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    What have I done? Cruel messages were splashed across her social media pages. She saw disgust and revulsion in the eyes of her friends and family. She knew no man would ever want her again. She was tainted for life — and there was nothing she could do. In that second, Emma made her decision.

    She stepped closer to the platform edge. So why am I sharing this tragic story with you today? Because not only did Emma miraculously survive And you can do it too. So why has herpes been so difficult to beat up until now? Herpes works by invading healthy cells and taking control of them. In fact, this cellular search and destroy mission could treat all of your painful and embarrassing symptoms in as little as 48 HOURS… … And best of all, treat this horrible disease in as little as a few weeks from today.

    Including professional athletes, international business leaders and Hollywood celebrities — people you know by name. So you need to take this opportunity to watch it now, and until the very end, while you still have the chance. So if you want to treat the herpes virus - both types 1 and 2. And do it in as little as a few weeks.

    Then be sure to keep watching, because… The secret lies in nothing more than these 3 ingredients, enjoyed by the people of Morocco for centuries Yep, three cheap, readily available and delicious ingredients that you can pick up from your local grocery store today. But before we get to that, let me first introduce myself, and explain why I decided to create this presentation. But before I reveal how, let me first tell you a quick story.

    The second we met, sparks flew. All the things I was looking for. To be honest, she was perfect. And for me at least, it was love at first sight. But after just a couple months, our blissful little bubble would burst in the cruelest way possible. I was at home in the kitchen when suddenly there was a loud bang on the door. Her eyes were bright red and filled with tears.

    A second later she slapped me round the face with such force she cut me above my left eye. I literally had no idea what she was talking about.

    It was ugly, and it made her feel self-conscious. So she decided to stay in for a few days until it scabbed over and healed. The problem was, a few days after that, she started to feel unbearable pain downstairs. She said it was like someone was stabbing her in the crotch, while giving her rug burn, while pouring acid over the top. The next day she spotted a couple of little sores down there. She freaked out and went to see her doctor the same day who did a test.

    A few days later and the tests came back. She had both forms of herpes — at the same time Imagine that. Because you can have both forms of herpes caused by the same type of herpes virus at the same time. Emma was convinced that I must have given the disease to her.

    But as far I knew, I was clean. So I agreed to get tested. I had herpes too. Remember, it likes to hide. Because the person who gave it to you may not have even known they had it themselves. But of course, at the time that meant nothing to me.

    For weeks she suffered from puss-filled blisters on her lip. A raging, burning sensation down below. And pain and discomfort with every step.

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    Because although the physical pain of herpes felt like torture to Emma, the emotional pain would become even worse after word of her diagnosis spread. People from our home town started leaving disgusting messages on her Facebook page, and posting sick jokes on Twitter, which left her crying for days.

    And lifelong friends started behaving differently around her. Over time, they stopped calling. The invitations to nights out and parties dried up. So what did she do about it? Well, take a look at this. Because it will make you mad. The doc started her on Zovirax and later Famvir. Emma suffered from headaches, fatigue, stomach pain, diarrhea and frequent vomiting. So the doc switched her to Valtrex. But not long after, she began to complain about a dull pain in her lower back, which we later realized was due to her kidneys breaking down.

    According to a study into the drug and its effect on the kidneys, scientists discovered that the renal function of healthy human subjects was damaged as quickly as 12 — 48 hours after the drug was administered.

    The virus just kept on coming back again and again. And why did this continually happen? Or even prevent the spread of the disease to other people! They NEVER attempt to get to the root cause of the virus in order to actually treat it and stop it from coming back. And get rid of the symptoms a little faster?

    Which is exactly what happened to Emma. The attacks became more and more severe and painful, took far longer to heal, and began to cover larger areas of her body. Brain Atrophy A recent study in Sweden found that people with herpes are TWICE as likely to develop dementia, with more than 30 experts now in agreement that the herpes virus is one of the major causes of dementia.

    Ocular Herpes The type 1 herpes simplex virus, which results in cold sores, is also proven to cause eye herpes, or ocular herpes. This is a common and recurring viral infection of the cornea that can lead to scarring, vision loss and blindness. To illustrate how serious this risk is, a massive 50, new and recurring cases are reported every year, according to The National Eye Institute. Which can lead to brain damage, blindness, or even death.

