Cold Sores

(Oral Herpes, Fever Blister)

Cold sores, also known as fever blisters, are caused by a virus. They usually appear around the mouth and on the lips. They are highly contagious but not dangerous.

About 60% of the population have suffered cold sores at some point in their lives. On average, people who get cold sores have 2 or 3 episodes a year, but this figure can vary significantly from person to person.

The virus that causes cold sores is herpes simplex 1, a cousin of herpes simplex 2, which causes the well-known sexual disease. About 80% of the people in North America have dormant (inactive) herpes 1 virus living permanently in their body.

The virus typically resides in a dormant state within the body's nerve cells. The body's immune system is normally able to keep the virus in its inactive state. When an infected person is exposed to a "trigger," or if the immune system is weakened, then the virus quickly multiplies and spreads down the nerve cell and out onto the skin, usually on the lips. This produces the characteristic tingling sensation and subsequent clusters of blisters.

Specific triggers include:

cold weatherfatiguefever, such as from stomach flu or other infectionsmenstrual periodsmental or physical stressphysical irritation of the lips (e.g., following a visit to the dentist)sunlight or sunburn

You can catch the virus if you come into direct contact with the cold sore blisters or the fluid inside them, which contains a high number of the viruses. This can easily happen through touching the hands of someone who has touched their blisters. It can also occur through sharing toothbrushes, cups, cutlery, face cloths, towels, lipstick, or other personal items that have been contaminated with fluid from the blisters. Once the blisters have stopped oozing or have crusted over, the person is no longer contagious.

People who get cold sores may feel some unusual sensations around the lips in the 24 hours before the blisters appear, including tingling, burning, pain, or numbness. This is called a prodrome or warning sign that cold sores will appear at these spots. The skin turns red and blisters form. They ooze a clear liquid for a few days that dries to a yellow crust over a period of about 3 to 5 days. There is usually some pain in the first few days after the cold sores break out, but this often disappears as the cold sore crusts over. Complete healing takes from 10 to 14 days.

The condition typically causes a cluster of lesions or blisters at a site around the lips. Areas other than the lips such as the inside of the mouth, around the nostrils, or even the surface of the eyes, can also be affected. It is possible to spread the virus to other parts of your body if you touch the blisters and then touch yourself elsewhere. Cold sores inside the mouth can be problematic, interfering with talking and eating. If the virus infects the eye, it can damage the surface leading to vision loss. Very rarely, it can get into the brain, causing viral meningitis or encephalitis. The virus that causes cold sores, herpes simplex 1, can also be spread to the genitals during oral sex, leading to genital herpes.

Herpes simplex 1 never goes away completely, so cold sores can return later on if they are triggered again. Most cold sores don't leave scars; however, if an open blister becomes infected with bacteria or the lesions tend to return at the same site, scarring may result. People with weakened immune systems tend to get more cold sores and heal slower.

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Disclosing cold sores (oral herpes HSV-1) to potential partners before kissing?

This is a question brought up a lot on the Herpes Opportunity forums.

“Should I / How do I disclose that I get cold sores to potential partners before kissing them?”

The answer can be a confusing one, simply because it’s up to the individual on what’s right or not. And there has been a great debate on the forum before about it, and recently another question on this topic has been thrown into the ring …

So let’s get into this question a bit deeper, shall we?

“If 80% of people have cold sores, whose responsibility is it to bring it up? Those who have it or those who don’t?”

The reason this conversation is a bit hard to pin down is because when it comes to oral herpes (HSV-1) specifically, 80% of Americans 14-49 years old have it. Now that’s a VAST majority of people, isn’t it? We’re not just talking a measly barely-tipping-the-scales 51% majority or anything. So considering this statistic, with whom does the responsibility to bring up the topic fall? (In a perfect world, we all would be talking about every aspect of our sexual and intimate histories with each other before getting intimate, but that ain’t the world we live in.)

Here’s another way to think of this without herpes specifically as the topic … Here’s the scenario: Eight out of 10 people in a room are sick with the flu virus. All 10 people know before walking into the room that 80% of the people in that room are sick with the flu. Which group should be covering their mouths? The 8 people who are sick or the 2 people who aren’t? You’ll find people to argue either point. What it comes down to is this: What does your integrity tell you to do considering the circumstances? Would you feel guilty if you kissed someone without telling them you have oral herpes (cold sores)?

