The herpes virus is one of the most prevalent viral diseases known to man. As much as eighty percent of all people, worldwide, have herpes simplex virus type 1 (HSV1), and twenty percent have herpes simplex virus type 2 (HSV2). This may sound like scary statistics, but most infected people suffer only mild discomfort. The more common form, HSV1, usually causes the occasional blister-like sores on or around the mouth. These blisters are called cold sores or fever blisters and, as most sufferers know, they are annoying and mildly painful but rarely dangerous.
If the sores are left alone, they will generally heal up in five to twenty days. The less common version, HSV2, has the same symptoms except that the sores are usually found on or around the genitals. However, either type can be found in other places on the body and, in rare cases, the virus can cause serious problems. Ocular herpes (an infection of the eye) can cause blindness, and herpes encephalitis (an infection of the brain) can cause brain damage or death. We have no cure for the herpes virus at this time; once you have the virus, you have it for life.
After the virus invades a new host, it incubates for two to twenty days. Then blister-like sores start to form, and in the initial breakout there can be fever, muscle aches and a general feeling of illness. What is a virus? Viruses are the smallest infectious agents known; too small to be seen with a normal microscope, an electron microscope is necessary to be able to see a virus. According to Oates, J. K. in Herpes: the facts (1983) ” … an average bacteria is roughly 1,000 nanometers in diameter, while viruses range in size from 300 to as little as 10 nanometers. ” and that ” … a human red blood cell, …
is between 7 and 8 thousand nanometers … ” (p. 21). Viruses are nucleic acid, RNA or DNA, coated with a protective layer of protein called a capsid. Some viruses also have an outer bag of lipo-protein called an envelope. After a virus attaches to a living cell, it either enters the cell to release the genetic information, or, the virus injects the information through the cells outer lining. Thus changing the cells natural functions and forcing the cell to spend its energy to create copies of the virus. The cell will go on making copies of the virus until the cell is used up and dies.
The virus then leaves the dead cell and invades a nearby cell and the process starts all over. There are five types of human herpes virus: Varicella zoster which causes chickenpox, Epstein Barr virus which causes infectious mononucleosis, cytomegalovirus which can cause cytomegalic inclusion disease in infants, and herpes simplex viruses 1 and 2. Herpes Simplex Viruses 1 and 2 Oates states that “the herpes virus [HSV1 &ump; 2] is a roughly rounded particle, with its protein coat made up of a large number of hollow protein units. The whole is surrounded by a loose, ‘baggy’ envelope and measures about 100 nanometers …
“(p. 22). The herpes virus is transferred through body-to-body contact, most commonly when sores are present. However, the virus can be spread when there are no signs or symptoms of an outbreak. HSV usually infects the mucous membranes around the mouth or genital areas, but sores can form anywhere on the body. Once inside a living cell HSV takes over and the cell starts producing copies of the virus. Oates explains that “This activity usually leads to the cell dying and the release of mature particles of virus which acquire their envelope as they leave the dying cell to infect others.
” (p. 35). The dying cells release approximately two-hundred HSV particles. Primary breakouts are more sever then recurrent breakouts and last for up to twenty days. The infection starts with a tingling, burning or itching sensation, followed by the appearance of small red bumps. In primary breakouts, there is often fever, swollen lymph glands, and a general feeling of illness that is not present in recurrent breakouts. The mayo clinic website (2009) briefly describes, “They [the red bumps] then rupture, becoming ulcers that ooze or bleed.
Eventually, scabs form and the ulcers heal. ” (para. 3) A good description but a bit simplistic, doctor Hamilton, R. in The herpes book (1980) describes the process “Scab formation generally marks a turning point in both the way the sores look and the way the affected person feels. Local swelling, inflammation, and pain begin to subside, and general symptoms start to diminish. ” He goes on to say “As new mucous membrane or skin develops, the scab falls off and, generally, by the end of the second week most patients are completely recovered—or so it would appear. ” (p. 29).
But in fact you never actually recover because shortly after the virus entered a cell and began to multiply some of the virus particles found a nerve and started traveling up that nerve to the ganglia, where the virus will hide in a dormant state. In Human herpes simplex labialis, Fatahzadeh, M. and Schwartz, R. A. (2007) explains, “Following primary oral infections, HSV-1 migrates centripetally along the nerve tracts from the oral mucosa to the trigeminal ganglion. ” (p. 626). Occasionally the virus will travel back down the nerve to the original site of infection and a new breakout will occur.
Not everyone will have recurrences, and, in most cases, the recurrences are less frequent and less severe as time goes by. Herpes complications In very rare cases, HSV can cause a serious infection in the brain, called herpes encephalitis. Herpes encephalitis occurs when the herpes simplex virus infects brain cells. According to Pritz, T. in Herpes simplex encephalitis (2010) “Brain infection is thought to occur by means of direct neuronal transmission of the virus from a peripheral site to the brain via the trigeminal or olfactory nerve.
Factors that precipitate herpes simplex encephalitis are unknown. ” (para. 4). Herpes encephalitis infections usually occur in primary infections of people under the age of twenty, or in recurrent infections of people over the age of fifty. Pritz adds “In children older than 3 months and in adults, herpes simplex encephalitis (HSE) is usually localized to the temporal and frontal lobes and is caused by … (HSV-1). ” (para 1). And that “In neonates … brain involvement is generalized, and the usual cause is … (HSV-2), which is acquired at the time of delivery.
” (para 2). However, with regular screening for genital lesions in the weeks prior to delivery, most cases, of herpes encephalitis, in newborns can be prevented. If lesions are present then the baby will be delivered by caesarian section. The other major complication that can occur with HSV is ocular herpes. The herpes virus gets into the eye and according to Langston, D. P. in her article Herpes simplex virus in the eye (2010) ” When the virus first enters the body, … it travels through the nerves up to the same center, which also sends nerves to the eye.
… Occasionally … instead of traveling back down the nerves to the mouth or nose, it goes to the eye causing the illness there. ” (para. 2). In addition, a person can get ocular herpes by touching an active HSV lesion and then rubbing their eye. This is called autoinoculation, and it is possible to autoinoculate any part of the body where there is a cut or break in the skin. Langston continued with There are several forms of ocular herpes. The most common is … the viral infection, i. e.
a cold sore in the eye. Typically it causes a branching sore or ulcer on the surface of the cornea … Other forms include … sterile ulcers that are slow to heal because of mechanical damage FROM the preceding virus infection, … allergic or immune haze deeper in the cornea due to reaction to virus proteins left after the infection has cleared, and … iritis or inflammation of the blue or brown part of the eye located behind the cornea. The immune form of corneal disease causes the greatest scarring.