    And I agreed to give Emma some space. I heard nothing from her for months. Until I got a phone call that made my blood run cold. It was from her brother, James, who I still kept in contact with. Apparently, Emma had sunk into a deep depression and had become isolated and withdrawn. James said how it seemed like the light in her had been turned off. She knew she had to be truthful about her virus before things went any further.

    So after a few dates, she plucked up the courage to tell him. The next morning, on the way to work, Emma was standing on the edge of the subway platform. A man standing beside her had noticed how upset she looked. And how she kept creeping closer and closer to the platform edge. He tried to talk to her, but Emma ignored him, keeping her eyes fixed firmly on the tracks. The man had a bad feeling in his stomach, and decided to inch closer to this pretty young girl with sadness in her eyes.

    As the train hurtled through the station, Emma suddenly JUMPED Anticipating what might happen, the man was able to grab her arm just in time, pulling her to safety as the pair of them collapsed in a heap on the platform as the subway train thundered by. When James told me this, I felt sick.

    A painful group of blisters filled with yellow puss appeared on my top lip, and I was ashamed to show my face for weeks.

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    My own herpes virus had finally come out of hiding. Like Emma, I believed what the doctors told me. And all I could do was try to lessen the symptoms with expensive drugs.

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    I was resigned to the fact that the both of us would be stuck with this disease for the rest of our lives, and there was nothing we could do to change it. And although I no longer saw Emma, for years I prayed to God to look after her. And at the beginning ofI think he finally heard me.

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    Not that I knew it at the time. The training camp was designed to combat extremist organizations. And our base was a small fishing village called Tifnit in the South of Morocco, with more than 2, military personnel from 24 African and Western countries. Not me, I might add.
    A three-dimensional reconstruction and animation of a tail-like assembly on HSV-1 capsid 3D reconstruction of the HSV-1 capsid Animal herpes viruses all share some common properties.

    The structure of herpes viruses consists of a relatively large, double-stranded, linear DNA genome encased within an icosahedral protein cage called the capsidwhich is wrapped in a lipid bilayer called the envelope. The envelope is joined to the capsid by means of a tegument. This complete particle is known as the virion. These genes and their functions are summarized in the table below.

    Early gene expression follows, to allow the synthesis of enzymes involved in DNA replication and the production of certain envelope glycoproteins. Expression of late genes occurs last; this group of genes predominantly encode proteins that form the virion particle. Many of these receptors are then pulled inwards by the cell, which is thought to open a ring of three gHgL heterodimers stabilizing a compact conformation of the gB glycoprotein, so that it springs out and punctures the cell membrane.

    The sequential stages of HSV entry are analogous to those of other viruses. At first, complementary receptors on the virus and the cell surface bring the viral and cell membranes into proximity. Interactions of these molecules then form a stable entry pore through which the viral envelope contents are introduced to the host cell.

    The virus can also be endocytosed after binding to the receptors, and the fusion could occur at the endosome. In electron micrographs, the outer leaflets of the viral and cellular lipid bilayers have been seen merged; [17] this hemifusion may be on the usual path to entry or it may usually be an arrested state more likely to be captured than a transient entry mechanism. In the case of a herpes virus, initial interactions occur when two viral envelope glycoprotein called glycoprotein C gC and glycoprotein B gB bind to a cell surface particle called heparan sulfate.

    Next, the major receptor binding protein, glycoprotein D gDbinds specifically to at least one of three known entry receptors. The nectin receptors usually produce cell-cell adhesion, to provide a strong point of attachment for the virus to the host cell.

    The interaction of these membrane proteins may result in a hemifusion state. Once attached to the nucleus at a nuclear entry pore, the capsid ejects its DNA contents via the capsid portal. The capsid portal is formed by 12 copies of portal protein, UL6, arranged as a ring; the proteins contain a leucine zipper sequence of amino acidswhich allow them to adhere to each other. Viral epitope presentation with MHC class I is a requirement for activation of cytotoxic T-lymphocytes CTLsthe major effectors of the cell-mediated immune response against virally-infected cells.

    Replication[ edit ] Micrograph showing the viral cytopathic effect of HSV multinucleation, ground glass chromatin Following infection of a cell, a cascade of herpes virus proteins, called immediate-early, earlyand late, is produced.