My personal opinion is we just have the conversation, regardless of whether or not herpes is on the mouth or genitals. It’s still an opportunity to have an important conversation and care about someone else’s health. Imagine if before we even kissed, a nonchalant “Hey, just FYI I get cold sores — just like 80% of us — and just wanted to let you know. Do you get cold sores?” Doesn’t have to be a dealbreaker-feeling conversation. No shame. No guilt. No weirdness. Just a simple conversation about herpes. No biggie. That’s the world I want to live in. Where everyone can talk openly about something simple like herpes so it can open the door to deeper conversations and deeper connection.

So what do YOU think? Click here for the post if you’d like to join in on the discussion.

“Yeah, but what about ‘down there’? Ahem, (oral sex) …”

This leads to the obvious next question that’s asked … what about herpes and oral sex? You see, this is where this discussion gets fascinating (as far as I’m concerned). Why? Because what if someone has genital herpes of the HSV-1 variety (read about the differences between HSV-1 and HSV-2) and their partner goes down on them (after a proper herpes talk, of course), then what makes the potential of passing HSV-1 to that person’s mouth any different than passing it to their mouth if you have oral herpes and kiss them? The end result is the same: HSV-1 is passed to their mouth (to recap, which 80% of Americans ages 14-49 have). [Sidenote: There are also a lot of questions about receiving oral sex when you have HSV-2; there is less than a 1% chance of passing genital HSV-2 to your partner.]

This confusing double standard between no shame in oral herpes, but mucho shame in genital herpes is proof positive to me that our culture has a severe sexual shaming problem. The fact that we get something through kissing doesn’t have any stigma, but if we get something through expressing ourselves in a sexual manner, we might want to consider shaming our natural urges? Bull honkey. Yeah, I said it. Bull honkey. Time to realize that sex is a natural, beautiful thing. No shame belongs in sex. So how do we shift it? With ourselves first. Accept yourself with herpes. Disclose with self-acceptance and integrity. The stigma will shift, I promise you. Start now.

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Cold sores actually have nothing to do with colds

Fever blisters can be treated in most cases by applying a topical antiviral to the lesion. (Fotolia.com / December 18, 2012)

http://www.kidsdr.com

Fever blisters are fairly common and are also often called cold sores, but have nothing to do with a cold.

These sores typically appear on the outside of the mouth, on the lips. The vast majority (about 95percent) of fever blisters are due to a virus, typically herpes type 1. Because these blisters are caused by a virus, they are contagious and most people will be exposed to the virus during their lifetime.

Children are typically exposed via contact with an adult, sibling, or relative who has a fever blister, or with other children who've mouthed toys, cups, etc., contaminated with the virus.

In many cases, exposure may be asymptomatic. Others who pick up the virus develop painful vesicles appearing both inside the mouth and on the tongue and gums, as well as on the lips, three to five days after exposure.

This initial illness is called herpetic gingivostomatitis. The initial infection tends to be more uncomfortable, and it may take up to two weeks for the lesions to resolve. The most difficult aspect to deal with is oral discomfort, so it's important to make sure young children with the virus stay hydrated. Popsicles are often helpful for this.

Once you've been exposed to the herpes virus, this virus remains in nerve endings where it may remain dormant and asymptomatic for years. About 60 percent of children are positive for HSV-1 by adolescence.

At other times, the virus may become active (in times of stress, after sun exposure, or accompanying fever or menstrual periods), resulting in a fever blister. If a child develops a fever blister, they also are contagious and may spread the illness by touching or picking at the lesion, then touching other people or objects with their mouths.

Fever blisters can be treated in most cases by applying a topical antiviral to the lesion. These prescription medications may shorten the duration of the fever blister by a day or two, especially if started early and applied frequently. If your children experience recurrent fever blisters, speak with your pediatrician about the use of oral antiviral medications.

Remember, if you have a fever blister, don't kiss your baby. Although most viral shedding occurs after the initial HSV infection, you remain contagious with each fever blister so it's better to take precautions for a few days.

(Dr. Sue Hubbard is a nationally known pediatrician and co-host of "The Kid's Doctor" radio show. Submit questions at http://www.kidsdr.com.)

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

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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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Goodbye cold sores

ScienceDaily (June 27, 2011) — Herpes infections on the lips, in the eyes or on the nose are painful, long-lasting and unpleasant. A new 3D herpes infection model brings hope: active ingredients and new treatments can be reliably tested with this model. Animal tests could soon be a thing of the past.

