0000000000275650
AUTHOR
Kanoktip Puttaraksa
Parvovirus B19V Nonstructural Protein NS1 Induces Double-Stranded Deoxyribonucleic Acid Autoantibodies and End-Organ Damage in Nonautoimmune Mice
Abstract Background Viral infection is implicated in development of autoimmunity. Parvovirus B19 (B19V) nonstructural protein, NS1, a helicase, covalently modifies self double-stranded deoxyribonucleic acid (dsDNA) and induces apoptosis. This study tested whether resulting apoptotic bodies (ApoBods) containing virally modified dsDNA could induce autoimmunity in an animal model. Methods BALB/c mice were inoculated with (1) pristane-induced, (2) B19V NS1-induced, or (3) staurosporine-induced ApoBods. Serum was tested for dsDNA autoantibodies by Crithidia luciliae staining and enzyme-linked immunosorbent assay. Brain, heart, liver, and kidney pathology was examined. Deposition of self-antigens…
Pathogenic mechanisms of how human parvovirus breaks self-tolerance
It is known that viral infections can cause acute, chronic, and autoimmune diseases (ADs). However, the mechanism of how a persistent viral infection contributes to ADs remains still unclear. In this thesis, pathological and immunological aspects of how common viruses can initiate autoimmunity were investigated, and human parvovirus B19 (B19V) was employed as a model virus. B19V non-structural protein 1 (NS1), a superfamily 3 (SF3) helicase, initiated DNA damage resulting in cellular apoptosis. The apoptotic bodies (ApoBods) induced by B19V NS1 were purified and characterized. These ApoBods contained viral NS1 proteins with modified autoimmune-associated self-antigens, e.g. DNA, Smith, Apol…