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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 …

herpes forum


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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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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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Sleeping Beauty hooks up with herpes to fight brain disease

ScienceDaily (Jan. 9, 2010) — Neuroscientists have forged an unlikely molecular union as part of their fight against diseases of the brain and nervous system.

The team has brought together the herpes virus and a molecule known as Sleeping Beauty to improve a technology known as gene therapy, which aims to manipulate genes to correct for molecular flaws that cause disease.

The work, detailed in a paper published online in Gene Therapy, has allowed scientists at the University of Rochester Medical Center to reach a long-sought goal: Shuttling into brain cells a relatively large gene that can remain on for an extended period of time.

"We've broken what is in effect a size barrier -- a limit to how much genetic material we can put into the nucleus of a cell and keep functioning for a long period of time," said neuroscientist William Bowers, Ph.D., a scientist in the Center for Neural Development and Disease and the leader of the team. "That opens up more diseases to possible treatment with gene therapy."

The first author of the paper is Biochemistry graduate student Suresh de Silva, who defends his doctoral thesis later this month.

The molecular rendezvous of Sleeping Beauty and herpes in human brain cells could spell good news in the search for treatments for horrific brain diseases known as pediatric leukodystrophies, or a group of diseases known as lysosomal storage disorders. In many of these diseases, even though just a single gene or protein is defective, the effects are devastating -- the diseases slowly rob children of their brain cells and are often fatal after years of severe symptoms.

The findings bolster the tools that researchers have when approaching certain diseases, said Bowers, including Usher syndrome, which results in deafness and vision loss; Niemann-Pick disease Type C, a fatal childhood lysosomal storage disorder; and von Willebrand disease, an inherited disease that causes extensive, chronic bleeding.

"The field of gene therapy is just beginning to yield some successes for patients. Improvements like this are crucial for increasing the number of patients who might benefit from such an approach," said Bowers, who is an associate professor of Neurology, Microbiology and Immunology, and of Pharmacology and Physiology.

The research is part of a decades-long endeavor by scientists trying to get the right genes into the right cells at the right time to improve human health.

In the new work, scientists dramatically increased the size of the "genetic payload" they can deliver to brain cells compared to some conventional techniques, nearly tripling the amount of genetic material by some measures. They hope to deliver even bigger genes in the future.

The team did this by bringing together in a new way two molecular players, herpes and Sleeping Beauty, which are commonly used in molecular technology.

For years Bowers' team has been using the herpes virus -- HSV-1, the type that causes cold sores -- to shuttle genes into cells. Viruses like herpes are adept at infecting human cells, and scientists like Bowers use such viruses to carry into cells genes that would help people who are sick. Bowers and colleagues modify the viruses extensively, removing the portions that could make a person sick and using the portions that the virus uses to gain access to human cells.

Many scientists use other viruses, such as lentiviruses or a cold-related virus known as adeno-associated virus (AAV), to do a similar job. Each virus has its strengths and weaknesses when it comes to gene therapy. Herpes, for instance, readily infects cells, and it can carry a huge amount of genetic material, typically 15 to 30 times the amount of DNA that other viruses can carry into a cell.

But herpes as a genetic tool has a couple of big weaknesses. While the virus can deliver DNA into the nucleus of a cell, the genetic payload it carries does not become part of the package of genes that cells pass from one to another. Simply put, herpes cannot integrate the new DNA into the host genome. Instead, the DNA is adrift in the nucleus, where it's silenced within a few weeks. The short time span spells trouble when scientists are trying to treat a disease that requires the genes to be active for months or years.

That's where Sleeping Beauty comes in.

In molecular biology, Sleeping Beauty is a mobile genetic element that jumps into and out of longer segments of DNA. It's normally silent, but years ago a team of scientists was able to activate or "awaken" the snippet -- hence, Sleeping Beauty. Since Sleeping Beauty actually integrates segments of DNA into mammalian genomes, it sidesteps the main difficulties that herpes encounters inside a cell: Genes integrated within the cell's chromosomes by Sleeping Beauty operate for much longer periods of time. The drawback: The molecule can insert only small snippets of DNA.

