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Friday, December 14, 2012

Genital herpes stigma as an opportunity to help

Guest author from our community: Shannon (SingBlueSilver)

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

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

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

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

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

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

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

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

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

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

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

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

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

herpes forum


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What I wish I knew when I was first diagnosed with herpes

Guest author from our community: WhoopsiDaysi

I can remember when I was first diagnosed with herpes. It was around December 3, 2011. I had a few things come at me – I became an empty nester and about six weeks later my husband left. My life was turned upside down, to say the least, and then I got herpes symptoms that would suggest my worst nightmare (probably as a result of all the stress I was feeling). I tried to ignore the symptoms for a few days, tried my own remedies, tried to rationalize that it was nothing, but eventually I gave in and went for testing because it wasn’t going away. I wish I would have known then what I know now …

I wish I had known all the personal growth that would come as a result of having herpes.

I had a partner about 9 years previous who had herpes but, to that point, I hadn’t had any real symptoms or “The Herpes Outbreak.” It was always in the back of my mind, though, and the one thing I always dreaded. So off I went to see the doctor. Now just making the appointment was hard enough. “Why do you want to see the doctor?” the receptionist asks. Hmmm … how to phrase this delicately to a complete stranger while standing in their waiting room? I may as well have had a blow horn to announce to the world “I need to check to see if I have herpes.” Death by herpes number 1.

I got in to see the nurse. She did the exam and as soon as she looked, yep, it looks like herpes, or it could be syphilis. Now, I admit, this is the first time in my life I was rooting for syphilis. The tests were done and the waiting began. A few days later I went in and got the diagnosis – “I have herpes, type 2.” My doctor was sympathetic but wasn’t exactly a fountain of herpes statistics. She said that I had to use protection when I had sex with a partner and that I would pass it along to anyone I had sex with. When I asked about herpes medication, she said I could go on drug therapy if I chose but that it wouldn’t stop the transmission of herpes, just the outbreaks and the amount of herpes viral shedding. She then sent me on my merry way, without so much as a pamphlet or a single word of encouragement. I left with a lump in my throat and feeling like the bottom of my world had just finally fallen out. That was the last straw for me.

I was devastated. I came home and processed the news. I remember feeling like my life was pretty much over – I will never, ever, ever, ever have sex again, never have another relationship and that my life was pretty much over as far as love goes. Who would accept someone like me? Herpes! Wow, you may as well have said I had The Plague or leprosy. It would have hit me just as hard. I took a bit of time to process and then I decided to reach out to see what resources were out there. I needed more information, I needed to understand this and I needed to know if I was the only one on the planet with this “sentence.”

I found some support sites for people who had herpes and I started reaching out and talking to people. I joined a local herpes support group and then other herpes social sites and through all these sites I started to develop friendships and to see from the experience of others that maybe my life was not, in fact, over. I went on outings with my local group and developed some really nice friendships and started to see that herpes does not need to define us or degrade us. I have had the pleasure of meeting some of the most interesting, intelligent, caring people through this experience with herpes. I could see from these outings that we are just people and that herpes doesn’t make us any less of a person. In fact, it made us more understanding and accepting of ourselves and others. On our outings, herpes was definitely not the focus of our conversation. Being with them made me feel normal and accepted and human again and it really helped me to start to heal and get my perspective on what this really all meant.

What I wish I would have known

Now that it has been almost a year since my first diagnosis, there are things that I wished I had known on December 3, 2011. I wished I had known how many amazing people I would meet along the way and how many great friendships I would form as a result. I have met people from all over the United States, Canada and locally and have formed some really great friendships with people who have made my life so much richer for having met them. I have a much broader view of life and have learned so much about myself and what my priorities really are.

I wish I had known all the personal growth that would come as a result of having herpes. For the first time in my life, because of herpes, I took the time after my divorce to really examine what happened, to do the work required to heal and to take the time for me that I had never done in my life before. Before herpes, I just went from one bad relationship to another looking for the approval that I really needed to give to myself. Now, with herpes, I have taken time to really focus on me and what I want and need and where I want my life to go and what I really want it to look like. I have had time to examine my past, explore my dreams and create an amazing new life. I have taken courses to help me grow and to examine what I really believe and become much happier, mature and peaceful.

I wish I had known that love was still available to me and that not everyone is going to reject me because of herpes. There are people in the community of herpes to date and there are also people who don’t have herpes who will see that I am a great person who happens to have herpes. I have a lot more to offer than herpes can take away.