It burns and itches on your upper lip: a herpes infection is on the advance. Caught early, the number and size blisters can be controlled with virus-controlling salves, but the herpes simplex virus can recur at any time. "About 90 percent of the world's population carry it in them all their lives, once infected, and become sick again in stress situations," explains Dr. Anke Burger-Kentischer of the Fraunhofer Institute for Interfacial Engineering and Biotechnology IGB in Stuttgart. Coming down with a herpes virus is not always without its dangers. In the worst cases the nervous system and the brain become inflamed. The researcher, together with her team and the cell systems department, developed a 3D herpes infection model. This makes it possible for the first time to integrate the complicated dormant stage of the virus into a model of the skin. A patent application has been submitted for the new process.

The expert explains the particularity of the virus: "After the blisters subside, the herpes virus retreats to the nerve cells and rests there. At this stage, only the virus' DNA can be proven." As soon as a human suffers too much stress or is even exposed to too much intense sun, the nerve cell may release the virus. It travels along the neural pathways to sites where it has occurred several times before, and the new infection becomes visible.

To date the skin models used for drug testing and to detect the virus have been very simple and unable to simulate the dormancy state of the virus. "We have integrated a neuronal cell line into the certified skin model of the IGB and are able to detect this latency stage for the first time. Just like in the human nerve cells, the particles of the virus itself cannot be seen; only the presence of its DNA can be proven by means of a PCR (polymerase chain reaction) analysis," explains the expert.

The researcher and her team then exposed the skin model to ultraviolet radiation at wave lengths of 280 to 315 nanometers (UVB). This reactivated the herpes virus, and there was an infection on the skin model. Proof of this reactivation was also possible on a co-culture. For this, the researchers introduced the latently infected neuronal cell line to a carrier with pores. Subsequently the cells were also irradiated with UVB. The virus was reactivated and penetrated these pores, infecting the cutaneous keratinocytes -- the keratinizing cells cultivated previously. To verify the infection, the scientists used a specific antibody that binds to a specific protein on the outer layer of the virus. The coloration of this antibody made it possible to clearly show the infection of the skin cells with the reactivated virus from the nerve cells.

"The 3-D herpes infection model therefore simulates an in-vivo situation exactly. Animal experiments will in the future become largely unnecessary," happily explain Burger-Kentischer and the doctoral candidate, Ina Hogk, who has worked on the development of the model from the beginning.

Research on active ingredients can profit from the 3D herpes infection model of the researchers from IGB, a model that also enables improved study of infection mechanisms. This procedure might also be used to test new medications for shingles, which is also caused by a variant strain of the herpes virus.

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

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

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

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

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

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

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

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

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

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

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

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

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Journal Reference:

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

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Gene is first linked to herpes-related cold sores

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

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

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

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

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

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

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

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

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

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Journal Reference:

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

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The Kid's Doctor: Cold season often brings contagious cold sores

Fever blisters -- also called cold sores -- are fairly common, but they have nothing to do with a cold.

These sores typically appear on the outside of the mouth, on the lips. The majority (about 95 percent) of fever blisters are due to a virus, typically herpes type 1. Because the sores are due to a virus, they're contagious and most people will be exposed to the virus during their lifetime.

Children are typically exposed via contact with an adult, sibling or relative who has a fever blister, or with other children who've mouthed toys or other objects that may have been contaminated with the virus.

In many cases, exposure is asymptomatic, while other children will develop painful vesicles appearing both inside the mouth, on the tongue and gums, as well as on the lips 3-5 days after exposure.

This initial illness is called herpetic gingivostomatitis. The initial infection tends to be more uncomfortable and may take up to two weeks to resolve. The most difficult aspect is oral discomfort, so it's important to make sure infected youngsters stay hydrated. Popsicles are often helpful for this.

Once you've been exposed to the herpes virus, it remains in your nerve endings, where it may be dormant and asymptomatic for years. About 60 percent of children are positive for HSV-1 by adolescence. At times of stress, sun exposure, fever, or menstrual periods, the virus may become active again, and result in a fever blister.

Children who develop a fever blister are also contagious and may spread the virus to others by touching them, or picking at the lesion and then touching other people or objects with their mouths.

Fever blisters may be treated in most cases with a topical antiviral applied directly to the lesion. Prescription medications are available that may shorten the duration of a fever blister by a day or two, especially if started early and applied frequently. If you child experiences recurrent core sores, speak with your pediatrician about the use of oral antiviral medications.