So the Rochester team brought herpes and Sleeping Beauty together in an attempt to get the best of both worlds: Delivery of the bigger genetic package made possible by herpes, and the integration of the DNA into the host genome made possible by Sleeping Beauty.

And that's exactly what happened. In the tag-team approach funded by the National Institute of Neurological Disorders and Stroke, herpes gets the genetic package into the right neighborhood, the cell's nucleus, and then Sleeping Beauty delivers the package precisely where it needs to go to be most effective -- into the cellular genome.

In the current experiments, the herpes virus carried into cell nuclei the gene for green fluorescent protein, which allows scientists to track where the gene is active. The team also outfitted the herpes package with special molecular signals that Sleeping Beauty would recognize. Separately, the team introduced Sleeping Beauty into the cells. When the two met, Sleeping Beauty transferred the gene for GFP from the herpes package to the genome of the human cells, where the gene was stably expressed.

The team has previously shown that the Sleeping Beauty/herpes combination works efficiently in brain cells known as neural progenitor cells, which go on to form brain cells known as neurons. Modifying these cells -- perhaps by adding a gene that creates a protein crucial for health -- is one technique scientists are experimenting with to try to treat several brain diseases that are currently untreatable.

The gene segment used in the experiment described in Gene Therapy was about 12 kilobases long, which is larger than the limit of either AAV (4.5 kb) or lentiviruses (9 kb). Those few kilobases matter, a lot. The ability to transfer bigger genes gives scientists room to try to address more diseases with a gene therapy approach. The added space also makes it possible to include more regulatory elements -- instructions that help determine how and when genes are turned on or off. This allows scientists to package additional safety directives, in the form of more DNA, along with the gene designed to treat the disease.

In addition to de Silva and Bowers, authors include technical associates Michael Mastrangelo, Louis T. Lotta Jr., and Clark Burris, as well as Howard J. Federoff, M.D., Ph.D., a former Rochester faculty member who is now executive vice president for health sciences at Georgetown University.

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Friday, December 7, 2012

How and why herpes viruses reactivate to cause disease

ScienceDaily (Oct. 31, 2012) — The mere mention of the word "herpes" usually conjures negative images and stereotypes, but most people have been infected with some form of the virus. For most, a sore appears, heals and is forgotten, although the virus remains latent just waiting for the right circumstances to come back. Now, the mystery behind what triggers the virus to become active again is closer to being solved thanks to new research published in the Journal of Leukocyte Biology's November 2012 issue.

In the report, scientists show how the immune system may lose its control over the virus when facing new microbial threats, such as when it must fend off other viral invaders or bacteria.

"Because almost all people are infected by one or more herpes family viruses during their lifetime, the potential impact of these findings are significant," said Charles H. Cook, M.D., FACS, FCCM, director of surgical critical care at The Ohio State University College of Medicine in Columbus, Ohio, and a researcher involved in the work. "We hope that by understanding how these latent viral infections are controlled that we can prevent reactivation events and improve people's lives."

To make this discovery, researchers studied mice with latent herpes family cytomegalovirus (CMV) during severe bacterial infections. They found that T-cells responsible for CMV control were reduced significantly during a new infection with bacteria. This, in effect, reduced the "brakes" which kept the virus under control, allowing the virus to reactivate and cause disease. When the immune system eventually sensed the reactivation, the memory T-cell levels returned to normal, effectively restoring the body's control over the virus.

"Finding ways to control herpes flare ups is important, not only for the health of the person with the virus, but also for preventing its transmission," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "This report highlights the important interplay when we are 'co-infected' with more than one microbe and provides important insights into why the immune system sometimes fails as well as how it can regain control of latent herpes virus infections."