I wished I had known that one day herpes wouldn’t be on my mind night and day and that it is more of an inconvenience than anything else and that the first herpes outbreak is the worst. I had gotten through the worst of it already and I wouldn’t really need to think about it much. It’s been almost a year and I haven’t had another outbreak and most likely won’t again for a long time. Herpes is there but it doesn’t determine what kind of life I am going to have; I do.

I wished I had known that I can still do the things I want to do. A friend of mine told her story of how she was worried after her herpes diagnosis that she wouldn’t be able to give blood, which was something she wanted to do in honor of her Dad. After being told by one nurse that no she couldn’t donate because she had herpes, she was relieved to find out when she decided to go through the screening process anyway that she could absolutely still give blood.

I wished I had known that the good that would come out of having herpes would far outweigh the negatives and that, at the end of the day, it is just a skin condition – a cold sore in a tender location, nothing more.

Finally, I wished I had known that I would actually be happier as a result of moving through it and it would all be okay. All I needed to do was reach out and to accept myself. And for the first time, I have really done that and that is the gift I received from having herpes – it is all going to be okay and I am amazing just the way I am.

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Destroy your herpes shame and embrace your imperfections

Guest author from our community: breatheandletgo

It’s nearly impossible for many of us who have genital herpes to say the word without feeling shame. I am one of those people, though I am actively working on changing this. And as I’ve worked on the change in myself, I’ve asked a lot of questions about shame, its roots and what strategies are effective in overcoming its paralyzing effects.

You’ve shut down and pulled away from others to protect yourself, but what you really want to do is let go of the shame, feel okay as you are and become brave enough to risk being loved?

The roots of my own shame aren’t a big mystery. I experienced some pretty serious abuse growing up and I have relied on the guidance and wisdom of caring and supportive counselors, spiritual mind-body practices, and more often than not, research to find ways to heal my wounds. Those of you, like me, who weren’t blessed to come into the world celebrated and loved the way you deserved to be know the kind of the work you will do to come back from abuse is the work you do just to stay alive.

But once you find your footing, you’ll soon discover your next mountain to climb is the one where you unlearn all of the habits you learned to survive, because survivors do whatever it takes to stay alive. We squash our dreams. We close our hearts to hope so it won’t hurt so much when something comes along we might love and lose or just be tempted to believe we deserve — because for all we know it will probably only hurt in the end. And our survivor brains tell us one more hurt is the only thing separating us from an abyss of pain we won’t escape because we’re convinced we’re alone.

And even if you’ve had a healthy start in life with supportive caregivers and opportunity to grow and thrive, shame is something everyone deals with on some level, and no doubt a diagnosis of herpes is an opportunity for most people to discover where they are in regard to shame and healthy self-concept, and even the strongest will likely feel the ripple effect for some time after they are diagnosed. Acceptance is a journey.


Shame and imperfection

I’ve researched and read about the relationship between shame and imperfection, and I’ve learned in order to fight shame and truly embrace our imperfections, we have to become keen observers of our own thought life. We have to be mental shame ninjas, monitoring our thoughts and inner conversations with ourselves and others. And in my own practice of shame busting, I have learned to use two words to fight my own inner shame thoughts. They are really profound. Are you ready? The words are: “Who says?” So when my shame voice says, “No one is ever going to want to be with you now,” I force myself to ask myself, “Who says?” Sometimes that’s all of the fight I’ve got to throw at a shame thought, but it is a start. This simple question brings awareness and consciousness to such automatic negative thoughts.

We have to fight every thought that says being imperfect is the same as being inadequate or unlovable. Our shame comes from believing we are unlovable as we are, and that is a lie. How do I know? Because everyone alive has imperfections! Pema Chodron, a Tibetan Buddhist Nun says it like this: “Our brilliance, our juiciness, our spiciness, is all mixed up with our craziness and our confusion, therefore it doesn’t do any good to try to get rid of our so-called negative aspects, because in that process we also get rid of our basic wonderfulness.” I love that quote! And isn’t it true? This world would be a pretty vanilla place without you, without me, without all kinds of people and their wonderfulness. Herpes is not who we are, or even a small part of us, but so many of us find ourselves struggling mightily with fear and shame as we attempt to integrate this small virus into our self-concept, myself included.

