Herpes: can it be treated?

Genital herpes cannot be cured, but it can be treated. Antiviral medications are available to help reduce the symptoms of genital herpes and decrease the number of recurrences. These antiviral medications include acyclovir, famciclovir, and valacyclovir. Valacyclovir can also be used to reduce the risk of transmitting herpes to your sex partner(s). It should be used in combination with safer sex. You should discuss the value of using antiviral medications with your physician.

Here are some suggestions if you have, or think you may have, a first episode of genital herpes:

Go to your doctor or clinic as soon as possible. Early diagnosis and treatment will help you to feel substantially better more quickly.Have a trained professional diagnose the problem and confirm the presence of herpes by a virus test taken from the affected area (a culture test is the most common method, but a blood test for antibodies may also be used). A blood test for syphilis, HIV, and possibly hepatitis B may also be performed.If the pain is severe, you may wish to take a prescription pain reliever.If it is helpful, take very warm showers to run warm water over the area 3 or 4 times a day.When you get out of the shower or bath, blow dry the genital area with a hair dryer. Set the temperature on low or cool.Make sure you are passing urine without difficulty. Try urinating in the shower or tub to decrease the sting. Pouring a glass of warm water over the area may also be helpful. Some people have found that drinking a lot of water (8 glasses a day) dilutes the urine enough that it hurts less.If you cannot pass urine and you've tried several times, wait a couple of hours - even 3 or 4. If there is still no result, you must get medical attention. Not passing urine can lead to serious problems, but they can generally be prevented. Either visit your own doctor or go to the emergency room of a local hospital.Avoid wearing tight underwear. If possible, do without underwear altogether. Try wearing loose clothes made of pure cotton. When you get home, take a shower or soak in the tub. Leave your clothes off if you can.Talk to your physician about the value to you of using antiviral medications.Avoid (because they may be worse than doing nothing):cortisone cream or ointmentantibiotic cream or ointmentany cream or ointment that does not contain a useful, specific antiherpes drugpetrolatum (e.g., Vaseline®)antibiotics (unless you have a clear-cut secondary infection)alcohol (because it stings)ether (because it stings and can catch fire)DMSO (dimethyl sulfoxide)Avoid (because they are of no proven benefit):

If you have your first episode of herpes during pregnancy, consult your physician as soon as possible about what you can do to reduce your baby's risk of infection. Take care of yourself by giving yourself time to heal, treating any other infections, and treating your herpes.

It is hard to learn and figure out everything all at once, but the answers will come. Your ability to cope and your methods for coping will also evolve. Speak to your doctor about how to cope with herpes and reduce the risk of passing the infection on to your sex partner(s).

With recurrent herpes, it is important to fully understand the active phases of infection so you can avoid contact when necessary. It is also important to use safer sex precautions, such as condoms and dental dams, for the prevention of herpes and other sexually transmitted infections. Since people can spread the herpes virus even when they have no noticeable symptoms, it's important to take these precautions at all times. It's important to know that condoms don't provide complete protection from herpes, since they don't always cover all affected skin.

If you are facing issues such as loneliness and the fear of discussing herpes with new partners, keep in mind that these are very common issues and that frustrations can be overcome through a commitment to yourself and to your ability to grow from this experience. In addition, you may wish to have treatment for recurrent herpes. People with recurrent genital herpes now have choices to make regarding antiviral treatment for control of the infection. Talk to your doctor about medications that might help treat your symptoms, reduce the number of outbreaks, or reduce your risk of passing on herpes to your sex partner(s).

Stephen L. Sacks, MD, FRCPC, with revisions by the MediResource clinical team

View the original article here

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.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by NIH/National Institute of Allergy and Infectious Diseases, via EurekAlert!, a service of AAAS.

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

Journal 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

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

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

View the original article here

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

ScienceDaily (Aug. 2, 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.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by NIH/National Institute of Allergy and Infectious Diseases, via EurekAlert!, a service of AAAS.

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

Journal 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

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

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

View the original article here

How Can Genital Herpes Be Treated?

Genital herpes is one of the most common and highly infectious sexually transmitted conditions. As the name suggests, it is caused by the Herpes Simplex virus (HSV). The HSV-1 is responsible for causing fever blisters and it can spread through kissing or exchange or saliva. This strand of the herpes virus is also spread through sexual contact and this causes genital herpes. Sores caused by either of these viruses, HSV -1 and HSV -2 look the same. When this virus is transmitted from an infected person to a non-infected one, small blisters develop in and around the genitals.

This health condition cannot be cured, but you can certainly treat it and minimize its symptoms. Both, men and women suffer from this health condition and can infect others. Genital herpes spreads very fast and this is the reason why millions of people are affected by it. Moreover, this health condition can also be transmitted through carriers. Statistics reveal that more than two million people are affected by this virus each year and around 80-90% of people who contract it do not experience any type of symptoms. Infected people can experience symptoms after a week, a month or even a year. Some people never have symptoms but they can still spread it to anyone else.

It is seen that the poor, destitute and less educated people are most infected with genital herpes and this is because these people are not aware of it. Also, individuals who abuse drugs such as cocaine and then have multiple sexual partners are more susceptible to this problem. It can spread when a non-infected person comes in contact with an infected person. Sexual intercourse and oral sex are the most common ways through which genital herpes spreads. But, at times, herpes also spreads through skin to skin contact.

Since more than 90% of the people fail to recognize symptoms of this health condition, you should always go for a routine checkup at regular intervals. Once you are diagnosed with genital herpes, you should use medications such as Famvir or Valtrex to treat those problems. These medications will help you minimize the risk of the virus spreading further.

Famvir

This antiviral drug slows down the growth and spread of herpes virus. This gives the body more time to fight off the infection. Again, this medication does not cure herpes but it certainly helps in treating it. Famvir is used for the treatment of genital herpes, cold sores, shingles, and chicken pox. Use this medication for the entire period of time as recommended by the doctor. Continue taking it even if your symptoms start getting better before the whole course is over. Start using this medication as soon as you see the first symptoms of this health condition.

Valtrex

Valtrex is an antiviral drug that slows down the growth and spread of herpes virus. Valtrex does not cure herpes but it certainly helps in treating it. It is used for the treatment of genital herpes, cold sores, shingles, and chicken pox. Use this medication for the entire period of time as recommended by the doctor.

An online clinic HealthExpress for the treatment of genital herpes, with prescription drug like Valtrex, Famvir treatment of Genital herpes. For more information on Valtrex and Famvir online visit Healthexpress.co.uk.

View the original article here