    Research using flow cytometry on another member of the herpes virus family, Kaposi's sarcoma-associated herpesvirusindicates the possibility of an additional lytic stagedelayed-late.

    In the case of HSV-1, no protein products are detected during latency, whereas they are detected during the lytic cycle. The early proteins transcribed are used in the regulation of genetic replication of the virus. The viral genome immediately travels to the nucleus, but the VHS protein remains in the cytoplasm.

    Here, concatemers of the viral genome are separated by cleavage and are placed into formed capsids. HSV-1 undergoes a process of primary and secondary envelopment. The primary envelope is acquired by budding into the inner nuclear membrane of the cell. This then fuses with the outer nuclear membrane, releasing a naked capsid into the cytoplasm.

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    The virus acquires its final envelope by budding into cytoplasmic vesicles. LAT regulates the host cell genome and interferes with natural cell death mechanisms. By maintaining the host cells, LAT expression preserves a reservoir of the virus, which allows subsequent, usually symptomatic, periodic recurrences or "outbreaks" characteristic of nonlatency. Whether or not recurrences are symptomatic, viral shedding occurs to infect a new host.

    A protein found in neurons may bind to herpes virus DNA and regulate latency. When bound to the viral DNA elements, histone deacetylation occurs atop the ICP4 gene sequence to prevent initiation of transcription from this gene, thereby preventing transcription of other viral genes involved in the lytic cycle.
    Herpes simplex virus 2 is typically contracted through direct skin-to-skin contact with an infected individual, but can also be contracted by exposure to infected saliva, semen, vaginal fluid, or the fluid from herpetic blisters.

    Even microscopic abrasions on mucous membranes are sufficient to allow viral entry. HSV asymptomatic shedding occurs at some time in most individuals infected with herpes. Concurrent infection with HIV increases the frequency and duration of asymptomatic shedding.

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    Herpes simplex is a double-stranded DNA virus. The appearance and distribution of sores in these individuals typically presents as multiple, round, superficial oral ulcers, accompanied by acute gingivitis. Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms from the similar symptoms of other disorders, such as allergic stomatitis. When lesions do not appear inside the mouth, primary orofacial herpes is sometimes mistaken for impetigoa bacterial infection.

    Common mouth ulcers aphthous ulcer also resemble intraoral herpes, but do not present a vesicular stage. Laboratory tests include culture of the virus, direct fluorescent antibody DFA studies to detect virus, skin biopsyand polymerase chain reaction to test for presence of viral DNA. Although these procedures produce highly sensitive and specific diagnoses, their high costs and time constraints discourage their regular use in clinical practice.

    The differential diagnosis includes hand, foot and mouth disease due to similar lesions on the skin. Prevention Barrier protection, such as a condomcan reduce the risk of herpes transmission. As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men. Condom use also reduces the transmission risk significantly. In many infections, the first symptom people will have of their own infections is the horizontal transmission to a sexual partner or the vertical transmission of neonatal herpes to a newborn at term.

    Since most asymptomatic individuals are unaware of their infection, they are considered at high risk for spreading HSV. Neither type of condom prevents contact with the scrotum, anus, buttocks, or upper thighs, areas that may come in contact with ulcers or genital secretions during sexual activity. Protection against herpes simplex depends on the site of the ulcer; therefore, if ulcers appear on areas not covered by condoms, abstaining from sexual activity until the ulcers are fully healed is one way to limit risk of transmission.

    When one partner has a herpes simplex infection and the other does not, the use of antiviral medication, such as valaciclovirin conjunction with a condom, further decreases the chances of transmission to the uninfected partner. To prevent neonatal infections, seronegative women are recommended to avoid unprotected oral-genital contact with an HSVseropositive partner and conventional sex with a partner having a genital infection during the last trimester of pregnancy.

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    Mothers infected with HSV are advised to avoid procedures that would cause trauma to the infant during birth e. The use of valaciclovir and famciclovir, while potentially improving compliance, have less-well-determined safety in pregnancy. Management No method eradicates herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Analgesics such as ibuprofen and paracetamol acetaminophen can reduce pain and fever.

    Topical anesthetic treatments such as prilocainelidocainebenzocaineor tetracaine can also relieve itching and pain. Acyclovir was the first discovered and is now available in generic. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the nucleus of a nerve's cell body.

    HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated transcript. Prodromal symptoms include tingling paresthesiaitching, and pain where lumbosacral nerves innervate the skin. Prodrome may occur as long as several days or as short as a few hours before lesions develop. Beginning antiviral treatment when prodrome is experienced can reduce the appearance and duration of lesions in some individuals.

    During recurrence, fewer lesions are likely to develop and are less painful and heal faster within 5—10 days without antiviral treatment than those occurring during the primary infection.

    The causes of reactivation are uncertain, but several potential triggers have been documented. A study showed the protein VP16 plays a key role in reactivation of the dormant virus.

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    Reactivation due to other infections is the likely source of the historic terms 'cold sore' and 'fever blister'.

    Other identified triggers include local injury to the face, lips, eyes, or mouth; trauma; surgery; radiotherapy ; and exposure to wind, ultraviolet lightor sunlight.

    Some individuals' outbreaks can be quite debilitating, with large, painful lesions persisting for several weeks, while others experience only minor itching or burning for a few days. Some evidence indicates genetics play a role in the frequency of cold sore outbreaks. An area of human chromosome 21 that includes six genes has been linked to frequent oral herpes outbreaks. An immunity to the virus is built over time. Most infected individuals experience fewer outbreaks and outbreak symptoms often become less severe.

    After several years, some people become perpetually asymptomatic and no longer experience outbreaks, though they may still be contagious to others. Immunocompromised individuals may experience longer, more frequent, and more severe episodes.

    Antiviral medication has been proven to shorten the frequency and duration of outbreaks. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs. HSVinfected individuals are at higher risk for acquiring HIV when practicing unprotected sex with HIV-positive persons, in particular during an outbreak with active lesions.

    As many as one in seven Canadians aged 14 to 59 may be infected with herpes simplex type 2 virus [80] and more than 90 per cent of them may be unaware of their status, a new study suggests. Emperor Tiberius is said to have banned kissing in Rome for a time due to so many people having cold sores. In the 16th-century Romeo and Julietblisters "o'er ladies' lips" are mentioned.

    In the 18th century, it was so common among prostitutes that it was called "a vocational disease of women". Herpes was not found to be a virus until the s. The original use was against normally fatal or debilitating illnesses such as adult encephalitis, [87] keratitis, [88] in immunocompromised transplant patients, [89] or disseminated herpes zoster. The usage expanded to include topical treatment of herpes simplex, [92] zoster, and varicella.

    Vidarabine was the first systemically administered antiviral medication with activity against HSV for which therapeutic efficacy outweighed toxicity for the management of life-threatening HSV disease. Intravenous vidarabine was licensed for use by the U. Food and Drug Administration in Other experimental antivirals of that period included: It was merely a cold sore in an unusual place until the s.

    As late asa study of "Psychological morbidity in a clinic for sexually transmitted disease" does not mention herpes simplex because at that time, no significant morbidity problem i.

    Most had hardly heard of genital herpes Feelings can include depressionfear of rejection, feelings of isolationfear of being found out, and self-destructive feelings. Much of the hysteria and stigma surrounding herpes stems from a media campaign beginning in the late s and peaking in the early s. Multiple articles were worded in fear-mongering and anxiety-provoking terminology, such as the now-ubiquitous "attacks", "outbreaks", "victims", and "sufferers".

    At one point, the term "herpetic" even entered the popular lexicon. The articles were published by Reader's Digest, U. News, and Time magazine, among others.

    A made-for-TV movie was named Intimate Agony. The peak was when Time magazine had 'Herpes: The New Scarlet Letter' on the cover in Augustforever stigmatizing the word in the public mind. People with the herpes virus are often hesitant to divulge to other people, including friends and family, that they are infected. This is especially true of new or potential sexual partners whom they consider casual. One of the diseases that increased dramatically was genital herpes.

    The HRC was designed to meet the growing need for education and awareness about the virus. The goal of these HELP groups was to provide a safe, confidential environment where participants can get accurate information and share experiences, fears, and feelings with others who are concerned about herpes. The charity started as a string of local group meetings before acquiring an office and a national spread. Herpes simplex research Research has gone into vaccines for both prevention and treatment of herpes infections.

    Unsuccessful clinical trials have been conducted for some glycoprotein subunit vaccines. As ofthe future pipeline includes several promising replication-incompetent vaccine proposals while two replication-competent live-attenuated HSV vaccine are undergoing human testing.