Remember, if you have a fever blister, don't kiss your baby! Although the most viral shedding occurs after the initial HSV infection, you remain contagious with each fever blister, so it is best to take precautions for a few days after an outbreak.

(Dr. Sue Hubbard is a nationally known pediatrician and co-host of "The Kid's Doctor" radio show. Submit questions at www.kidsdr.comat www.kidsdr.com.)

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Ambushed by recurring cold sores? Here's why

For such a ubiquitous plague, cold sores can be mighty shaming.

In addition to the indignity of wearing a bulging, weepy blister on your lip, sufferers also must contend with the stigma of its source: HSV-1, a type of herpes simplex virus.

But unlike HSV-2, the virus that usually causes genital herpes, cold sores are not usually sexually transmitted (though they can be). Most people get infected with HSV-1 as kids, from kissy adults.

"It is one of the most common viral infections, and yet you're a pariah," said Dr. Adam Friedman, director of dermatologic research at Albert Einstein College of Medicine at Yeshiva University in New York. "People look at you like you're a leper."

About 70 percent of Americans are infected with HSV-1, but just a third of those infected have cold sore outbreaks, said Bryan Cullen, professor in the department of molecular genetics and microbiology at Duke University Medical Center. Genetics likely separates the lucky from the unlucky, he said.

The hardy virus, which stays in your body your whole life, survives by moving up the sensory nerves after initial infection and vacationing in nerve bundles, where immune cells can't find and destroy it. Triggers such as stress, fatigue, sun exposure, picking at your lip or having a cold or the flu can reactivate some infected cells, which travel back to the initial infection site to cause a new outbreak.

There is no cure. Cullen and fellow researchers hope to find a way to disrupt the processes that keep the virus latent, so that they can coax it out of hiding all at once and ambush it with medication. But they're not close to clinical trials, Cullen said.

HSV-1 has been implicated in a number of diseases, including Alzheimer's, though that link is disputed. Though there are rare cases of severe complications from HSV-1 — such as when the virus spreads to the brain in immunocompromised people, causing death or neurological damage — for the most part "the worst part about (HSV-1) is probably the social stigma," Friedman said.

Prevention and treatment

Though the virus is most contagious during an outbreak, when the virus is "shedding," it's also possible to transmit when no outbreak is visible. According to a study published in 2008 in an oral medicine journal, at least 70 percent of people with HSV-1 shed asymptomatically at least once a month.

Friedman recommends keeping your mouth away from others when you feel a cold sore coming, during the outbreak and for a few days after it goes away. That includes oral sex, as HSV-1 can be transmitted from mouth to genitals (HSV-2 also can be transmitted from genitals to mouth).

Taking prescription antivirals such as acyclovir (Zovirax) or valacyclovir (Valtrex) can reduce healing time or prevent a blister from forming at all, clinical trials have shown. It's best to attack during the "prodrome" stage, when many people feel tingling or itching at the infection site, or have flulike symptoms, before a blister appears.

Friedman suggests applying ice at the first hint of a cold sore, holding it against the infected site for no more than 15 minutes, to reduce swelling. You might also soak a cotton ball in whole milk and hold it against the sore for 10 to 15 minutes daily, Friedman said. Milk contains the protein monocaprin, which can halt HSV-1.

Finally, cover a blister with a thick emollient such as petroleum jelly to speed healing and protect the wound from bacteria, Friedman said.

aelejalderuiz@tribune.com

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

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

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

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

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

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

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

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

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

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

About Herpes

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

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Journal Reference:

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

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

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

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

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

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

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

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

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

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

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

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

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

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Journal Reference:

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

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Goodbye cold sores

ScienceDaily (June 27, 2011) — Herpes infections on the lips, in the eyes or on the nose are painful, long-lasting and unpleasant. A new 3D herpes infection model brings hope: active ingredients and new treatments can be reliably tested with this model. Animal tests could soon be a thing of the past.

It burns and itches on your upper lip: a herpes infection is on the advance. Caught early, the number and size blisters can be controlled with virus-controlling salves, but the herpes simplex virus can recur at any time. "About 90 percent of the world's population carry it in them all their lives, once infected, and become sick again in stress situations," explains Dr. Anke Burger-Kentischer of the Fraunhofer Institute for Interfacial Engineering and Biotechnology IGB in Stuttgart. Coming down with a herpes virus is not always without its dangers. In the worst cases the nervous system and the brain become inflamed. The researcher, together with her team and the cell systems department, developed a 3D herpes infection model. This makes it possible for the first time to integrate the complicated dormant stage of the virus into a model of the skin. A patent application has been submitted for the new process.

