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Cold Sores and Herpes Facts


The word ‘herpes’ comes to us via Latin, derived from the Greek root ‘herpein’ – ἕρπης herpēs, meaning ‘to creep’ or ‘latent’.  Herpes viruses are a family of viruses that include, among others:

Herpes Simplex Virus Type 1 (HSV-1)

HSV-1 primarily affects the oral and facial areas and mucous membranes, but can also affect the genital area, the eyes, and in rarer cases different areas of the body; this is the virus that most commonly causes the outbreaks known as ‘Cold Sores’, which are, in reality, herpes virus outbreaks.

Herpes Simplex Virus Type 2 (HSV-2)

HSV-2 primarily affects the genital area but can also affect other parts of the body.  Since the herpes virus is transmitted by direct contact from an infected individual, and as we live in a more and more sexually permissive society, the incidence of HSV-1 and HSV-2 affecting the oral / facial areas as well as the genital areas or both is increasing.

Other viruses in the herpes virus family (Herpesviridae) include:

  • Varicella-zoster virus (chickenpox and shingles)
  • Human cytomegalovirus (infectious mononucleosis)
  • Epstein-Barr virus (a co-factor in human cancers)
  • Karposi’s sarcoma Herpesvirus (a cofactor in Karposi’s sarcoma, a complication associated with AIDS)

But by far, the herpes viruses that affect the most people are HSV-1 and HSV-2.

The family of herpes viruses can often be ‘silent’, and cause people little or no adverse effects, or run the gamut to severely painful and recurrent outbreaks that have devastating social consequences, and advanced stages may lead to more serious disease.

A Note About Cold Sores and Herpes

Often referred to by the more socially acceptable terms ‘cold sores’, or ‘fever blisters’, the eruptions that occur in and around the oral / facial area are the result of the action of the herpes simplex virus Type 1 (HSV-1).  As the HSV-1 virus is primarily transmitted through direct contact, kissing and sexual activity, for decades, “having herpes” was considered a sign of promiscuous sexual behavior, and more socially friendly terms, like ‘cold sores’, were coined.

But the cold facts are that ‘cold sores’ and ‘fever blisters’ are indeed outbreaks caused by the herpes virus.  And it’s nothing to be ashamed of.  In fact, the herpes virus is primarily transmitted as much by ‘viral shedding’ (explained a little later), as it is by direct sexual contact. Almost half of people infected with the herpes virus don’t even know it, as they may never have experienced a visible outbreak, or didn’t know that certain symptoms were those of herpes. If you’ve ever had a cold sore, you have the HSV-1 virus in your system.

While there is NO CURE for the herpes virus (no matter what you may have heard or read), and it stays in your system for your entire life, taking care to avoid outbreak triggers, and learning about the many viable options that may help to reduce the symptoms, frequency, severity and length of any outbreaks you may experience are important steps to better health.

Another variant of the herpes virus is herpes simplex Type 2 (HSV-2), which is also referred to as ‘genital herpes’, as it primarily affects the genital region of your body.  HSV-2 is primarily transmitted through sexual contact and is highly contagious, both during outbreaks and when there are no visible symptoms.

Other than the specific area of the body affected, both HSV-1 and HSV-2 function in very similar ways, result in very similar symptoms, are triggered by similar events, and may be reduced in frequency and severity by a number of prescription and non-prescription treatments and immune system supporting supplements.

Herpes Simplex Statistics, Symptoms and Triggers

If you have experienced, been diagnosed or know you have been infected with a herpes virus you need to know you are not alone.

Herpes is one of the most common virus infections in the world, and one of the fastest spreading viruses known.  There are two main types of herpes virus infections that are of great concern to both men and women: HSV-1 (oral herpes) and HSV-2 (genital herpes).

General Statistics About HSV Viruses

It is important to note that statistics on herpes virus infections vary depending on the source of the information, the nature of the study or sampling methods used, and the time of the data collection.  We present the latest available statistics, verified through the most credible sources available, including the CDC (Centers for Disease Control), NIH (National Institutes of Health), as well as other governmental, medical school and STD research facilities.

  • One out of five adolescents and adults is infected with genital Herpes in the United States
  • Infection is more common in women (approximately one out of four women or greater) than in men (approximately one out of five or greater)
  • Male-to-female transmission is more likely and more common than female-to-male transmission
  • One in five Americans (approximately 20%) have genital Herpes (yet at least 80 percent of those with HSV-2 – genital Herpes – are unaware they have it)
  • About 80 percent of American adults have oral Herpes (cold sores) – that’s over 260 million Americans
  • An estimated 25 percent of American adults have genital Herpes
  • Approximately two-thirds of people who acquire STDs in the United States are younger than 25
  • About one in five people in the United States over age 12 (approximately million+ individuals) are infected with HSV-2, the virus that causes genital Herpes
  • At least one in four Americans will contract an STD at some point in their lives
  • Up to 1 million new HSV-2 infections may be transmitted each year in the United States
  • Genital Herpes infection also is more common among African Americans (45.9%) than among White Caucasians (17.6%)
  • Since the late 1970s, the number of Americans with genital Herpes infection has increased 30%, and continues to increase
  • The largest increase of genital Herpes is among young Caucasian teenagers
  • Genital Herpes infection is now five times more common in 12- to 19-year old Caucasian adolescents than over the past 30 years
  • Genital Herpes is twice as common among young adults ages 20 to 29 than it was 20 years ago

A Summary of the Science Behind Herpes Viruses

Herpes viruses are extremely common with more than 100 varieties having been identified in a variety of animal species, including at least 8 variations that affect humans.

