PublisherThe University of Arizona.
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AbstractThe link between autoimmune diseases and viral infections has long been under scrutiny, with potential mechanisms including viral persistence and viral transactivation of cellular cytokine promoters coupling the two phenomenon. In this study, the relationship between autoimmune disease and the persistence of non-structural NS1 human parvovirusB19 (B19V) protein in serum from patients with SLE and RA was investigated. The hypothesis was that due to a failure in the viral host’s ability to silence persistent viral protein transcripts, non-structural NS1 protein remains elevated in individuals with autoimmune disease (post-infection) and contributes to exacerbation of the disease. To test this hypothesis, anti-PARVO non-structural NS1 antibodies were detected in the serum of 15 SLE subjects. B-cell hybridomas from a patient with SLE secreting elevated levels of anti-PARVO non-structural NS1 IgG were generated, which secreted stable human IgG mAbs specific to non-structural NS1. Six mAb hybridoma sub-clones were isolated with low binding titers to the full length (FLNS1). The sub-clones, however, demonstrated increased binding activity to the nuclease domain of NS1. Optimization of the mAb screening system will be performed for future research, which will facilitate the purification and characterization of the human anti-PARVO non-structural NS1 mAbs.
Degree ProgramHonors College
Biochemistry & Molecular Biophysics