The expert explains the particularity of the virus: "After the blisters subside, the herpes virus retreats to the nerve cells and rests there. At this stage, only the virus' DNA can be proven." As soon as a human suffers too much stress or is even exposed to too much intense sun, the nerve cell may release the virus. It travels along the neural pathways to sites where it has occurred several times before, and the new infection becomes visible.

To date the skin models used for drug testing and to detect the virus have been very simple and unable to simulate the dormancy state of the virus. "We have integrated a neuronal cell line into the certified skin model of the IGB and are able to detect this latency stage for the first time. Just like in the human nerve cells, the particles of the virus itself cannot be seen; only the presence of its DNA can be proven by means of a PCR (polymerase chain reaction) analysis," explains the expert.

The researcher and her team then exposed the skin model to ultraviolet radiation at wave lengths of 280 to 315 nanometers (UVB). This reactivated the herpes virus, and there was an infection on the skin model. Proof of this reactivation was also possible on a co-culture. For this, the researchers introduced the latently infected neuronal cell line to a carrier with pores. Subsequently the cells were also irradiated with UVB. The virus was reactivated and penetrated these pores, infecting the cutaneous keratinocytes -- the keratinizing cells cultivated previously. To verify the infection, the scientists used a specific antibody that binds to a specific protein on the outer layer of the virus. The coloration of this antibody made it possible to clearly show the infection of the skin cells with the reactivated virus from the nerve cells.

"The 3-D herpes infection model therefore simulates an in-vivo situation exactly. Animal experiments will in the future become largely unnecessary," happily explain Burger-Kentischer and the doctoral candidate, Ina Hogk, who has worked on the development of the model from the beginning.

Research on active ingredients can profit from the 3D herpes infection model of the researchers from IGB, a model that also enables improved study of infection mechanisms. This procedure might also be used to test new medications for shingles, which is also caused by a variant strain of the herpes virus.

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Gene is first linked to herpes-related cold sores

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

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

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

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

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

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

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

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

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

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Journal Reference:

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

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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.

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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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How to Get Rid of Cold Sores

Cold sores can be pesky little things. They always occur at the wrong time, like right before a date or an important job interview. Cold sores occur on the lips or in the area surrounding the mouth. Cold sores are also referred to as "fever blisters".

Cold sores or "fever blisters" are caused by the Herpes Simplex 1 virus. Type 1 refers to herpetic lesions of the upper body. Genital herpes do not fall into this category. Since cold sores are caused by a virus, they are treatable but not curable. Also, cold sores are highly contagious. Even slight contact with a lesion can transmit virus particles from one person to another. Treatments exist both over the counter and prescription to keep cold sores under control and get rid of those unsightly lip lesions.

1. Over the counter treatments. Cold sores can be treated with creams and ointments purchased from your local pharmacy. Abreva® is a cold sore treatment that speeds healing as well as any prescription medication. The treatment should be used during the first couple of days of the infection which is called the "tingle stage". During this stage of the infection, outward signs are not yet visible on the skin. An infected person may feel burning, tingling, or itching around the mouth where the cold sore is preparing to form. Abreva® works best at this stage to shorten what could be a two week ordeal from start to finish. Other products that can be used include Herpecin-L®, Zilactin®, and Anbesol Cold Sore Therapy®. Carmex®, Neosporin(TM), and Chapstick® are used to prevent cracking, itching, and redness during the later stages of the infection when the sore is drying out and scabbing over.

2. Prescription medications. If over the counter remedies are not resolving the cold sore problem to your satisfaction, then see a doctor about prescription treatments. The Food and Drug Administration (FDA) has approved two medications for the treatment of cold sores: Denavir® cream 1% and Zovirax® cream 5%. These creams are best applied during the "tingle stage" of cold sore formation. The logic is that if the treatment is applied early enough before the herpes virus has time to replicate itself the duration of the outbreak will decrease. An important point to note is that even with treatment, a person experiencing a cold sore is still considered contagious until the sore completely disappears.

While cold sores are not a major health problem, they are a form of herpes simplex virus and should be treated appropriately. Steps should be taken to avoid re-infection and transmittance of the virus. Treatment does not cure, but does keep cold sore symptoms under control.

Visit http://www.LearnHowToRemove.com for a growing library of tips to remove those annoying messes in your life.

