Herpes – The Gift That Keeps On Giving

Herpes is a viral infection that typically manifests on the skin as vesicular lesions in a vesicular lesion or vesicle, like a blister. These will eventually ulcerate and even crust and scab over as healing occurs. 

Now herpes is caused by one of two different viruses. However, there have been people that have contracted both, one is called herpes simplex virus type 1 or HSV-1, and the other is called herpes simplex virus type 2 or hsv2. Now, hsv1 is most often associated with sores around the mouth and the lips. 

Often referred to as cold sores or fever blisters, whereas hsv2 is most often associated with sores around the genital structures and even the anus. Still, there is some potential crossover between these two viruses, and that has to do with how you contract them. 

HSV-1 is typically contracted or spread through direct contact with infected oral secretions from someone with HSV-1. This is often done during childhood, say when a parent or sibling has a visible, active lesion, and oral secretion gets.

Transfer

It is transferred from kissing or sharing of other various items that eventually make it to the mouth. 

Now keep in mind you don’t technically always have to have a visible lesion to spread HSV-1 because some people have these mild reactivations of this infection, which we’ll get to in a minute,

When there are visible larger lesions, these lesions tend to shed more virus and have an increased viral load, increasing the risk of transmission. 

Now because of how hsv1 is typically spread like this through these infected oral secretions, it’s not technically or generally classified as a sexually transmitted infection. 

Although there are some exceptions to this however, hsv2 is typically classified as a sexually transmitted infection because, again, it is most commonly transferred or contracted through direct contact with genital structures from an infected person. 

Let’s cover one thing that many of you are probably thinking about is it possible to get hsv1 in the general region and hsv2 around the mouth or the lips, the answer is yes. 

Both virus types have been isolated from both genital and oral lesions. It’s just that, more commonly again, hsv1 is found around the mouth and hsv2 around the genital structures. 

Now, this transfer would occur through oral forms of intercourse, say if somebody had an active infection or hsv1 around the mouth and they performed a form of oral intercourse that could transfer HSV-1 to the genital structure and vice versa. 

It’s also true somebody had hsv2 in the general region, and it could get transferred to the mouth through oral intercourse. 

So now we need to discuss why herpes is the gift that keeps giving.

In other words, why does our immune system have such a hard time eradicating this virus? 

Because those of you who’ve experienced herpes, like cold sores or other various manifestations of the infection, may have got a pretty good idea that you can have flares where the lesions show up, and then they heal and go away.

You can have another flare, and there’s a lot of variability on how often or how frequently people can experience these flares. To understand how this is working, we need to talk about what’s known as the primary infection. 

How the virus sets up in this latent phase and then can reactivate periodically, so when a person is first exposed to the virus, the virus will infect epithelial cells, which make up the surface of your skin.

The mucous membrane would be the inside lining of your mouth, but this virus will get inside these epithelial cells and start to replicate and copy itself.

This virus will move into a sensory neuron close by or associated with that skin area or epithelial cells. Once it moves into that sensory neuron, it will travel up the neuron towards something called a sensory ganglion. 

I know ganglion is a weird word, but stick with me a second because the sensory ganglion is an important collection of neuron cell bodies. 

The cell body of neurons where you’d find like the nucleus and other organelles now if this is an oral infection, it’s going to set up in this ganglion called the trigeminal ganglion. Many of you may have heard of the trigeminal nerve. It’s the great sensory nerve of the face. It serves much of the skin of the face. 

If it’s a genital infection, it will go into a sacral ganglion. Now I’m bringing up this discussion about the ganglion because this is where the virus evades parts of our immune response and sets up this latent lifelong infection.  

Let me go back to the beginning of this process when the virus first enters those epithelial cells. This is the start of what’s known as the primary infection, and what’s interesting about the primary infection is that many people are asymptomatic. 

But when people do have symptoms, that can include these painful vesicular lesions, swollen lymph nodes, and even things like headache, fever, and even malaise which is this term for I don’t feel well now. 

This is when symptoms are present. They can start anywhere from 2 to 12 days after exposure. 

As the vesicular lesions are present, those can last anywhere from one to three weeks, with the genital HSV lesions tending to last closer to that two to three-week range, so what happens after our body deals with a primary infection? 