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J. Campbell, J. Trgovcich, M. Kincaid, P. D. Zimmerman, P. Klenerman, S. Sims, C. H. Cook. Transient CD8-memory contraction: a potential contributor to latent cytomegalovirus reactivation. Journal of Leukocyte Biology, 2012; 92 (5): 933 DOI: 10.1189/jlb.1211635

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Thursday, December 6, 2012

Genital herpes virus reactivates widely throughout genital tract

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

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

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

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

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

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Compound discovered that boosts effect of vaccines against HIV and flu

ScienceDaily (Aug. 26, 2012) — Oxford University scientists have discovered a compound that greatly boosts the effect of vaccines against viruses like flu, HIV and herpes in mice.

An 'adjuvant' is a substance added to a vaccine to enhance the immune response and offer better protection against infection.

The Oxford University team, along with Swedish and US colleagues, have shown that a type of polymer called polyethyleneimine (PEI) is a potent adjuvant for test vaccines against HIV, flu and herpes when given in mice.

The researchers were part-funded by the UK Medical Research Council and report their findings in the journal Nature Biotechnology.

Mice given a single dose of a flu vaccine including PEI via a nasal droplet were completely protected against a lethal dose of flu. This was a marked improvement over mice given the flu vaccine without an adjuvant or in formulations with other adjuvants.

The Oxford researchers now intend to test the PEI adjuvant in ferrets, a better animal model for studying flu. They also want to understand how long the protection lasts for. It is likely to be a couple of years before a flu vaccine using the adjuvant could be tested in clinical trials in humans, the researchers say.

'Gaining complete protection against flu from just one immunisation is pretty unheard of, even in a study in mice,' says Professor Quentin Sattentau of the Dunn School of Pathology at Oxford University, who led the work. 'This gives us confidence that PEI has the potential to be a potent adjuvant for vaccines against viruses like flu or HIV, though there are many steps ahead if it is ever to be used in humans.'

HIV, flu and herpes are some of the most difficult targets to develop vaccines against. HIV and flu viruses are able to change and evolve to escape immune responses stimulated by vaccines. There aren't any effective vaccines against HIV and herpes as yet, and the flu vaccine needs reformulating each year and doesn't offer complete protection to everyone who receives it. Finding better adjuvants could help in developing more effective vaccines against these diseases.

Most vaccines include an adjuvant. The main ingredient of the vaccine -- whether it is a dead or disabled pathogen, or just a part of the virus or bacteria causing the disease -- primes the body's immune system so it knows what to attack in case of infection. But the adjuvant is needed as well to stimulate this process.

While the need for adjuvants in vaccines has been recognised for nearly 100 years, the way adjuvants work has only recently been understood. The result has been that only a small set of adjuvants is used in current vaccines, often for historical reasons.

The most common adjuvant by far is alum, an aluminium-containing compound that has been given in many different vaccines worldwide for decades. However, alum is not the most potent adjuvant for many vaccine designs.

'There is a need to develop new adjuvants to get the most appropriate immune response from vaccines,' says Professor Sattentau, who is also a James Martin Senior Fellow at the Oxford Martin School, University of Oxford.

The Oxford University team found that PEI, a standard polymer often used in genetic and cell biology, has strong adjuvant activity.

When included in a vaccine with a protein from HIV, flu or herpes virus, mice subsequently mounted a strong immune response against that virus. The immune response was stronger than with other adjuvants that are currently being investigated.

The team also showed that PEI is a potent adjuvant in rabbits, showing the effect is not just specific to mice and could be general.

Another potential advantage of PEI is that it works well as an adjuvant for 'mucosal vaccines'. These vaccines are taken up the nose or in the mouth and absorbed through the mucus-lined tissues there, getting rid of any pain and anxiety from a needle. Mucosal vaccines may also be better in some ways as mucosal tissues are the sites of infection for these diseases (airways for respiratory diseases, genital mucosa for HIV and herpes).