How to Treat Cold Sores So They Don't Spread - Or Wreck Your Social Life

The chances are that unless you have a very effective cold sore treatment plan in place, you, like so many others are going to suffer from many more outbreaks of these painful and embarrassing sores. Although everyone who has suffered from the Herpes Simplex 1 Virus has come to dread the pain and embarrassment that comes with these outbreaks, what most people worry about most is the unfortunate impact that these outbreaks can have on their social life.

It is difficult to date and find the companionship that we all need if you cannot kiss or allow the other person to touch your face. It is also very difficult to meet new friends and truly enjoy yourself at social functions if you have to worry about preventing others from coming in contact with your face.

Of course, it can be quite difficult when others shy away from you or talk behind your back because of the sores on your mouth as well. All of these things come together to explain why those who suffer with this form of Herpes often suffer a lower self-esteem and higher amounts of anxiety.

The good news is you can treat cold sores and even eliminate future outbreaks entirely, enabling you to enjoy an active social life! There are two different aspects that come into play here: preventing the spread of Herpes and implementing a personalized cold sore treatment plan.

Preventing Virus Spread

It's true that trying to prevent others from getting the virus is what causes much of the social discomfort when you have the sores on your lips. While most people will recognize the cold sores and actively avoid making contact with your face, many may not know that they can get the virus by eating or drinking after you. Literally anything that your sores come in contact with could spread the virus!

The best way to prevent the spread of Herpes is to pay very close attention to the initial signs that you are getting them. In many cases the virus is spread during the very first stage of an outbreak before the sores are visibly showing. The virus can still be present on the skin even if it is not seen, so you should be extra alert to notice what your initial signs are so you can identify them right away.

For many people the initial signs are tingling or itching, red skin, or a rough patch of skin.

Implementing a Cold Sore Treatment Plan

The absolute best way to prevent spreading Herpes would be to force the virus to remain inactive inside your body and never make a public appearance on your face, right? This can actually be done by implementing a cold sore treatment plan that allows you to treat cold sores effectively and essentially inactivate the virus.

Here are some ideas of what should be included in a treatment plan:

* Working around outbreak triggers to avoid outbreaks.
* Correcting any deficiencies inside the body.
* Supplying the body with a well balanced, nourishing diet.
* Protecting the skin from sun and other potential damage.

If you just continue to live your life day to day and treat cold sores only after an outbreak develops, you will be living the social consequences the rest of your life. Take charge now and have the active social life you deserve!

Mouth Cold Sores - What Are They, Treatment (and Why You Might Not Have a Cold Sore at All)

A Quick Primer On Cold Sores and Herpes Simplex--Also, You May Not Have A Cold Sore After All!

A mouth cold sore, otherwise known as oral herpes, is the most common manifestation of the herpes simplex virus, the second most common is genital herpes. If you're getting a cold sore in your mouth, on the other hand, that's almost definitely not a cold sore because it's extremely rare that cold sores will occur inside someone's mouth--it's most likely a canker sore, which is completely different from a cold sore. A canker sore, otherwise known as an aphthous ulcer, is a bacterial infection and has nothing to do with the herpes virus and requires a completely different treatment.

Cold sores can also occur on the nose, probably the second most common place that they pop up on the face, but are almost always on, or right around the edge of, the lip. This is the specific problem that we will be addressing today.

Cold sores cycle between active and dormant periods--active periods typically last 2-21 days where there are blisters on the skin containing infectious virus particles, followed by a remission period--this is the state the virus is in the great majority of the time. During the remission period, the virus resides entirely in the sensory nerve cells, not doing anything whatsoever, where it will remain for the rest of the infected person's life. Over time the frequency and duration of active outbreaks lessen.

The Home Treatment for Mouth Cold Sores That I've Found To Be The Most Effective

1. Keep the cold sore clean and dry by washing it every few hours with a damp wash cloth and soap. Use some good quality facial soap if you can to keep from drying out your skin too much.

2. Apply an ice cube for a few minutes to the cold sore right after you wash it. Not only will this will cause the itching and pain to dissipate, but it will also lessen the severity of the outbreak by slowing down the virus' metabolism and decreasing its replication rate.

3. Apply some witch hazel with a q-tip after you've iced it, this is by far one of the most effective treatments I've found to date--I heard about it on an internet alternative health forum and tried it out myself, witch hazel is just amazing stuff. I can't tell you how it works, but I know from my own personal experience treating several cold sores with it over the last few year that it works.

