Date of Submission

3-2026

Document Type

Thesis

Degree Name

Master of Science in Cellular and Molecular Biology

Department

Biology and Environmental Sciences

Advisor

Anna Kloc, Ph.D.

Committee Member

Anthony Melillo, M.S.

Committee Member

Haresha Samaranayake, Ph.D.

Keywords

Myocarditis, Parvovirus B19, NS1 protein, Synonymous Mutations, HEK293T, Cell Cycle Arrest

MeSH

Myocarditis, Parvovirus B19, Human, Viral Nonstructural Proteins, Silent Mutation, HEK293 Cells, Cellular Senescence

LCSH

Myocarditis, Parvovirus infections

Abstract

Myocarditis is a persistent cause of dilated cardiomyopathy and sudden cardiac death which is generally caused from cardiotropic viral infection followed by active inflammatory destruction of the myocardium. Parvovirus B19 is a single stranded virus with 5,596 nucleotides. It causes the Fifth disease (erythema infectiosum), and it is also commonly found in clinical human heart tissue samples. Parvovirus B19 NS1 protein plays an important role in viral replication and the host cell cycle regulation. NS1 is mainly known to induce a G1 and G2 cell cycle arrest, but the functional role of specific NS1 mutations is not fully understood. This is particularly important in a clinical setting, because specific mutations may impact the outcome of the viral infection. The objective of this study is to identify and analyze mutations in the NS1 gene in human heart sample with history of non ischemic heart condition. The NS1 gene was identified in three layers of the human heart; epicardium, myocardium and endocardium. Each layer displayed different genetic mutations that impacted the sequence of the NS1 protein. A mutated NS1 gene was introduced into a mammalian gene expression vector and transfected into HEK293 cells. The transfected HEK296 cells with the mutated NS1 gene showed phenotypic changes which could be due to G2 cell cycle arrest. These findings are important for the understanding of functional impact of NS1 mutations and underlying molecular mechanism of Parvovirus B19 pathogenesis.

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