Herpes shame and isolation

A residual effect of shame winning the fight for our self-worth is isolation. I know this all too well. I remember telling the counselor I was seeing a while back about a recurring dream where I’d show up to a party wearing combat gear of some kind. I thought it was a silly dream, but when I told her about it, she instantly had insight into where these costume party nightmares were coming from. In my combat gear I felt safe … but no one could see me. No one could love me. I couldn’t feel anything. I knew she was right as soon as she began to ask me the first question.

Maybe you’re like me? Maybe you’ve discovered that you’ve developed some really great survival skills along the way that no longer work in your real life, or find yourself working on some new ones as a result of getting herpes. You’ve shut down and pulled away from others to protect yourself, but what you really want to do is let go of the shame, feel okay as you are and become brave enough to risk being loved?

“Referred pain”

A while ago, I read about this phenomenon called referred pain. Referred pain happens a lot in undiagnosed cancer patients. It’s pain that shows up repeatedly and would seem to have nothing to do with cancer. For example, a golfer might experience a repetitive pull in her shoulder muscle and treat the shoulder pain thinking he has a hurt shoulder, but in reality, she has cancer growing in her cervix or abdomen. This is serious stuff! When I read about referred pain I immediately thought about how the herpes changes so many of our internal journeys. Yeah, I was diagnosed with herpes, but what I really got was a wake-up call to a lot of internal work I needed to do. I learned I’d have to go deep inside to love and accept myself in this new reality on a whole other level before I would be healthy enough to disclose my status to someone new.

Pain is a gift to tell us to check things out. Pain says, hey…make no assumptions. Look at this. Take it apart and get to the source. You can ice a shoulder if you have referred pain, but it won’t do a thing for your cancer. Pain with herpes is a lot like referred pain. It is its own pain, especially during those first few breakouts, but after the physical pain fades, the emotional pain lingers. It comes up in the way we think and feel about ourselves. They way we perceive our value and worth. And if we’re not careful, we can put ourselves on the damaged goods shelf and stick a discount sticker on our foreheads that communicates something far beneath our true worth. Shame does that.

If we are brave, we will challenge the assumptions we make about ourselves and others and learn to love ourselves on a whole new level. Brené Brown, an amazing author, teacher and researcher on the topic of shame and embracing imperfection, talks about developing what she calls shame resilience. People with shame resilience do a few things well:

They recognize their own shame triggers and learn to avoid and/or manage them effectivelyThey become critical thinkers by challenging their shaming assumptionsThey reach out to others for help and support.

Our herpes support community here is a great place to begin reaching out, to hear a friend say “who says?” and to begin to tell ourselves new stories and create new realities to keep shame from stealing our destiny.

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Thursday, December 13, 2012

“Good” herpes virus, “bad” herpes virus: The Truth about HSV-1 and HSV-2

Many thanks to the American Social Health Association for this article.

How alike are HSV-1 and HSV-2? 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 herpes infection to oral herpes, or cold sores. How apt is the comparison? In spite of scientific facts, the herpes 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).

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 HSV-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.

Under a microscope, HSV-1 and HSV-2 are virtually identical, sharing approximately 50% of their DNA. 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.” HSV-1 usually establishes latency in the trigeminal ganglion, a collection of nerve cells near the ear. 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.

Even this difference is not absolute either type can reside in either or both parts of the body and infect oral and/or genital areas. 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.

“People don’t understand that you can have type 1 genitally or orally, that the two types are essentially the same virus,’ says Marshall Clover, manager of the National Herpes Hotline.” One type is associated with stigma, the other is “just a cold sore” — our society has a euphemism for it so we don’t even have to acknowledge that it’s herpes.”

The common myth is that HSV-1 causes a mild infection that is occasionally bothersome, but never dangerous. The reality? 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. “This is heresy, but I think type 1 is a more significant infection than type 2,” says Spotswood Spruance, MD, an oral HSV specialist at the University of Utah. “Type 1, and the morbidity associated with it, are underestimated.”

By comparison, HSV-2 is widely believed to be a painful, dangerous infection that affects only people with very active sex lives. The reality? Some 16% of adult Americans from all backgrounds, income levels, and ethnic groups have HSV-2. Like HSV-1, type 2 is usually mild — so mild that 80% 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.

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-2. 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.

How Many Herpes Outbreaks?

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.

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 100 million Americans who are infected acquired the virus when they were children. By the time they’re adults, only some 5% of people are bothered enough to consider oral HSV-1 a medical problem, according to Spruance.

