An Investigation of Endoplasmic Reticulum-Associated Proteins Implicated in Efficient Murine Polyomavirus Infection

Undergraduate Honors Thesis

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Citeable URL: https://scholar.colorado.edu/concern/undergraduate_honors_theses/3r074v373

Abstract

Polyomaviruses are nonenveloped DNA tumor viruses that begin infection by trafficking through the endoplasmic reticulum (ER) en route to the nucleus. However, the mechanism by which the virus escapes the ER prior to nuclear entry is poorly understood. Previous research with Simian Virus 40 identified several ER-resident proteins involved in the Endoplasmic Reticulum Associated protein Degradation (ERAD) pathway as being necessary for efficient infection. In an attempt to better elucidate this potential mechanism and its possible similarity to SV40 infection, mouse A31-3T3 cells were transduced with lentiviral shRNAs targeted against the previously identified proteins and were then infected with murine polyomavirus (MuPyV). The results of these experiments suggested that several DNAJ molecular co-chaperones, two Derlin family retrotranslocons, and one ER sorting protein, BAP31, are indeed necessary for efficient MuPyV infection in mouse cells. Further studies of these proteins will provide insight into the molecular mechanisms of general polyomavirus infection and ER quality control function.

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