Professor Sattentau suggests that: 'In the best of all possible worlds, you could imagine people would have one dose of flu vaccine that they'd just sniff up their nose or put under their tongue. And that would be it: no injections and they'd be protected from flu for a number of years.

'It's just a vision for the future at the moment, but this promising adjuvant suggests it is a vision that is at least possible.'

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Shingles Raises Risk Of Stroke By 30 Percent Or More In Adults, Study Finds

ScienceDaily (Oct. 9, 2009) — Adults with shingles were about 30 percent more likely to have a stroke during a one-year follow-up than adults without shingles, in a study reported in Stroke: Journal of the American Heart Association.

The risk was even greater when the infection involved the eyes.

Shingles, also called herpes zoster, is a painful skin rash caused by the varicella zoster virus (VZV). VZV is the same virus that causes chickenpox. After a person recovers from chickenpox, the virus stays in the body. Usually the virus doesn’t cause problems, but it can reappear years later, causing shingles.

Shingles is not caused by the same virus that causes genital herpes, a sexually transmitted disease.

“Many studies have shown that people with herpes zoster infection are more likely to develop stroke. But ours is the first to demonstrate the actual risk of stroke following herpes zoster infection,” said Jiunn-Horng Kang, M.D., M.Sc., lead author of the study and attending physician in the Department of Physical Medicine and Rehabilitation and chair of the Sleep Physiological Lab at Taipei Medical University Hospital.

Kang and his associates studied 7,760 patients 18 years and older who received shingles treatment between 1997 and 2001. These people were matched by age and gender with 23,280 adults who weren’t treated for shingles (controls). Their average age was 47.

During the one-year follow-up, 133 shingles patients (about 1.7 percent) and 306 of the controls (about 1.3 percent) had strokes. After adjusting for general factors for stroke risk, the researchers found:

People treated for a shingles infection were 31 percent more likely to have a stroke, compared with patients without a shingles infection.Patients with shingles infections that involved the skin around the eye and the eye itself (herpes zoster ophthalmicus) were 4.28 times more likely to have a stroke than patients without shingles. When the researchers analyzed the risk of stroke by stroke type, they found:Shingles patients were 31 percent more likely to develop an ischemic stroke during the one-year follow-up than those without shingles.The risk of hemorrhagic (bleeding) stroke was 2.79 times higher for people with shingles infection than for people without shingles.

Ischemic strokes, which are caused by the blockage of an artery, account for 87 percent of the new or recurrent strokes that strike about 780,000 Americans annually, according to the American Heart Association.

“Herpes zoster infection is very easy to diagnose, and antiviral medication can be used to treat the infection in the early stages,” Kang said. “While the mechanism by which shingles increases stroke risk remains unclear, the possibility of developing a stroke after a shingles attack should not be overlooked.

Doctors and patients must pay extra attention to controlling other risk factors for stroke, such as high blood pressure, smoking and diabetes.”

Shingles usually starts as a rash on one side of the face or body. The rash starts as blisters that scab after three to five days and usually clears within two to four weeks. There is often pain, itching or tingling in the area where the rash develops.

Researchers didn’t design the study to determine how shingles infection raises stroke risk. But other research suggests that as the herpes zoster virus replicates and attacks the vessel wall, the vessel wall becomes damaged and inflamed. This in turn can cause the vessel to close up, or occlude, blocking blood flow to the brain. Shingles is also the only recognized human virus able to invade cerebral arteries.

In addition, shingles is also associated with severe pain, and the stress of that chronic pain may raise the risk of cardiovascular disease theoretically, Kang said.

Co-authors are Jau-Der Ho, M.D., Ph.D.; Yi-Hua Chen, Ph.D.; and Herng-Ching Lin, Ph.D. Individual author disclosures are on the manuscript.