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-2. While experts estimate that some 30% of genital herpes infections in the United States may be caused by HSV-1, only 2- 5% of recurring genital outbreaks are caused by HSV-1. Research conducted by Lawrence Corey, MD, and colleagues at the University of Washington in Seattle shows that genital HSV-2 recurs 10 times more often than genital HSV-1.

According to a study by Wald et al. (New England Journal of Medicine, 1995), among 110 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, 1994).

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., New England Journal of Medicine, 1987), oral HSV-2 recurred an average of 0.01 times a year in newly infected people. “I’ve never convincingly seen an oral type 2 recurrence,” says Spruance.

A possible fourth factor affecting recurrence rate is viral type. According to the Lafferty study, genital HSV-2 infections were the most frequently recurring herpes infections, followed by oral HSV-1, genital HSV-1, and last of all, oral HSV-2.

How Easily Does Herpes Spread?

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. According to Spruance, people with recurrent oral HSV-1 shed virus in their saliva about 5% of the time even when they show no symptoms. In the first year of infection, people with genital HSV-2 shed virus from the genital area about 6-10% of days when they show no symptoms, and less often over time. (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 the time they’re teenagers or young adults, about 50% of Americans have HSV-1 antibodies in their blood. By the time they are over age 50, some 80-90% of Americans have HSV-1 antibodies.

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-2. According to one study (Mertz, Annals of Internal Medicine,1992), previous oral HSV-1 infection reduces the acquisition of subsequent HSV-2 infection by 40%.

A prior infection with oral HSV-1 lowers the risk of acquiring genital HSV-1 even further. Studies show that genital HSV-1 infections almost always occur in people who have no prior infection with HSV of either type (Corey, Annals of Internal Medicine, 1983).

In the absence of prior oral infection, however, HSV-1 spreads easily to the genital area, usually through oral sex. In some countries, such as Japan and parts of Great Britain, genital HSV-1 is as common as genital HSV- 2, or more common.

“Prevalence rates of genital HSV-1 differ based on the practice of oral sex and on the percentage of people who are HSV-1 positive from childhood,” explains Anna Wald, MD researcher at the University of Washington at Seattle.

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. A prior genital infection with HSV-1, for example, may give more protection against genital HSV-2 than a prior oral infection with HSV-1.

What does all this mean on a practical level? Let’s look at some examples to find out. Say you have genital HSV-1 and your partner has genital HSV-2. 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. “We have documented cases where a person acquires HSV-2 after a prior genital HSV- 1 infection,” says Wald. “I don’t think it happens often, but it does happen.”

On the other hand, it’s very unlikely that your partner will get genital HSV- 1 from you. “I’ve never seen a case of a person acquiring HSV-1 on top of HSV-2,” says Wald. “It’s possible, but it would be unusual.”

What if your partner has genital HSV-2 and you perform oral sex on him or her? 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, 1994) and the prevalence of genital HSV-2 infection, you might expect oral HSV-2 to be relatively common. It’s not.

According to one study, almost 100% of recognizable HSV-2 infection is genital (Nahmias, Scandinavian Journal of Infectious Diseases Supplement, 1990). 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. Only about one quarter of people with genital HSV- 1 shed virus at all in the absence of symptoms, while 55% of people with HSV-2 do (Wald, New England Journal of Medicine, 1995). “Shedding data appear to parallel recurrence data, meaning that people who have a lot of recurrences also have a lot of shedding,” says Wald.

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.” In other words, genital HSV-1 can be spread through genital sex, even when there are no symptoms. “Good” Virus/ “Bad” Virus

If HSV infection is as easily transmitted from the mouth as from the genitals, then why do people take steps to prevent genital but not oral infection? Why don’t we kiss through dental dams ?

“It’s ironic, isn’t it?” says Wald. “It’s not about health, it’s about social acceptability.”

Scientists can tell us all day that the main difference between the two viral types is simply their site of preference-whether they typically occur above the waist or below. But the unspoken attitudes of our society send a different message. That’s just the problem, social attitudes whisper. Below the waist is bad.

“People think of oral herpes as the “good” herpes and genital herpes as the “bad” kind,” says Glover of the National Herpes Hotline. “It’s partly that they don’t understand the similarities between HSV-1 and 2. But it’s also that good and bad is how our culture views sex and our bodies.”

The inescapable fact is that HSV-1 is usually spread through contact with infected lips, while HSV-2 usually spread through contact with infected genitals. 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. “People have more trouble explaining to a new partner that they have genital herpes, even if it’s HSV- 1, than if they have a cold sore,” says Glover. “Just saying the word “genital” is like an anvil that pulls the sentence down”.

