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Chapter 40 : Papillomavirus

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Papillomavirus, Page 1 of 2

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Abstract:

Human papillomaviruses (HPV) are a large group of viruses (more than 200 types identified) that infect the epithelium of the skin and mucous membranes. The infections can be latent, subclinical, or clinically manifest, causing lesions that range from the benign (warts, papillomas, condylomas) to the malignant. Some of these viruses are responsible for cutaneous warts; a different group of HPVs (types 6 and 11) is responsible for most genital warts. The major importance of HPVs is because 20 types (especially HPV-16 and -18) are regarded as the necessary, if not sufficient, cause of cervical cancer as well as other cancers of the vagina, vulva, penis, anus, and oropharynx. Although most sexually active individuals get infected with genital HPVs, most of these infections are transient and innocuous. It is the persistence of the high-risk oncogenic HPVs that leads to malignant transformation. Cancer caused by these viruses is preceded by a precancerous stage whose detection is the basis of cytologic screening (Pap smear) for cervical cancer. Ten years ago HPV vaccines were introduced for the prevention of diseases associated with HPV-16 and -18 and for the prevention of anogenital warts caused by HPV-6 and -11. The introduction of HPV vaccination has been a major advance because it is the first time a vaccine has been able to directly prevent virally induced cancers. When used broadly before the onset of sexual activity, HPV vaccination has caused a dramatic reduction in the incidence of genital warts and HPV-related cervical lesions. This should be the harbinger of a decline in the rates of cervical and other cancers.

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Figures

Image of FIGURE 1
FIGURE 1

Phylogenetic tree of 99 human papillomaviruses, their genuses and species. The tree was established on the concatenated amino acids and nucleotide sequences of six open reading frames (E6, E7, E1, E2, L2, and L1) (reprinted from reference with permission).

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Image of FIGURE 2
FIGURE 2

Structure of the papillomavirus virion. A cryoelectron micrograph of the HPV-1 capsid is shown (diameter, 60 nm). (Reprinted from reference with permission.)

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Image of FIGURE 3
FIGURE 3

HPV genetic maps. (C) linearized HPV-16 DNA map; (B) linearized HPV-11 DNA map; (A) HPV-11 transcription map. By convention, the map origin of papillomaviruses is defined as the position homologous to the HpaI single restriction site of HPV-1. The open boxes correspond to the ORFs in the respective translation frames. The numbers above each ORF indicate the nucleotide position of the preceding stop codon (left solid vertical line)/start codon (dashed vertical line)/stop codon (right vertical line). Each HPV-11 mRNA is depicted with its cap site (solid circle), exons (thick line), introns (thin angled line), and poly(A) site (arrow). The putative corresponding proteins are indicated on the right of the mRNAs.

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Image of FIGURE 4
FIGURE 4

Organization of the HPV-16 URR. The URR begins after the stop codon of the L1 ORF and finishes at the cap site of the E6 mRNAs. The positions of some of the potential binding sites of various viral and cellular factors are indicated by the symbols placed on and below the line. E1BS, E1 binding site; E2BS, E2 binding site; ori, origin of replication; TATA, TATA box; GRE, glucocorticoid responsive element. AP-1, Oct-1, NF-1, NF-kB, Sp1, TEF-1, TFIID, and YY1 are cellular transcription factors.

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Image of FIGURE 5
FIGURE 5

Epithelial growth factor (EGF) receptor, phorbol ester, and HPV E5 protein interactions. (A) Upon exposure to a phorbol ester, phosphokinase C (PKC) is activated and phosphorylates the EGF receptor. This allows the binding of a complex of proteins, Grb2 and Sos, that are brought in contact with the cytoplasmic membrane. The Ras protein becomes activated by Sos after exchange of GDP for GTP. This is the trigger for the actuation of a cascade of protein kinases, Raf-1, MEK, MAPK, that ultimately induces the expression of the transcription factor AP-1, which is made up of two proto-oncoproteins, Fos and Jun. The net result is a stimulation of cell proliferation and differentiation. (B) Under physiological conditions, the EGF receptor is activated by the binding of its ligand, EGF. Autophosphorylation ensues, which precipitates the sequence of events detailed in panel A. Eventually, the process stops when the EGF receptor becomes internalized by endocytosis. As the endosome becomes acidic, the EGF receptor is degraded. The acidification of the endosome is dependent on a proton pump that includes a p16 protein subunit. Papillomavirus E5 inactivates the proton pump by binding to the p16 subunit. It is believed that the undegraded EGF receptor is then recycled to the cytoplasmic membrane. The overall effect is an increase of cellular differentiation and proliferation.

