Golgi-Dependent Cgas/Sting Responses To Human Papillomavirus And Rhinovirus Infection

Abstract

At the onset of infection, papillomaviruses (HPV) evade detection from our immune system by waiting for the host cell to enter mitosis so that the Golgi structure is vesiculated and unable to tether transmembrane protein STING, a necessary event in order to initiate interferon responses downstream that would otherwise fight viral infection. The Golgi-dependence of functional STING/interferon signaling prompted us to investigate if other viruses actively disable this innate immune pathway by perturbation of the Golgi structure. Human rhinovirus (HRV), the most common viral infectious agent in humans and a member of the family of viruses that are the predominant cause of the common cold, have been shown to trigger Golgi vesiculation. In this study, we have investigated the activation or evasion of STING-dependent interferon regulatory factor (IRF3) by HPV, HRV, and poxviruses. Based on our findings with HPV, we predict that vesiculation of Golgi structure during active HRV infection may contribute to antagonism of cellular STING/IFN responses. Understanding the mechanisms of immunoevasion and immunoantagonism by HPV and HRV may help identify potential targets for therapeutic interventions against the diseases these pathogens cause.