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My name is Richard Whitley.
I am a professor of pediatrics, microbiology, medicine,
and neurosurgery at the University of Alabama at Birmingham.
Over the next 45 minutes,
I would like to discuss with you the Natural History and
pathogenesis of herpes virus infections.
It is important to recognize that there are eight human herpes viruses.
Three are in the alpha herpes virus subfamily,
three are in the beta herpes virus subfamily,
and two are in the gamma family.
Herpes simplex type one,
herpes simplex type two,
and varicella zoster virus comprise the alpha herpes virus family.
Cytomegalovirus, human herpes virus six,
human herpes virus seven,
comprise the beta herpes virus family.
While Epstein Barr virus,
and human herpes virus eight or
Kaposi sarcoma virus are members of the Gamma herpes virus family.
These three subfamilies reflect where
the virus has established latency as I will mention later,
and how they can potentially be reactivated.
It is important to recognize the natural history of
herpes simplex because it serves as a model for HSV1,
HSV2, and varicella zoster virus infection.
Primary infection is the consequence of exposure of
an uninfected individual to virus at a mucosal surface.
Virus is then transported to
the dorsal root ganglia where an initial round of replication will occur.
Virus is maintained in a latent state,
in its episomal form.
This is illustrated on the slide in front of you now.
Shown in the upper left panel,
is Episomal latent herpes simplex virus DNA.
With a proper provocative stimulus,
the virus is reactivated and transported back down
the nerve root to a muco-cutaneous surface where either lesions,
or asymptomatic shedding will occur.
Herpes simplex can infect multiple body sites as illustrated on the present slide.