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Tuesday, December 4, 2012

Herpes medication does not reduce risk of HIV transmission, study finds

ScienceDaily (Jan. 25, 2010) — A five-year international multi-center clinical trial has found that acyclovir, a drug widely used as a safe and effective treatment taken twice daily to suppress herpes simplex virus-2 (HSV-2), which is the most common cause of genital herpes, does not reduce the risk of HIV transmission when taken by people infected with both HIV and HSV-2.

The results of the study are published in the New England Journal of Medicine.

Up to 90% of people with HIV infection also have HSV-2 infection. Most people who are infected with HSV-2 do not know they have the virus because symptoms can be mild or absent. HSV-2 infection can cause recurrent sores and breaks in the skin of the genital region, which can be mild and often go unnoticed. HSV-2 infection also attracts immune cells called CD4 T-cells to the genital region, which HIV uses to establish or pass infection.

Multiple studies have shown that frequent genital herpes recurrences increase the amount of HIV in the blood and genital tract. The HIV virus is also shed from genital herpes ulcers and persons with such ulcers transmit HIV to others more efficiently. Five preliminary studies showed that it is possible to decrease the amount of HIV in the blood and genital tract through treatment to suppress HSV-2, but these studies did not measure whether this translated into a reduction in HIV transmission. Researchers had hoped that acyclovir's ability to suppress the herpes virus, which causes symptomatic genital sores and breaks in the skin but also frequently is active without symptoms, could reduce the likelihood of sexual transmission of HIV from a person with HIV and HSV-2. The study is the first to determine whether twice daily use of acyclovir by individuals who are infected with both HSV-2 and HIV reduced the transmission of HIV to their sexual partners. The authors conclude that daily acyclovir therapy did not reduce the risk of transmission of HIV, in spite of the fact that acyclovir reduced plasma HIV RNA by a ¼ log and the occurrence of genital ulcers due to HSV-2 by 73%.

Led by the University of Washington in Seattle and funded by the Bill & Melinda Gates Foundation, the Partners in Prevention HSV/HIV Transmission Study was conducted among 3,408 African HIV serodiscordant couples, in which one partner had HIV and the other did not. In all the couples, the partner who had HIV also had HSV-2 infection. The study took place at 14 sites in seven countries in eastern and southern Africa (Botswana, Kenya, Rwanda, South Africa, Tanzania, Uganda and Zambia). In sub-Saharan Africa, the majority of new HIV infections occur among heterosexual HIV discordant couples, many of whom are in stable partnerships and unaware that one partner has HIV and the other does not. Genital herpes is thought to be a factor in a substantial proportion of new HIV infections in Africa.

The study began recruitment in Nov. 2004 and ended follow-up of participants in Oct. 2008. Results were first announced in May 2009 and were presented at the International AIDS Society (IAS) meeting in Cape Town, South Africa, on July 22, 2009.

In the primary analysis of HIV transmissions determined by laboratory testing to have occurred within the couple and not acquired from an outside partner, there were 41 infections in the acyclovir arm and 43 in the placebo arm -- not a significant difference. Of the partners who were infected with HIV, 68 % were women. Acyclovir suppressive treatment did show significant reductions in the frequency of genital ulcers (by 73%) and the average amount of HIV in the blood (by 0.25 log10 copies/milliliter, a reduction of 40%), compared to the placebo arm.

"As is often the case with large efficacy trials, you learn to expect surprises," said Dr. Connie Celum, the leader of the study and a UW professor of Global Health and Medicine in the Division of Allergy and Infectious Diseases. "We found that, in spite of a significant reduction in plasma HIV levels and genital ulcer disease with acyclovir suppressive therapy, there was no reduction in HIV transmission. This was a disappointing finding, but a critical outcome of this study is the understanding that interventions must achieve a bigger reduction in HIV levels in order to reduce HIV transmission, especially among persons with high HIV levels. This will be important in informing future interventions to reduce HIV infectiousness."

