Conner's response contained just the type of source material I was looking for. Thanks Conner -- let us all +1 him. Allow me to summarize the specifics of the article in relation to my question:
PVs are transmitted through direct or indirect contact with an
individual who has the lesion. Dysfunctions in the epithelial barrier
by trauma, minor injuries or maceration cause loss of solution of
continuity in the skin, thus allowing viral infection. After
inoculation, the incubation period varies from 3 weeks to 8 months.
Spontaneous regression is observed in most cases.
Infection begins when the PV reaches the cells of the basal layer;
there is no viral replication at this location and the virus just
keeps its genome by amplification of a low number of copies.
The replicative phase and protein synthesis occur in the suprabasal
differentiated keratinocytes. Progression time and type of lesion
correlates with the quantity of viral particles detected. Younger
warts present a higher viral amount when compared to old warts.
Plantar warts have a higher viral load than common warts. The center
of the lesion appears to be the main site of viral concentration.
PVs appear to remain in their host for long periods of life. A variety
of different types of PVs can be detected in random sites of normal
skin in humans and animals. This reinforces that a latent life cycle
is often a characteristic of these viruses.
- There are no known PVs that infect more than one species.
- To date, about 100 different types of HPVs have been fully characterized.
- Human PVs does not grow on conventional culture media. The diagnosis of HPV infection is made by histopathology of lesions