Epidemiology of herpes simplex diseases]

The epidemiological principle of the herpes simplex virus (HSV) infections is to have the affected host survive, to persist in it and thus to make it to be a life long starting point for new infection chains. There is an accurately tuned correlation between virus and host organism, in which the persistence of the virus as a latent infection in the ganglion cells of sensory neurones is of central importance. In this state the virus cannot be attacked by the defensive power of the body. When changing from latency in the ganglion cell to activity in the periphery it utilizes the nerve conduction. It has not yet been cleared which factors are responsible for the change-over from the productive, cytocide infection to the latent infection, how the latency is being stabilized and how the reactivation to the herpes recidivans takes place. The organ and tissue specifity of both the HSV types 1 and 2 seems to be bound to the entire pathogenetic complex so that inspite of occasional reverse infections HSV type 1 remains epidemiologically the facial virus type and HSV type 2 the genital one. Apparent and inapparent rimary infections and relapes lead to numerous uncontrolled contacts so that the rate of infection is 50% until the age of puberty and 80% in middle-age adults. The contamination with the mainly venerically transmitted HSV type 2 starts with the age of puberty and reaches abt. 10 to 15% of our population. In patients suffering from cervix carcinoma antibodies against herpes simplex virus type 2 are more frequently demonstrated. Comparative examinations have shown that an increased exposition cannot be the sole cause for this prevalence. The kind of relationship between herpes genitalis and cervix carcinoma remains, however, unclear.