4. Take some nail polish remover on a q-tip (a new one), and finally apply it to the cold sore--this stuff is awesome at soaking up any last little bit of nasty yellow virus fluid that your cold sore is inevitably leaking out. I've heard you can use Clearasil, too, but that it doesn't work as well as the nail polish remover.

Bonus Tip

Studies have shown that taking lysine every day at a dosage of 1000mg 3 times a day not only reduces the number of the outbreaks you get over the course of a year but also greatly reduces the length and severity of an outbreak when you do get one.

To get even further information on mouth cold sores, I'd suggest the you visit my friend's blog (click the link to the left)--she and her friends have been experimenting with home remedies for oral herpes for years now and have taken their findings and distilled the information down to precisely what works and what doesn't, very interesting stuff.

Are Cold Sores Herpes?

Many people have herpes and many people have cold sores. Both ailments are caused by viruses, and people who are infected often experience outbreaks in the form of a rash, pimples or sores that break open. There are differences in the two ailments, and there are many similarities too. This article will clarify any confusion you might have about herpes and cold sores.

Cold sores are technically called HSV type 1, HSV - 1, oral herpes, or herpes simplex, and outbreaks most commonly occur on the lips, though they can occur on the inside of the mouth, tongue and genitals too. In non medical terms, cold sores are also called fever blisters. Most people would rather call the outbreaks cold sores or fever blisters, rather than oral herpes.

The initial infection with the herpes simplex or cold sore virus, usually occurs in early childhood. A child can get infected by a kiss from an aunt or grandmother for example, and then a child can infect another child with a kiss or slobbering on the other child, or by sharing a cup or spoon. If you think back to situations you were in as a child, or situations you see children in now, you can see how easy it is to spread the infection. For this reason, it is estimated that up to 80% of the adult population has the cold sore virus in them. But for most people, the virus is dormant, and causes them no concern at all.

For others, outbreaks around the lips may be common or even frequent, and such outbreaks may tend to occur when the person is anticipating something which may be stressful, such as a date or a job interview. For some people, chocolate, nuts or sunshine can cause a cold sore to appear.

When the term herpes is used, it usually refers to any infections or outbreaks below the belt. It is technically called HSV type 2, or HSV 2, or herpes simplex 2. The virus is usually transmitted or passed along to someone else through sexual contact. The symptoms can include a tingling in the limbs and sores in the form of small pimples or larger pimples which usually break open, and then scab over and finally go away.

The viruses for HSV 1 and HSV 2, are similar, but not exactly the same, from a scientific standpoint. But from a practical standpoint, the sores and symptoms are similar. The cold sore, or HSV 1 virus, can be transferred to genitals through oral sex. And the herpes, or HSV 2 virus, can be transferred to the lips, also through oral sex.

As the viruses for both are very similar, the treatments for both are also similar. Treatments can include anti viral prescription drugs, or herbal formulas.

If you want to end cold sores or herpes, my site below has a guaranteed formula for herpes prevention. My website explains how it works, and from my website, you can email me with any questions you might have. I answer emails confidentially, and you will not get on any mailing list.
http://www.herpesgone.com

What Causes Cold Sores and How Do I Prevent Them From Happening?

What causes cold sores? Many folks ask this question everyday. One ultimate trigger causes most of these unpleasant and embarrassing sores for nearly everyone. Let me tell you about it.

I am sure you are aware that a cold sore is the byproduct of the herpes simplex virus during its replication process. This virus destroys a lot of your cells while creating new virus particles.

Usually, this virus is inactive and hiding in the root cells of your facial nerves. If conditions become right, it will activate, travel up the nerve fiber and create a massive sore on your face.

Yes, the herpes simplex virus is what causes all cold sores. However, over a third of those that carry this virus never get an outbreak even though nearly 90% of the population is infected.

So, if we want to determine what causes cold sores, we need to uncover the ultimate trigger that activates the sleeping virus.

Both physical and mental stress is a common trigger that causes cold sores. Often, people get an outbreak when they come down suffer from cold or flu symptoms.

Mental stress can be such things as an upcoming big event, like a wedding. One woman just wrote that she always gets one before a big date. Terrible luck for sure.

You cannot always reduce or eliminate stress. Stress is part of being alive and active. You do not need to control the stress as much as what it does to your body.

The ultimate trigger for these sores - for activating the herpes virus - is an acid pH balance. Stress, cold weather and poor intake of vegetables will cause your body to dip into the acid zone.

