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.
Highlights
Human papillomaviruses (HPV) are the main causative agents of cervical cancer and represent the most common sexually transmitted infection worldwide [1,2]
While most studies using cell lines show an inhibition of the nuclear factor-κB (NF-κB) pathway, in cervical intraepithelial neoplasia (CIN) and cervical cancer, HPV seems to induce the expression of inflammatory cytokines, which correlates with cancer progression [124,125]
Several reports have demonstrated that different HPV efficiently evade the cellular antiviral signalling pathways using diverse strategies throughout their life cycle
Summary
Human papillomaviruses (HPV) are the main causative agents of cervical cancer and represent the most common sexually transmitted infection worldwide [1,2]. Cellular PRRs can detect either viral RNA or DNA, and they can be either associated with membranes or localize freely in the cytosol [7,8] These different classes of PRRs use common pathways to convey their signals, culminating in the expression of pro-inflammatory cytokines, such as type I interferons (IFNs), and IFN-stimulated genes (ISGs), restricting infection establishment and spreading [9]. This is accomplished by triggering the activation of downstream. We review and clarify these different evasion mechanisms and discuss their correlation with cancer progression during infection
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