    A genomic study of the herpes simplex type 1 virus confirmed the human migration pattern theory known as the out-of-Africa hypothesis.

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    Archived from the original on 31 December Retrieved 31 December Dental clinics of North America.
    In this feature, we look at the latest scientific facts about the two types of herpes simplex virus, as well as social attitudes toward oral and genital herpes. When many people first tell someone they have genital herpes, they start by comparing the infection to oral herpes, or cold sores.

    How apt is the comparison? In spite of scientific facts, the social stigma and emotional attitudes surrounding genital herpes can make it hard to compare it objectively with an oral infection that most people casually accept. Following the unspoken assumptions of our society, many people still believe there is a "good" herpes virus-HSV- 1, the usual cause of cold sores-and a "bad" herpes virus-HSV-2, the usual cause of genital herpes.

    In this feature, we take a look at HSV- 1 and 2 to see how alike and different the two viral types really are. We asked leading researchers how the two compare in terms of severity, recurrences, and transmission rates.

    We asked how often each occurs outside its usual site of preference, and how each behaves in the genital area. We questioned how much immunity having one type orally or genitally provides against getting the second type. In addition, we looked at the way our society views oral and genital herpes. What's behind the very different images the two types carry? And what can we do about it? In an interview, counselors at the National Herpes Hotline suggest ways to help replace judgmental social assumptions with a healthy attitude.

    Both types infect the body's mucosal surfaces, usually the mouth or genitals, and then establish latency in the nervous system. For both types, at least two-thirds of infected people have no symptoms, or symptoms too mild to notice. However, both types can recur and spread even when no symptoms are present. The primary difference between the two viral types is in where they typically establish latency in the body- their "site of preference. From there, it tends to recur on the lower lip or face.

    HSV-2 usually sets up residence in the sacral ganglion at the base of the spine. From there, it recurs in the genital area. Unfortunately, many people aren't aware of this, which contributes both to the spread of type 1 and to the misperception that the two types are fundamentally different.

    HSV-1 is usually mild, especially when it infects the lips, face, or genitals. However, in some cases type 1 can recur spontaneously in the eye, causing ocular herpes, a potentially serious infection which can lead to blindness. In very rare cases HSV- 1 can spread spontaneously to the brain, causing herpes encephalitis, a dangerous infection that can lead to death.

    HSV-1 is also the usual cause of herpes whitlow, an infection on the finger, and "wrestler's herpes," herpes gladiatorum a herpes infection on the chest or face. The range and potential severity of HSV-1 infections lead some experts to view the virus as more risky than usually perceived.

    Like HSV-1, type 2 is usually mild-so mild that two- thirds of infected people don't even know they have it. Type 2 rarely causes complications or spreads to other parts of the body. It is the most common cause of neonatal herpes, a rare but dangerous infection in newborns; however, type 1 causes up to one-third of neonatal infections.

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    The two types do behave somewhat differently depending on whether they are residing in their site of preference-the mouth and face for HSV-1, and the genital area for HSV But both types are quite common, and under most circumstances neither is a major health threat. That's one reason medical professionals tend to dismiss HSV -2 despite the emotional trauma a diagnosis can cause for a patient. While HSV can be a frustrating and painful condition for some people, in general the virus is less a medical problem than a social problem.

    For most of us, genital herpes is no more dangerous than a cold sore. Just how much of a physical problem HSV poses for a person depends largely on three factors. The first is how well the person's immune system is able to control the infection.

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    Differences in immune response may be the main reason that some people are bothered by frequent cold sores or genital herpes outbreaks while others are not. It's also the reason that both HSV-1 and 2 can pose serious challenges for infants, who have a limited immune response; and for people with compromised immune systems, including people with cancer, AIDS, severe burns, and people taking immunosuppressant medications. The second factor affecting outbreaks is how long a person has had the infection.

    Over time, recurrences of both HSV- 1 and 2 tend to decrease, for reasons that aren't entirely clear. In the case of oral HSV-1, many of the approximately million Americans who are infected acquired the virus when they were children. On the other hand, almost all of the approximately 40 million Americans infected with HSV-2 acquired the virus as teenagers or adults. In the first year, those who have recurring outbreaks experience an average of four to six episodes.