All of the herpes viruses are members of one family, the Herpesviridae, and have specific common characteristics, such as the ability to establish latency (a period when the virus will become inactive, or ‘dormant’) during a primary (first) exposure and infection.

This means that following initial infection the herpes virus may lie dormant for periods of time. It resides (or ‘hides’) within the nervous system and other cells in the body as protection from the antibodies produced by the immune system.

When inactive (dormant or latent) the virus inhabits the cell in the latent stage and does not replicate or travel throughout the body.  When stimulated by various factors (triggers) such as stress, illness, poor nutrition, excessive activity and even sunlight coupled with a weakened immune system, the herpes virus re-awakens and travels through and around nerve pathways to the site of the outbreak.

The herpes virus remains in a latent stage that can last for weeks, months or even years.  During this inactive stage it does not reproduce or spread or result in classic herpes outbreaks.  Most likely, during this latent stage, the protein coating remains strong and antibodies from the human immune system cannot reach or effectively eliminate the virus.

A good time to attack the virus is in its active stage when it leaves the host cell and attempts to attach to and inhabit cells weakened by massive replication – this process is referred to as the VIRUS ATTACHMENT stage.

Viruses are sub-cellular organisms, extremely small in size (approximately 1/100th the size of the average bacterium) and are vulnerable the immune system when not attached to or inside of a host cell.

When outside of a human host cell, they are typically dormant, and they may be residing in latency, or seeking a new host cell to attach to.  They cannot reproduce by themselves and may even die or be eliminated by our immune system, but when they enter a host cell, they take over the host cell’s metabolism to effect their own replication.

The herpes virus’ most essential objective is to take over control of the host cell DNA and use it to make copies of its own DNA (or in some viruses like HIV, the genetic material may be RNA which is slightly different), replicating wildly, and then releasing newly-formed virus particles into the system, spreading to and attaching to new host cells, where the process repeats itself over and over.

In every reproducing cell there are DNA and RNA, which contain the genetic blueprint for the cell and the body.  Viruses genetically contain either RNA or DNA but not both.  Since viruses have only half the genetic material for reproduction they cannot reproduce unless they attach themselves to human host cells, insert their genetic material inside the host cell, and literally hijack the host cell’s capabilities to replicate this generic material, making new virus particles. 

Once inside the cell viruses can then reproduce.  They essentially turn the host cell into a ‘virus production factory’ which may lead to that cell dying or being engulfed by the host’s immune system.

The herpes virus that inhabits a cell acts like a parasite and will drain energy from the host cell.

The virus, encased in protein coating, moves through the intercellular fluid in our bodies from cell to cell and multiplies rapidly in each.  Left unchallenged by a strong immune system, one virus particle can explode into thousands and each of these into thousands or millions more. This is the action of the herpes virus.  As the total number of virus particles in the system (called the ‘viral load’) increases, the likelihood of an outbreak increases quickly.  Thus, the objective is to regulate virus reproduction as much as possible, as early and continuously as possible.

Again, it is important to note that if a herpes virus cannot successfully attach to a host cell or cannot insert its DNA or RNA into the host cell, it cannot reproduce, and will likely die off in a single generation.  It is also susceptible to attack by a healthy immune system which can eliminate the un-attached viruses from the body.

There are two types of herpes simplex viruses that constitute the largest viral threat to humans in volume: (HSV): HSV-1 and HSV-2.

These constitute two of the at least 8 known Herpes viruses.  The DNA sequences of HSV-1 and HSV-2 are approximately 50% identical and their encoded proteins are even more closely related.

There are no genes unique to either virus.  HSV-1 is responsible for more than 90% of oro-labial herpes (‘cold sores’ or ‘fever blisters’) whereas HSV-2 is responsible for over 90% of genital herpes infections; but either type is also able to infect the other area through cross contamination or direct contact (such as oral sex).

Those suffering with the infection may shed the virus from the skin of the genitalia, even in the absence of symptoms.  This scenario is referred to as asymptomatic viral shedding.

The host immune system will try and get rid of the invading virus by mounting an antibody response, as well as producing white cells which will destroy cells that have been recognized as being viruses or virus infected.

Unfortunately, those antibodies which are produced early during the herpes simplex infection do not prevent recurrence of the active phase of the disease.  Further, the genetics of the herpes viruses also have the ability to hide signaling the body’s immune system, and to increase the virus’ ability to evade and resist the normal immune response.

This probably occurs because the extracellular virus is neutralized while intracellular virus replication and direct cell-to-cell transfer is unaffected.  In simple terms, virus particles that escape (are released) into the blood stream or intracellular fluids may be identified and killed, but those which stay inside host cells replicating, or lie dormant in nerve roots between outbreaks may not be easily identified by or eliminated by your immune system.

When a virus is detected by the immune system, the antibody will attach itself to one of the surface proteins of the virus.  This will wake up the body’s white cells to enable the antibody-marked virus to be destroyed.  This so-called ‘cell-mediated response’ is important in the modification of the herpes infection, as patients who suffer from a compromised cellular immune system may experience more severe bouts of herpes outbreaks, be more susceptible to infection, and have a lower ability to defend against the virus and its more serious side effects.


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