Well, this is when the latent phase of the infection starts, where that virus is kind of contained within that sensory ganglion. 

Remember that our body or immune system can deal with it to a certain degree even though it can’t entirely eradicate the virus. 

For example, our body heals and improves from that primary infection. With the recurrent infections we’re about to discuss, people who have experienced those know that the lesions can come. 

Then the body can heal, so our body does have this ability, especially from the perspective of the skin, to heal those skin lesions.  

It is of it the immune system pushing the virus back into that sensory ganglion, containing it until a potential reactivation infection occurs. 

When, how often, or how frequently do these reactivation infections occur? Even if they occur, there’s a variety of factors, post factors like your own immune system, things that are within you that are unique to you. 

Ultimately, there are environmental factors thought to influence the reactivation of this virus, things as immunodeficiency and the immune system not working correctly. 

Stress, sunlight, and even a fever. These are often referred to as cold sores or fever blisters because people will notice that they pop up when they have a cold or even a fever. 

When this reactivation phase occurs, the virus will re-enter its replication cycle and move back down that sensory neuron to the area of the skin that that sensory neuron serves and re-enter those epithelial cells. 

The virus starts to copy itself, which is when the vesicular lesions will start to reform. Now, this process also explains why some people will experience what is called prodromal symptoms. 

These symptoms can occur one to two days before the vesticular lesions or blisters form. These symptoms typically include things like pain burning, tingling, and even itching in the pathway of that neuron before the lesions even form.

Let me reiterate something I mentioned earlier: the frequency and severity of these reactivation infections, flare-ups, or outbreaks vary significantly among individuals. 

For example, plenty of patients have tested positive for HSV, especially hsv1, where they’re like, I’ve never had a cold sore in my life. I will tell them you’re one of those asymptomatic during the primary infection. 

At least the primary infection was very mild. You probably didn’t notice it much, and you just went on your way, and your body does a better job containing that infection rather than allowing it to have these flare-ups or outbreaks. 

Now another interesting thing to consider is that the primary infection, in general, the severity of this, correlates with the frequency and the severity of the outbreaks. The worse the primary infection, the more severe and infrequent the outbreaks or reactivation and actions can be something we want to consider.

Hsv2, the genital infection is also much less forgiving. What I mean by that is you are more likely to have outbreaks with HSV to genital infections than you are, say, with an oral HSV-1 infection. 

So if we can’t cure this or completely eradicate the virus, can we do anything about these reactivation infections or flare-ups? The answer is yes. 

For example, there are topical medications available that people will try to use, most of which are ointments that help with the discomfort. Topical lidocaine could help numb that pain and make the flare more bearable. 

But the medications that tend to have the most data and be the most effective are a group of antiviral medications. Some of the common antiviral medications used for HSV are things like valacyclovir, acycloviron, and even acyclovir. 

Now, these medications are relatively accessible generic, and reasonably inexpensive, and they tend to work if you use them properly. At least they tend to help because they don’t kill the virus. 

But what they do is help slow down the virus replication. Remember, during this reactivation infection or this flare, the virus will re-enter its replication cycle and start copying itself. 

These medications can help inhibit that and bolster the immune system to push this virus back into its latent phase. 

Again, as I mentioned earlier, these medications must be used correctly. What I mean by that is when a patient has, for example, these outbreaks, you need to initiate these medications as soon as you feel the sores might be coming on. 

Patients who do the best are those that recognize those prodromal symptoms that we mentioned earlier. Remember, sometimes people will notice tingling, that burning pain before the sores even form. As soon as they feel those symptoms, they initiate the medication because the medication again does not kill the virus. It just inhibits its replication.

Suppose somebody already has the sores formed for like a day or two. In that case, these antiviral medications won’t do much, but if they initiate them early enough, they’ll notice that the length of the outbreak and the time they’re experiencing discomfort tends to shorten. 

It helps with the severity. Another way I want to mention is that these medications could be used, which would be reserved for people with more severe and frequent outbreaks. 

A patient in this situation might opt with their health care provider to be on a lower dose or a lower maintenance dose, if you will, so they would be on a lower dose daily. 

It would help reduce the chances or the risk of these frequent and more severe outbreaks.