    Over time, as with oral infections, the number of outbreaks usually drops off. A third factor influencing the frequency of HSV -1 and 2 outbreaks is whether the virus is established in its site of preference. While HSV can infect both genital and oral areas, both types cause milder infections when they are away from "home" territory.

    Outside their site of preference, both type 1 and 2 lose most of their punch. For example, most people infected with HSV-1 in the genital area have few, if any, outbreaks after the initial episode, far fewer than is typical with either oral HSV-1 or genital HSV According to a study by Wald et al. New England Journal of Medicine,among women with genital herpes, the average number of recurrences per year for those with genital HSV-1 was zero.

    Other studies have shown an average of about one outbreak per year Benedetti, Annals of Internal Medicine, Similarly, HSV-2 infection in theoral area-outside its site of preference-very rarely causes problems. First of all, oral, HSV-2 infections are rare, for reasons discussed below. But even when an infection occurs, recurrent outbreaks are uncommon. In one study Lafferty et al. A possible fourth factor affecting recurrence rate is viral type.

    As a number of readers have attested over the years, many people with genital herpes are at least as concerned about transmission-the likelihood of spreading the virus to a partner-as about their own health. On the other hand, few people with oral herpes, share this concern. Is this because one type is more contagious than the other? The short answer is no. Both viral types are easily transmitted to their site of preference, and can also be spread to other sites.

    Both are most contagious during active outbreaks, but are often spread through viral shedding when there are no recognizable symptoms. Both of these figures reflect shedding as detected by viral culture. From here, however, the question of transmissibility gets more complicated. Acquisition of one type is more difficult-though certainly possible-if you already have the other type.

    This is because either type, contracted orally or genitally, causes the body to produce antibodies, some of which are active against both HSV-1 and 2. This acquired immune response gives some limited protection if the body encounters a second type. When a person with a prior HSV infection does contract the second type, the first episode tends to be less severe than when no prior antibodies are present.

    On a practical level, this means oral HSV-1 is often the most easily acquired herpes infection. Usually the first herpes simplex virus that people encounter, oral HSV-1, is typically spread simply by the kind of social kiss that a relative gives a child.

    Because children have no prior infection with any HSV type, they have no immune defense against the virus. By comparison, almost all HSV-2 is encountered after childhood, when people become sexually active. Those who have a prior infection with HSV-1 have an acquired immune response that lowers - though certainly doesn't eliminate-the risk of acquiring HSV In the absence of prior oral infection, however, HSV-1 spreads easily to the genital area, usually through oral sex.

    Finally, the question of immunity and HSV types is complicated by an additional issue. Some studies suggest that the ganglia themselves may acquire some immunity to HSV after they are exposed to one viral type. In the laboratory, infection of ganglia with more than one virus is difficult, suggesting that it may be more difficult to acquire a second HSV type in a location where you already have HSV.

    What does all this mean on a practical level? Let's look at some examples to find out. If you have unprotected sex, there is a small but real risk that you will get HSV-2, resulting in more outbreaks and more shedding. Will you get HSV- 2 in the mouth? Given the widespread practice of oral sex some three-quarters of all adults practice it, according to The Social Organization of Sexuality, and the prevalence of genital HSV-2 infection, you might expect oral HSV-2 to be relatively common.

    One reason is that most adults are already infected with HSV-1 orally, which provides some immunity against infection with HSV 2. Another reason is that oral HSV-2 rarely reactivates, so even if an infection does exist, no one knows. So far we've been talking about transmission of HSV-1 or 2 from its site of preference.

    What about transmission from another site? Say you acquire genital HSV-1 through oral sex. Can you spread the virus to a partner through genital sex? The answer is yes, but probably not as easily as it was spread through oral sex. The main reason is that the virus reactivates and sheds less often outside its site of preference.

    While HSV- 1 can be spread from genitals to genitals, "we think it is spread more easily through oral sex because HSV-1 reactivates more frequently in the oral area," says Wald. However, she warns, "transmission of genital HSV-1 during asymptomatic shedding has been documented. Why don't we kiss through dental dams? But the unspoken attitudes of our society send a different message. That's just the problem, social attitudes whisper.

    Below the waist is bad. But it's also that good and bad is how our culture views sex and our bodies. From a social point of view, the problem is not the disease; it's how you got it. Whether we like it or not, the social prejudice against genital herpes, no matter which virus causes it, is a reality.

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