Is this topic making you crazy? For people who have trouble dealing with social attitudes toward genital herpes, the blatant double standard society applies to oral herpes can be frustrating, to say the least.

“Talk to a wise friend,” suggests Rebecca, a health communication specialist on the National Herpes Hotline. “Join a support group. Find Someone you respect and exchange ideas them. It’s always reassuring to see that not everyone lives inside the walls our society builds around sexual issues and realities. ”

It’s also worth hoping that new research on the similarities between HSV-1 and 2, as well as increased public education about genital herpes, can help lower the level of misunderstanding about both types of the virus. Today, the greatest difference between HSV- 1 and 2 appears to be the way we think about them. Tomorrow, that may change …

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Wednesday, December 12, 2012

Unexpected bottleneck identified in spread of herpes simplex virus

ScienceDaily (Nov. 5, 2012) — New research suggests that just one or two individual herpes virus particles attack a skin cell in the first stage of an outbreak, resulting in a bottleneck in which the infection may be vulnerable to medical treatment.

Unlike most viruses that spread to new cells by bombarding them with millions of particles, herpes simplex virus type 1 (HSV-1) -- a virus that causes cold sores and genital lesions -- requires just one or two viral particles to infect a skin cell in the first stage of cold sore formation, Princeton University researchers reported in the Proceedings of the National Academy of Sciences.

"The fact that just one or two virus particles are involved is surprising because these viruses can replicate themselves hundreds of times in a single cell," said Matthew Taylor, first author on the study and a postdoctoral researcher in the laboratory of Lynn Enquist, the Henry L. Hillman Professor in Molecular Biology and the Princeton Neuroscience Institute.

The bottleneck occurs when HSV-1 particles, which can lie dormant in the cells of the nervous system for decades after initial infection, awaken and invade a nearby skin cell, the first stage in sore formation. Once inside the skin cell, a single viral particle multiplies and spreads millions of copies to nearby skin cells, creating a visible lesion or "cold sore." The virus can then spread to new individuals through skin-to-skin contact.

This restriction to one or two particles limits the genetic diversity of the virus that spreads to the next individual, Enquist said. This puts the virus at a disadvantage, he said, because having a variety of distinct genomes enhances the overall chances of the virus surviving and spreading. A well-known example of a virus that relies on genetic diversity to thrive is HIV, which involves large numbers of viral particles with distinct genomes.

In the case of herpes viruses, Enquist said: "The number of different genomes that infect the cell is remarkably low, so any mutations that weaken the virus are unlikely to survive. Only the most fit viral particles will survive and replicate in the epithelial [skin] cells, and be available to transmit to the next individual."

Although bottlenecks can ensure that only the most fit viruses are transmitted to the next individual, they also can be points at which the infection is more susceptible to immune system responses and drug treatments, according to Taylor. He and Enquist worked with co-author Oren Kobiler, a former Princeton postdoctoral researcher now at Tel Aviv University.

The researchers' findings suggest that other viruses related to HSV-1 -- known as alpha-herpes viruses -- may have similar bottlenecks, Taylor said, including herpes simplex viruses type 2, which causes cold sores and genital lesions, and varicella zoster virus, which causes chicken pox and shingles. It remains to be determined if this bottleneck exists for other viruses that spread from infected neurons, such as poliovirus and the West Nile virus, Taylor said.

Julie Pfeiffer, an associate professor of microbiology at the University of Texas Southwestern Medical Center, said the Princeton research is the first to tally how many viral particles are involved in HSV-1 infection -- and reveal that as the virus' weak point.

"This work changes the way that we think about herpes virus spread," said Pfeiffer, who is familiar with the study but had no role in it. "This study demonstrated that these neuron-to-epithelial cell viral-transmission events are surprisingly efficient, but they are initiated by a very small number of viruses. This work has interesting implications for herpesvirus transmission and evolution."

To determine the number of virus particles that infect the skin cell, the researchers constructed three genetically unique viral genomes labeled with either red, green or blue fluorescent tags, and then infected cells with the particles and analyzed them for the presence of the three colors. They counted the number of cells containing one, two or all three colors and used statistical analysis to determine the number of unique viral genomes expressed in each cell. The method, which was originally developed by Kobiler, Enquist and colleagues in Princeton's mathematics department and initially published in 2010 in Nature Communications, revealed that most skin cells express less than two viral genomes on average.