Celum said the study is a direct assessment of the impact of herpes suppression on HIV transmission and is the most direct way to see if it's possible to make a person less infectious and less likely to transmit HIV to their partner. Although the primary outcome of reducing HIV transmission was not observed, Celum said the study achieved many significant mile¬stones that will help to inform HIV prevention research in a number of ways. Among these were HIV testing of approximately 55,000 couples of unknown HIV serostatus, screening of more than 6,500 HIV serodiscordant couples, and enroll¬ment of 3,408 couples in which the HIV- infected partner was dually infected with HSV-2 and not eligible for antiretroviral therapy, based on national guidelines. Adherence to twice daily acyclovir was high, with 88% of doses dispensed (the drug was not dispensed during pregnancy or if visits were missed), and 96% of dispensed doses taken, as measured by pill counts. Retention of study participants at 24 months of follow-up was 92% for HIV infected partners and 84% for HIV uninfected partners.

The Partners in Prevention HSV/HIV Transmission Study is the first clinical trial to directly test whether suppressing HSV-2 infection in HIV-infected persons could reduce rates of HIV transmission and HIV disease progression. The study was randomized, placebo-controlled and double-blinded, meaning that both participants and the care providers did not know which treatment the participants were receiving. Both the placebo and treatment groups received standard HIV prevention services, which included being supplied with condoms, treated for other sexually transmitted infections, and provided care for HIV infection. All participants received extensive counseling, both individually and as a couple, throughout the study period, on how to reduce the risk of HIV infection.

"This was an ambitious study, and I applaud our collaborators at the University of Washington, the investigators and study teams in Africa, the study participants, and the communities where the study was done, for their dedication over the past five years," Celum said. "We will continue to learn from this study about risk factors for HIV transmission, which will bear fruit for both the HIV prevention and the vaccine fields for years to come."

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Journal Reference:

Celum C. et al. Acyclovir and Transmission of HIV-1 from Persons Infected with HIV-1 and HSV-2. New England Journal of Medicine, 2010; DOI: 10.1056/NEJMoa0904849

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STDs, midlife and beyond

Baby boomers, and even their parents and adult children, are experiencing a new type of boom-in acquiring sexually transmitted diseases (STDs). Why are STDs on the rise in the 45+ population, and what should we do about it?

Reasons for the Increase

A growing number of midlife and senior adults are engaging in sexual activity and ignoring the risks of unprotected sex. According to a study reported in U.S. Pharmacist, seniors are one-sixth less likely to use condoms than people in their 20s.

In their defense, seniors grew up when talking about sex was taboo, talking about STDs was even more taboo, and formal sex education-where they would have learned about STDs and how to prevent them-hadn't been "invented." But adults who did have formal sex education have no excuses, except laziness, denial--or skipping class.

Compounding the problem is that a decline in immunity in older people makes them more vulnerable to contracting STDs. Additionally, decreased vaginal lubrication and thinning of the vaginal walls increases the risk of micro-tears in post-menopausal women, and these tears facilitate the transmission of STDs.

The Evidence

Researchers at England's West Midlands Health Protection Agency found between 1996 and 2003, STD rates for Chlamydia, genital herpes, genital warts, gonorrhoea and syphilis more than doubled among people 45+. Males in the 55 to 59 age range were significantly more likely to be affected.

The American Geriatrics Society (AGS) Foundation for Health in Aging reports studies that found the same trend of increasing incidences of other STDs: the human papilloma virus, which causes genital and anal warts and cervical cancer, and the human immune deficiency virus ( HIV), which causes AIDS. The Centers for Disease Control and Prevention reports that adults aged 50+ make up 10 percent of all new AIDS cases.

The implications? Health care providers should talk routinely to their older patients about the dangers of unprotected sex.

