The Interplay between Antiviral Signalling and Carcinogenesis in Human Papillomavirus Infections

Abstract

Human papillomaviruses (HPV) are the causative agents of the most common sexually transmitted infection worldwide. While infection is generally asymptomatic and can be cleared by the host immune system, when persistence occurs, HPV can become a risk factor for malignant transformation. Progression to cancer is actually an unintended consequence of the complex HPV life cycle. Different antiviral defence mechanisms recognize HPV early in infection, leading to the activation of the innate immune response. However, the virus has evolved several specific strategies to efficiently evade the antiviral immune signalling. Here, we review and discuss the interplay between HPV and the host cell innate immunity. We further highlight the evasion strategies developed by different HPV to escape this cellular response and focus on the correlation with HPV-induced persistence and tumorigenesis.

High-Risk Human Papillomaviruses and Epstein–Barr Virus in Colorectal Cancer and Their Association with Clinicopathological Status

“…The combined oncogenic effects of viral infections have been recognized as potential oncogenic drivers in various cancers [ 6 ]. Oncoviruses can lead to the onset and progression of cancer via commonly shared pathways including WNT/β-catenin, JAK/STAT/SRC, PI3k/Akt/mTOR, and/or RAS/MEK/ERK signaling pathways [ 6 , 8 , 14 , 41 ]. A study conducted by Guidry and Scott [ 63 ] showed that co-infection by HPV and EBV enhances EBV persistence either via latency or increased viral replication or by aggregating HPV oncogene expression.…”

“…HPV is a small epitheliotropic, non-enveloped, double-stranded DNA virus that can be sexually transmitted. It infects the epidermal or mucosal epithelial cells, where HPVs can induce neoplastic transformation (both benign and malignant) [ 7 , 8 ]. The multiplication of the virus occurs in cell nuclei and is firmly linked to cell differentiation [ 9 ].…”

High-risk human papillomaviruses and Epstein–Barr virus in breast cancer in Lebanese women and their association with tumor grade: a molecular and tissue microarray study

“…Human papillomavirus (HPV), a non-enveloped double-stranded DNA virus is transmitted sexually [ 6 , 7 ]. The HPV genome consists of eight open reading frames (ORFs) and is separated into three functional elements; the early (E) region which encodes six proteins (E1, E2, E4–E7) and is involved in regulating viral transcription and replication, the late region that encodes the structural proteins (L1 and L2) and is involved in viral assembly, and, the long control region [ 8 ].…”

Vesicular trafficking permits evasion of cGAS/STING surveillance during initial human papillomavirus infection

“…Indeed, IFN responses are detrimental to persistent HPV infections, reducing cellular proliferation and causing apoptosis, episome loss, mutation, and/or integration [73][74][75][76][77]. Likewise, it is well known that some HPV early genes-E5, E6, and E7 -counteract these detrimental antiviral IFN and IFN-stimulated gene (ISG) responses through a variety of mechanisms [78][79][80][81].…”