Abstract
Simple SummaryA subset of carcinomas that arise in the head and neck region show a viral etiology. In fact, a subgroup of oropharyngeal cancers are caused by some types of human papillomavirus (HPV), so-called high-risk (HR)-HPVs, whereas undifferentiated nasopharyngeal carcinomas are etiologically related to Epstein–Barr virus (EBV). However, studies have reported the presence of both HR-HPV and EBV in some types of head and neck cancers. In this review, we discuss the potential contribution and role of HR-HPV/EBV coinfection in head and neck carcinogenesis, as well as the mechanisms that are potentially involved. In addition, HR-HPV/EBV interaction models are proposed.High-risk human papillomaviruses (HR-HPVs) and Epstein–Barr virus (EBV) are recognized oncogenic viruses involved in the development of a subset of head and neck cancers (HNCs). HR-HPVs are etiologically associated with a subset of oropharyngeal carcinomas (OPCs), whereas EBV is a recognized etiological agent of undifferentiated nasopharyngeal carcinomas (NPCs). In this review, we address epidemiological and mechanistic evidence regarding a potential cooperation between HR-HPV and EBV for HNC development. Considering that: (1) both HR-HPV and EBV infections require cofactors for carcinogenesis; and (2) both oropharyngeal and oral epithelium can be directly exposed to carcinogens, such as alcohol or tobacco smoke, we hypothesize possible interaction mechanisms. The epidemiological and experimental evidence suggests that HR-HPV/EBV cooperation for developing a subset of HNCs is plausible and warrants further investigation.
Highlights
Head and neck cancers (HNCs) encompass tumors of a variety of subsites, including the lips, oral cavity, nasopharynx, oropharynx, hypopharynx, larynx, and salivary glands
Some studies have reported the simultaneous presence of High-risk human papillomaviruses (HR-human papillomavirus (HPV)) and Epstein–Barr virus (EBV) in HNCs [6,7,8], proposing that HR-HPV/EBV coinfection could play a fundamental role in the development of these malignancies [6,9,10]
In the meta-analysis conducted by Tham et al (2020), an increased frequency of HPV/EBV copresence was found in World Health Organization (WHO) type I nasopharyngeal carcinomas (NPCs) when compared with WHO type II/III tumors (7.6% vs. 1.0%) [77]
Summary
Head and neck cancers (HNCs) encompass tumors of a variety of subsites, including the lips, oral cavity, nasopharynx, oropharynx, hypopharynx, larynx, and salivary glands. Head and neck squamous cell carcinomas (HNSCCs) constitute more than 90% of all HNCs [1]. These malignancies were the sixth leading cancer worldwide, with 931,931 new cases in 2020, excluding non-melanoma skin neoplasms. Some studies have reported the simultaneous presence of HR-HPV and EBV in HNCs [6,7,8], proposing that HR-HPV/EBV coinfection could play a fundamental role in the development of these malignancies [6,9,10]. We propose a mechanism by which HR-HPVmediated alterations facilitate EBV infection in epithelial tissues
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