Taylor then filmed individual virus particles of pseudorabies virus, a model alpha-herpes virus that infects animals, as the particles exited neurons and entered skin cells. He found that the bottleneck limiting infection to one or two particles exists for pseudorabies virus as well.

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The above story is reprinted from materials provided by Princeton University. The original article was written by Catherine Zandonella.

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Journal Reference:

M. P. Taylor, O. Kobiler, L. W. Enquist. Alphaherpesvirus axon-to-cell spread involves limited virion transmission. Proceedings of the National Academy of Sciences, 2012; 109 (42): 17046 DOI: 10.1073/pnas.1212926109

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Monday, December 10, 2012

Study Evaluates Use Of Corticosteroids And Antiviral Agents For Treatment Of Bell Palsy

ScienceDaily (Sep. 3, 2009) — Among patients with Bell Palsy, a facial paralysis with unknown cause, treatment with corticosteroids is associated with a reduced risk of an unsatisfactory recovery, and treatment with a combination of corticosteroids and antiviral agents may be associated with additional benefit, according to a systematic review and meta-analysis of previously published studies, reported in the September 2 issue of JAMA.

In background information provided by the authors, they note that Bell Palsy "is an acute weakness or paralysis of the facial nerve," and has an annual incidence of 20 to 30 per 100,000 population. "While 71 percent of untreated patients will completely recover and 84 percent will have complete or near normal recovery, the remainder will have persistent to moderate to severe weakness, facial contracture, or synkinesis [involuntary movement]." The authors explain that a herpes infection likely causes the disorder. DNA samples from patients have yielded herpes simplex virus type 1 (HSV-1). Varicella zoster virus (VZV) reactivation is also associated with Bell Palsy.

John R. de Almeida, M.D., from Sunnybrook Hospital and the University of Toronto, Canada, and colleagues conducted a search of the medical literature for randomized controlled trials comparing treatment with either corticosteroids or antiviral agents with a control measuring unsatisfactory facial recovery (four months or more), unsatisfactory short-term recovery (six weeks to less than four months), synkinesis and autonomic dysfunction, or adverse effects. The authors identified 854 studies, of which 18 were eligible for inclusion for evaluation. The 18 studies included 2,786 patients and were conducted in 12 countries and five continents.

"… high-quality evidence suggests that corticosteroids alone reduce the risk of unsatisfactory recovery by 9 percent in absolute terms, with a NNTB (number of patients needed to treat for one patient to experience benefit) of 11," the authors report. "Corticosteroid therapy combined with antiviral agents reduced the risk of unsatisfactory recovery compared with antiviral agents alone. Corticosteroids were also associated with a 14 percent absolute risk reduction of synkinesis and autonomic dysfunction (NNTB, 7; moderate quality of evidence). Corticosteroids were not associated with an increased risk of adverse effects."

"Our results suggest a possible incremental benefit of antiviral agents in addition to corticosteroids, with an absolute risk reduction of 5 percent compared with corticosteroids alone. This effect, however, is not definitive and did not quite reach statistical significance," the authors write. "Further primary studies are needed to definitively establish – or refute – an incremental benefit of combined therapy compared with corticosteroid mono therapy," the authors conclude.

Editorial: Treatment of Bell Palsy – Translating Uncertainty Into Practice

"The systematic review by de Almeida et al of medications for treatment of Bell palsy helps resolve lingering doubt about the benefits of corticosteroids, but raises questions about the adjunctive role of antiviral medications," John F. Steiner, M.D., M.P.H., of Kaiser Permanente Colorado, Denver, writes in an accompanying editorial.

"Until the next generation of clinical trials is completed, clinicians and patients will have to deal with substantial uncertainty in deciding whether to add antiviral drugs to corticosteroids for Bell palsy. By assessing how clinicians alter their prescribing patterns and how treatment guidelines are revised in response to this new evidence, it will be possible to learn more about how clinical uncertainty is translated into practice."

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Journal Reference:

John R. de Almeida; Murtadha Al Khabori; Gordon H. Guyatt; Ian J. Witterick; Vincent Y. W. Lin; Julian M. Nedzelski; Joseph M. Chen. Combined Corticosteroid and Antiviral Treatment for Bell Palsy: A Systematic Review and Meta-analysis. JAMA, 2009; 302 (9): 985-993 [link]

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Saturday, December 8, 2012

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.

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

Journal References:

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

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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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