There doesn't seem to be a lot of information available on research done on warts. What is the life cycle of a wart? How does it spread? -- specifically how does it recruit cells to spread it? What is the life cycle of a PV-infected dermal cell?


2 Answers 2


This article has some good information. It's certainly more than I want to know about warts.

Isolated warts may remain unaltered for months or years, or a large number of new lesions may develop rapidly in a short period of time. The development of warts is not predictable. Approximately 65% of warts disappear spontaneously within two years. The patient’s age and number of lesions do not seem to affect the prognosis.

There are many different types of warts and of HPV. Since warts cause a type of dysplasia their life cycle can be very variable and unpredictable.

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    $\begingroup$ Do you mind summarize some of the key points in the article. The link might die someday, and it'd just make a much more complete answer :). $\endgroup$ Commented Aug 14, 2012 at 0:01
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    $\begingroup$ Sure. I'm new to Biology beta. It seems to me that the nature of the site necessitates a lot of linking and referencing since there's no way to confirm someone's credentials. And even those with credentials need to cite their sources. $\endgroup$
    – Conner
    Commented Aug 14, 2012 at 0:06
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    $\begingroup$ Welcome :). Generally, when making a claim, a reference is just customary. The edited answer is great though, +1. $\endgroup$ Commented Aug 14, 2012 at 0:10

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.

Interesting Notes

  • 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

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