What You Need To Know

When having sex with a new partner:
Use a condom. Condoms are the most effective protection against STD transmittal. Use lubricants with the condom to reduce the chance of getting sores or small cuts on the penis or inside the vagina--sores and cuts facilitate STD transmittal.Both you and your partner should be tested for STDs and share your results.If your test results show you're both STD-free you can forego the condom as long as you remain monogamous.
For more information visit Global Action on Aging.

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Monday, December 3, 2012

Herpes healing comes in numbers

Seven years ago, Pam Wisniewski stood in her doctor's office and got some news she thought would ruin her life.

"You have genital herpes," a physician's assistant told her.

Wisniewski started sobbing. "I felt like I was going to be alone for the rest of my life," she said. Her dream of marriage to the perfect man and children faded.

"It was devastation at that point," she said.

Today, Wisniewski is living the dream she thought was lost. She and her husband, Mike, are approaching their one-year anniversary and plan on starting a family soon.

And she's helping others make the same transition.

The 29-year-old UNC Charlotte doctorate student moved to Charlotte, N.C., in 2005 and started a herpes and human papillomavirus, or HPV, support group.

She thought it might end up as "a group of 50 people who went out to a movie now and then," she said. Today, Charlotte H has 1,100 members and keeps growing.

At least 45 million people in the United States have contracted Herpes simplex virus, and most don't know it, according to the federal Centers for Disease Control and Prevention. During an outbreak, patients can experience painful blisters and sometimes flulike symptoms early on.

The virus is transmitted through kissing, oral sex and intercourse. Herpes can even spread when a couple uses a condom because the skin around the protected genital area could be infected.

About 20 million people have HPV, which causes benign warts in men and women and sometimes cervical cancer in women.

For those living with herpes or HPV, healing comes in numbers.

As support groups grow in Charlotte, members are transforming their experiences into lessons for the newly infected or longtime fighters suffering alone. For them, herpes or HPV aren't life-stoppers.

Here are some of their stories.

Carle: The Diagnosis

Carla, who requested her last name not be used, started dating a man she met in a divorce support group after her 10-year marriage ended.

Both had initially tested negative for sexually transmitted infections. But routine tests don't detect herpes unless a blood test is requested. Her partner, who did not have any symptoms, unknowingly gave her herpes even though they were using condoms.

Carla, 36, got tested for herpes when painful genital blisters erupted. The results were negative and she was sent home with a topical cream, but she tested positive after a second outbreak.

"It was a little bit to deal with coming off a marriage," she said.

Dr. Lena White at the Mecklenburg County, N.C., Health Department said a classic blister has a white head with a red halo around it. By the time many patients visit their doctors, the lesion may have subsided.

"Sometimes doctors don't have enough evidence to make the diagnosis," she said. Carla, an active member of the Charlotte-based Carolina H support group that started in March, is now in a long-term relationship. "The group keeps you grounded," she said.

John: Feeling Trapped

John, 40, contracted herpes from his girlfriend, who hid her secret from him. He had a reaction many have when they're diagnosed: He thought he might as well marry her because no one else would want him. John also asked that his last name not be used.

"At that time, not knowing anything or without doing any research, I thought we were the only two within three states to have herpes," he said. In fact, a lot of people who are diagnosed limit their dating to stay within the herpes community.

John joined a support group after ending his relationship. He made friends quickly and is now dating a Carolina H group member.

"There's someone there that you're going to relate to and who can show you the ropes" on navigating a new life, he said.

Strength In Numbers

For members, support groups are a chance for lessons and friendships. Some meetings are more social; others are educational. Charlotte H and Carolina H have scheduled gatherings or activities a few times a month.

"Sometimes we talk about it maybe one percent of the time," said Kirk, a Carolina H leader. "We talk about our group of friends probably two or three times a day."