This greatly reduces your resistance to disease and produces the perfect environment for activating the herpes virus - or any other virus for that matter.

It weakens your immune system and reduces your tissue levels of oxygen.

Your pH balance is quite fragile. It moves quite easily between 6.0 (slightly acid) to 7.5 (slightly alkaline). Your ideal target pH for best health is about 7.35. The farther you dip below 7, the more you are susceptible to viral attack.

Your ultimate cold sore trigger is a pH of 6.5 and below.

Your ultimate cold sore prevention program is keeping your pH above 7. You can easily achieve this with food and supplements.

If you get frequent or severe outbreaks, the first thing you should consider is to begin taking a top shelf vitamin and mineral program with a minimum of 1000 milligrams of calcium daily. Calcium is critical to prevent acidity in your body.

If this is not enough, you may need to evaluate your diet also.

Acid causing foods to restrict, especially during an outbreak, include processed sugar, white flour, carbonated beverages, table salt, pork, tobacco and coffee.

Helpful alkaline raising foods to increase in your diet are green vegetables (cabbage, broccoli, asparagus), wild rice, flax seed, apples and most citrus fruit.

Citrus fruit contains citric acid but it is not an acid causing food. Citric acid actually transforms to alkaline in your body.

You will have to experiment and determine what works best for you. You are unique and your body has needs unique to just you.

If you suffer, as I used to, from these terrible sores, please do not forget to start taking the best quality supplement you can afford. It will really make a difference. If need be, do not hesitate to take additional calcium supplements.

Once you start applying these simple treatment and prevention methods, then you will really benefit from the breakthroughs we have found in natural cold sore remedies.

You must have the basics right for best results. It is just that simple!

No matter what other cold sore remedies you choose to use, keeping your pH balance in the alkaline zone will greatly reduce the number of sores you get and their severity.

An acid tissue pH is truly what causes cold sores.

What causes cold sores in your life? Want some amazing Cold Sore Remedies? Stop by Denny Bodoh's wonderful web site where you will find answers to all your cold sore questions. Plus, you will get some truly amazing remedies that will quickly put a smile back on your face. Go to http://www.3DayColdSoreCure.com
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Are Cold Sores Herpes?

Many people have herpes and many people have cold sores. Both ailments are caused by viruses, and people who are infected often experience outbreaks in the form of a rash, pimples or sores that break open. There are differences in the two ailments, and there are many similarities too. This article will clarify any confusion you might have about herpes and cold sores.

Cold sores are technically called HSV type 1, HSV - 1, oral herpes, or herpes simplex, and outbreaks most commonly occur on the lips, though they can occur on the inside of the mouth, tongue and genitals too. In non medical terms, cold sores are also called fever blisters. Most people would rather call the outbreaks cold sores or fever blisters, rather than oral herpes.

The initial infection with the herpes simplex or cold sore virus, usually occurs in early childhood. A child can get infected by a kiss from an aunt or grandmother for example, and then a child can infect another child with a kiss or slobbering on the other child, or by sharing a cup or spoon. If you think back to situations you were in as a child, or situations you see children in now, you can see how easy it is to spread the infection. For this reason, it is estimated that up to 80% of the adult population has the cold sore virus in them. But for most people, the virus is dormant, and causes them no concern at all.

For others, outbreaks around the lips may be common or even frequent, and such outbreaks may tend to occur when the person is anticipating something which may be stressful, such as a date or a job interview. For some people, chocolate, nuts or sunshine can cause a cold sore to appear.

When the term herpes is used, it usually refers to any infections or outbreaks below the belt. It is technically called HSV type 2, or HSV 2, or herpes simplex 2. The virus is usually transmitted or passed along to someone else through sexual contact. The symptoms can include a tingling in the limbs and sores in the form of small pimples or larger pimples which usually break open, and then scab over and finally go away.

The viruses for HSV 1 and HSV 2, are similar, but not exactly the same, from a scientific standpoint. But from a practical standpoint, the sores and symptoms are similar. The cold sore, or HSV 1 virus, can be transferred to genitals through oral sex. And the herpes, or HSV 2 virus, can be transferred to the lips, also through oral sex.

As the viruses for both are very similar, the treatments for both are also similar. Treatments can include anti viral prescription drugs, or herbal formulas.

I help people prevent cold sores and herpes outbreaks with a herbal formula. My website explains how it works, and from my website, you can email me with any questions you might have. I answer emails confidentially, and you will not get on any mailing list.
http://www.herpes-herbs.com/

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