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Image of FIGURE 6
FIGURE 6

Model of the biological interactions of high-risk proteins with the cell cycle and apoptosis (see text for details). Symbols: ρ, activation; σ inhibition. Thick lines with open arrowheads (=J) indicate upregulation; the same lines with a broken end denote downregulation. Thick gray lines represent the regulations in normal cells, whereas the thick black lines show the regulations in HPV-infected cells; thin arrows (=R) show direct interactions. Note that the symbols are not drawn proportional to the protein molecular weights and that the protein complex aggregations are not necessarily concomitant or involve the direct protein-to-protein contacts shown. DP, differentiation-regulated transcription factor polypeptide; HDAC, histone deacetylase; mdm2, murine double minute 2 protein; DLG, disk large.

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Image of FIGURE 7
FIGURE 7

Model of HPV entry and DNA replication and encapsidation. (A) shows the cell surface events. Virions bind to heparin sulfate proteoglycans (HSPG) as well as to laminin-332 and growth factors. This induces the activation of growth factor receptors and integrins as well as a change in conformation of the viral capsid, which exposes the amino terminus of L2 for clipping by furin. The HPV particle is then transferred to a second receptor complex that includes tetraspanin before its cellular entry by endocytosis. (B) depicts the intracytoplasmic events with inside the endosome an acidification that leads to viral uncoating. The L2-viral DNA complex is moved through the trans-Golgi network with the help of retromer complexes. It is finally moved inside the nucleus where it accumulates at the PML nuclear bodies. (C) is a schematic rendition of the viral DNA replication and encapsidation, the latter being assisted by E2. Histones proteins (H2a, H2b, H3, and H4) are also incorporated. The virions are released with the death of the keratinocyte, terminally differentiated in a cornified shell. ( Figures 7A and 7B are slightly modified from reference , with permission.)

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Image of FIGURE 8
FIGURE 8

Drawing of the histologic features of normal skin and of a wart.

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Image of FIGURE 9
FIGURE 9

Pap smear demonstrating koilocytic atypia. In contrast to the histologic specimen, by cytology koilocytes have one or two relatively large, smooth, oval nuclei, surrounded by a very large halo of amorphous substance. (Courtesy of Clara E. Mesonero, Cape Cod Hospital, Cape Cod, MA.)

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Image of FIGURE 10
FIGURE 10

Histology of a cutaneous wart (hemalum-eosin stain; low-power view). The darkly stained layer is the stratum granulosum. Koilocytes are profuse and disrupt the stratum granulosum. The persistence of nuclei in the stratum corneum is a feature of parakeratosis. Note the thick stratum corneum. (Courtesy of Clara E. Mesonero, Cape Cod Hospital, Cape Cod, MA.)

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Image of FIGURE 11
FIGURE 11

Histology of condyloma acuminatum (hemalum-eosin stain; high-power view). The figure demonstrates many koilocytes in the stratum spinosum. Koilocytes are relatively large cells with a shrunken, irregular nucleus surrounded by a halo. (Courtesy of Clara E. Mesonero, Cape Cod Hospital, Cape Cod, MA.)

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Image of FIGURE 12
FIGURE 12

Diagrammatic representation of the nomenclature, histologic features, and distribution of associated HPV types in HPV-related cervical lesions. The dysplasia and the CIN classifications are primarily histologic classifications that are also used for cytology, whereas the Bethesda classification is designed mainly for cytology (see text for details). *This category in the Pap classification also included atypical squamous cells of the Bethesda classification.

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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Image of FIGURE 13
FIGURE 13

Immunocytochemistry of condyloma acuminatum with an antibody directed against the common papillomavirus antigen (high-power view). Several intense nuclear signals are visible. (Courtesy of Clara E. Mesonero, Cape Cod Hospital, Cape Cod, MA.)

Citation: Bonnez W. 2017. Papillomavirus, p 625-678. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch29
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