Document Type

Poster

Publication Date

2021

Abstract

Adenovirus has made major contributions in medicine by serving as a model DNA virus to study other viruses, such as human papillomavirus (HPV). Adenoviruses are a diverse family of nonenveloped, double-stranded DNA viruses that are ubiquitous to animals and humans. There are over 67 serotypes of human adenoviruses that can cause a variety of illnesses including, gastroenteritis, conjunctivitis and respiratory infections. Adenovirus can cause these infections by invading host cells and producing an environment that is favorable for viral replication. During the early phases of infection, adenovirus expresses various viral proteins such as E4 11k, which has multiple functions. One of these functions involves controlling host cell gene expression by preventing the expression of host proteins and enabling viral protein production. Recently, it was discovered that E4 11k also disrupts processing bodies (p-bodies) by relocalizing cellular proteins. It is hypothesized that disruption of p-bodies allows E4 11k to regulate gene expression. One protein found in p-bodies, Pat1b, is a scaffolding protein that participates in p-body assembly and gene expression. Its localization during an adenovirus infection is not well understood. In this study, we will observe the localization of Pat1b and other p-body proteins with E4 11k using immunofluorescence microscopy. We hypothesize that E4 11k will induce a different localization pattern for Pat1b during an adenovirus infection. Three variations of adenovirus will be utilized. If E4 11k is responsible for relocalization of Pat1b, it will only be observed with wild type virus and a virus that only expresses E4 11k. Different localization patterns are not expected with a virus that is deleted for E4 11k. Since cellular p-bodies are not well-understood, and other viruses have been shown to disrupt p-bodies, the effect of E4 11k on p-bodies could assist us in understanding the impact of p-bodies on healthy and virally-infected cells.

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