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Review
. 2019 Oct 9;11(10):922.
doi: 10.3390/v11100922.

A Current Update on Human Papillomavirus-Associated Head and Neck Cancers

Affiliations
Review

A Current Update on Human Papillomavirus-Associated Head and Neck Cancers

Ebenezer Tumban. Viruses. .

Abstract

Human papillomavirus (HPV) infection is the cause of a growing percentage of head and neck cancers (HNC); primarily, a subset of oral squamous cell carcinoma, oropharyngeal squamous cell carcinoma, and laryngeal squamous cell carcinoma. The majority of HPV-associated head and neck cancers (HPV + HNC) are caused by HPV16; additionally, co-factors such as smoking and immunosuppression contribute to the progression of HPV + HNC by interfering with tumor suppressor miRNA and impairing mediators of the immune system. This review summarizes current studies on HPV + HNC, ranging from potential modes of oral transmission of HPV (sexual, self-inoculation, vertical and horizontal transmissions), discrepancy in the distribution of HPV + HNC between anatomical sites in the head and neck region, and to studies showing that HPV vaccines have the potential to protect against oral HPV infection (especially against the HPV types included in the vaccines). The review concludes with a discussion of major challenges in the field and prospects for the future: challenges in diagnosing HPV + HNC at early stages of the disease, measures to reduce discrepancy in the prevalence of HPV + HNC cases between anatomical sites, and suggestions to assess whether fomites/breast milk can transmit HPV to the oral cavity.

Keywords: HIV and AIDS; HPV; HPV vaccines; head and neck cancer treatment; head and neck cancers; oral transmission.

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Conflict of interest statement

Ebenezer Tumban is a co-inventor of an L2-bacteriophage VLP-related patent application licensed to Agilvax Biotech. Interactions with Agilvax are managed by the University of New Mexico in accordance with its conflict of interest policies. The funding agency had no role in analyses or interpretation of data nor in the writing of the review; or the decision to publish the review paper.

Figures

Figure 1
Figure 1
A schematic of the genome of HPV16 and capsid proteins. Right image: genes that code for early proteins (E1, E2, E4, E5, E6, and E7), are shown in red and green colors; E5, E6, and E7 are oncogenes. Genes that code for late proteins (L1 and L2; capsid proteins) are shown in light blue color. URR (upstream regulatory region) contains origin of replication, enhancer elements, and early promoter (p97); URR controls viral replication. p670 is the late promoter. pAE and pAL are early polyadenylation and late polyadenylation sites, respectively. Left image: The L1 protein forms pentamers (one is circled) and each pentamer has an L2 protein at its center (not shown). Seventy-two copies of the pentamers assemble to form an icosahedral capsid.
Figure 2
Figure 2
The prevalence/contribution of human papillomavirus (HPV) types to HPV-associated head and neck cancers (HPV+ HNC) (adapted from Table 1).
Figure 3
Figure 3
Distribution of human papillomavirus-associated head and neck cancers (HPV + HNC) between anatomical sites. HPV is associated with 33.6% of OPSCC (lavender), 22.2% of OSCC (bright green), and 20.2% of LSCC (gold) worldwide.
Figure 4
Figure 4
Distribution of human papillomavirus-associated head and neck cancers (HPV + HNC) between geographical regions. Percent HPV + HNC cases in North America, Central/South America, Europe, Asia, and Africa.

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