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Chapter 196. Human Papilloma Virus

Infections

Elliot J. Androphy; Reinhard Kirnbauer

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Papillomavirus Infections at a Glance
Very common infection of skin and mucosa of children and adults.

Papules of variable size often with a rough scaly surface.

Caused by human papillomaviruses (HPV), a subset of which are associated with cervical,
penile, anal, and other epithelial malignancies.

Treatment often requires physical or immune mediated destruction of infected epithelial

cells.

A prophylactic vaccine effectively protects from infection with HPVs most commonly
identified in cervical cancer and genital warts.

Papillomaviruses (PVs) cause benign cutaneous and mucosal epithelial proliferations commonly
called warts or verrucae. PV infections do not produce acute local or systemic signs or symptoms
but induce slow, focal accumulations of keratinocytes. Lesions may remain subclinical for long
periods or may enlarge into fulminating masses that persist for months or even years. Persistent
lesions caused by certain types of human PV (HPV) can undergo neoplastic transformation.

Etiology and Pathogenesis

(See Also Chapter 191)
PVs comprise a large family of small DNA viruses that infect humans and many other species.1
PVs are highly host-specific, meaning that those from one species do not induce papillomas in
heterologous species, so HPVs infect only humans. Rabbit, bovine, and canine PVs have been
used in animal models of viral infection because biologic experiments cannot be performed in
humans using HPVs due to their oncogenic potential.
The PV genome is present within the viral particle as a single, covalently closed circle of doublestranded DNA. Each genome is composed of approximately 8,000 nucleotide base pairs and is
approximately one-twentieth the size of a herpesvirus genome. Based on their DNA sequences,
most human and animal PVs share a similar genetic organization (Fig. 196-1) that encodes only
eight to nine related proteins.2 PV proteins are labeled as E (early) and L (late). 3 The E proteins
are necessary for viral DNA replication and are not incorporated into the infectious virus particle.
Because the E genes do not encode a DNA polymerase or thymidine kinase, PV replication is not
selectively susceptible to inhibition by nucleoside analogues. Rather, PVs use host cell enzymes
and factors to replicate their DNA genomes. The L1 and L2 genes encode the structural proteins
that form the outer protein shell or capsid of the infectious viral particle, which is called the
virion. The spherical virion measures approximately 55 nm in diameter and packages the viral
DNA (Fig. 196-2).
Figure 196-1

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All papillomaviruses genomes are composed of approximately 8,000 nucleotide base pairs,
represented as a linear sequence but actually a closed circle of double-stranded DNA. The boxes
depict the viral genes, each of which encodes a protein. The regulatory region does not encode
proteins but is a DNA segment that controls expression of viral genes and replication of the viral
genome. E6, E7, ...