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Sunday, December 2, 2012

Towson biology professor developing silicone implant to battle herpes

Barry Margulies Barry Margulies uses a pasta maker to manufacture the implants that administer herpes treatment. (Kim Hairston, Baltimore Sun / July 24, 2012)

The space sure looked like a science lab, with beakers full of brightly-hued potions and a dry-erase board covered in graphs and mathematical scrawl. But at the heart of the operation sits a hunk of metal with a hand crank on the side.

"It's a pasta maker," said Barry Margulies, a biology professor who presides over the Towson University lab.

No joke. When it occurred to Margulies' graduate researcher that Williams Sonoma might have the answer to their prayers, it was a major breakthrough for the lab's efforts to treat one of America's most prevalent sexually transmitted diseases.

"I work in herpes," said Margulies, smiling a second later as he realized that sounded funny.

He's a jovial character who talks with his feet propped on his desk and decorates his office with pennants and balls from the Philadelphia teams he has cheered since his youth. A Janis Joplin CD peeks out from beside his keyboard.

Using the pasta maker, Margulies and his students make long strands of rubbery material that look like spaghetti noodles. The "noodles" are made of medical-grade silicone, blended with the drug Denavir.

Margulies said they could be the key to long-term, minimally invasive treatment of herpes simplex viruses type 1 and type 2. Inject one bit of the drugged silicone spaghetti in a strategic location, he explained, and the symptoms of the virus could be neutralized for up to five years.

At Massachusetts Institute of Technology, Margulies studied under Robert Langer, one of the nation's leading experts on time-release medication. As a doctoral student at the Johns Hopkins School of Medicine, he immersed himself in virology. The research insight that changed his career path combined the two experiences.

The idea struck him 20 years ago in graduate school. What if herpes patients didn't have to pop a pill or rub cream on their skin every day? What if the medication could be bound to a substance that would release it into the patient's body gradually?

Langer said the medications weren't good enough at the time, but when Margulies revived the idea more than a decade later, his mentor said it could work. The idea seemed so simple that he couldn't believe no one had tried it.

He has pursued the research since 2005, and his tests have found that in mice, the silicone implants reduce the recurrence of herpes. His lab is working on feline tests with counterparts from the University of California, Davis, and the early results are positive. Margulies has a patent pending on the silicone implants.

He has yet to test the implants on human subjects, and with several important questions — where does the drug go in the body when released and where is the optimal point of injection? — yet to be answered, he's not sure when that will happen. The effort might be out of his hands, licensed to a major drug company, by the time clinical trials begin.

"Sometimes, it's frustrating," he said of the protracted development period. "But I know that our sights are set on helping people."

Margulies has taught at Towson since 2001.

He knows some people might be surprised that a product of MIT and Hopkins is performing serious science at former commuter university with a lab staffed mostly by undergraduates. But he said he loves Towson's emphasis on teaching and on engaging students who are only a few years out of high school.

Shamsuddin Khan, a junior who works in the herpes lab, calls Margulies "fatherly" in the way he nurtures student input and fields endless questions. "If I keep asking something, many things one after another, he never feels tired," Khan said. "He keeps talking, applying many different ways to make lessons easier."

Through his work in the lab, Khan said, he has evolved from a scared novice to a scientist with plans to "do something big for the benefit of mankind."

Some of the key insights in developing the implants, such as the pasta maker revelation, have come from students.

"They think it's funny when I say, 'Your ideas can be as good as mine,'" Margulies said. "But the difference is just experience, and actually, experience can put blinders on you sometimes."

childs.walker@baltsun.com

Herpes facts

Definition: Sexually transmitted disease caused by the herpes simplex viruses type 1 (HSV-1) or type 2 (HSV-2). Most genital herpes is caused by HSV-2.

Prevalence: 1 out of 6 Americans ages 14 to 49 has HSV-2 infection.

Treatment: There is no cure. Sufferers can take antiviral medications to shorten and prevent outbreaks or daily suppressive therapy to help reduce transmission.

Source: Centers for Disease Control and Prevention

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