essential for people who suspect they may have contracted the virus and want to avoid passing it on to others, more especially to a sexual partner.

It is very important to note that it is possible to transmit genital herpes even if there are no visible outward signs of the virus. The virus is usually transmitted through direct skin on skin contact, through oral, vaginal or anal sex. It can also be transmitted by a person with a cold sore who kisses a partner’s genital area, so it is strongly recommended to avoid oral sex in the case of an outbreak of facial herpes.

Genital herpes transmission is not necessarily immediately apparent and people can be in a sexual relationship for a long time before developing symptoms for the first time. This can be the case when one of the partners in the relationship is, unknowingly, an asymptomatic carrier of HSV (herpes simplex virus), exhibiting no outward signs of having the virus. It is impossible to predict when asymptomatic shedding of the virus occurs, but it is estimated to be on a minimum of 5% of days in any given year.

This is an excellent argument in favour of testing for the herpes virus if you have had previous sexual partners and want to embark on a new relationship. Proper diagnosis is essential in determining the presence of the virus, the type of virus present and the best form for treatment for the virus.

In the case of active genital herpes, the use of condoms is an obvious way of avoiding genital herpes transmission along with that of a number of other sexually transmitted diseases. While using condoms is not 100% fail-safe, it can reduce the risk of transmission by up to 50%.

Being upfront with your partner about your genital herpes, while a difficult subject to broach, is essential in preventing its spread. It has been proven in scientific studies that those who reveal to a partner that they are carriers of the herpes virus are responsible for a reduction in its spread.

Another way in which you can avoid transmitting herpes is by watching out for any early warning signs or symptoms which may indicate that an attack is beginning. All sexual contact should be avoided whenever there is an attack in order to minimize the risk.

Choosing a treatment for genital herpes is another important factor in preventing the spread of the virus. You should talk to your medical practitioner about the kind of treatment which is best for you and for the type of herpes which you have contracted. Some people prefer to avoid traditional medication, while others find that suppressive therapy or the use of proven anti-virals is instrumental in avoiding the risk of transmission.

Whatever the course of treatment you decide on, the knowledge of what constitutes risk-taking behaviour, the ways in which the herpes simplex virus is transmitted and the ways in which you can tackle it will be essential in preventing genital herpes transmission.
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