Genital Herpes
Herpesviruses have been waging a war against man and winning. The herpesvirus family
is but one of hundreds of viral families that people deal with for most of their lives. The
influenza viruses, for example, cause the illness known as "the flu," while rhinoviruses are
responsible for causing the common cold. Both of these viral families have dozens of viral
strains that have similar traits, but are still very unique individuals. Herpesviruses are no
different and probably cause more human illness than any other viral group (Freedman 1). This
family includes varicella zoster virus, the cause of chicken pox in children and shingles in adults;
Epstein-Barr virus, the cause of infectious mononucleosis ("mono"); and herpes simplex virus,
type 1 and 2, the cause of cold sores and sexually transmitted genital herpes.
Since the 1970's, the number of Americans infected with genital herpes has grown to
almost epidemic proportions. The fear of human immunodeficiency virus (HIV) and AIDS
caused the American public to overlook other sexually transmitted diseases (STDs) allowing
genital herpes to spread very swiftly and silently through the population. Since the 1970's the
proportion of Americans infected with the herpes simplex type 2 virus (HSV-2) has increased by
almost one-third. Today, 45 million people over the age of 12 carry it--about 1 in 5. Women
generally are more susceptible to STDs, so the numbers climb even higher for women. One in
five white women is infected, versus one in seven white men. One in two black women has the
virus, compared with one in three black men (Carpenter 1). 3,000 to 4,000 newborns are also
infected each year (Edel 145). Unfortunately, education and awareness of genital herpes hasn't
spread quite as well. It wasn't until recently, that researchers discovered that most people
become infected without ever having any noticeable symptoms ("Symptoms…" 1). In fact, 80%
of people infected with genital herpes are unaware of their disease ("Factsheet" 1).
HSV-2 is spread through skin-to-skin contact and very rarely spread, if at all, by contact
with objects such as a toilet seat or hot tub ("Factsheet"). Contraction of the virus requires an
area of skin that is vulnerable to penetration like the soft skin cells of the genitals and moist
mucous membranes of the mouth, vagina, and anus. The thick skin of the arms, legs, and torso
has an increased amount of keratin, which makes the skin cells tougher and less likely to be
penetrated.
The relatively large herpesviruses are approximately 180-250 millimicrons in diameter,
have a core of deoxyribonucleic acid (DNA), and are shaped like 20 faceted crystal (Freedman
1). Once HSV-2 has penetrated the skin it begins to attack local skin and nerve cells. It does
this by attaching itself to the cells with a protein coat called the tegument that is held in place by
a lipid membrane produced by the infected cell ("Herpesviruses" 1). HSV-2 then injects its DNA
into the host cell, which makes its way to the nucleus of the cell where viral replication can
begin. The virus actually commands the infected cell to produce more of the viruses DNA using
its own machinery (Edel 7). Viral replication usually stops the host cell from living for itself so,
after the new virus particles are made, the cell bursts and dies, which scatters the new virus
particles to nearby cells where the cycle is repeated (Sacks 9).
Because HSV-2 is spread through direct contact between cells, it can avoid the
bloodstream and consequently, destruction by circulating antibodies ("Herpesviruses" 1).
Instead, HSV-2 prefers to travel along the sensory nerves from the skin to the nerve cells of the
sacral ganglia. The sacral ganlia is located near the base of the spine, and is one of dozens of
other nerve roots that run along the spine (Edel 15). Here the virus, for unknown reasons, goes
into a dormant stage where it waits to reactivate. During this latent stage the virus does not
replicate nor does it cause any detectable damage to the nerve cells ("Herpesviruses" 1). HSV-2
will remain in a state of "suspended animation" for weeks, months, or years until it is triggered
into reactivation (Edel 26). No one is quite sure what triggers the virus, but some researchers
believe stress, fever, trauma, and hormonal changes can stimulate reactivation ("Herpesviruses"
1).
Symptoms of initial infection vary from person to person, and may not appear for weeks,
months or years after the initial contraction of HSV. When symptoms do occur, their severity
will depend on the patient's past history of HSV. Typically there are two types of