Cervical cancer is the fourth most frequent cancer in women with an estimated 570,000 new cases globally in 2018. Treatment of advanced cervical cancer is often unsuccessful leading to high cancer-related mortality rates, especially in under-resourced countries. Recently, a possible role for the cell surface glycoprotein CD24 in host cell specificity of Zika virus was reported. As an extension of this work, Zika viruses have been proposed as oncolytic therapy for the treatment of neuroblastoma and other CD24 positive tumors. To determine the permissiveness of cervical cancer cells to Zika virus infection and its association with CD24, we assessed cytopathic effect (CPE) induced by Zika virus in cervical cancer cell lines (HeLa, SiHa and CaSki) by light microscopy and by cytotoxicity assay. Cervical cancer cells were susceptible to Zika virus-induced apoptosis. Upon infection, the morphology of cervical cancer cells changed, exhibiting Zika virus-induced CPE. Cervical cancer cell expression of viral non-structural protein 1 (NS1) after infection demonstrated viral protein translation. Quantitative plaque assays demonstrated the production of competent virions. Because CD24 expression was found to be important for Zika virus infection in neuroblastoma cells, CD24 expression was assessed in cervical cancer cells. Cervical cancer cells expressed low but measurable levels of CD24 mRNA and protein. siRNA-mediated knockdown of CD24 resulted in reduced NS1 expression and reduced levels of virus-induced apoptosis. Taken together our data suggest a possible role for CD24 in Zika virus-induced apoptosis in cervical cancer cells. Zika virus-induced apoptosis of cultured cervical cancer cells presents the possibility for the use of Zika virus as a potential oncolytic therapy for cervical cancer.
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Master of Science (M.S.)
College of Medicine
Length of Campus-only Access
Masters Thesis (Campus-only Access)
Krishnapura, Harini, "Zika Virus-induced Lysis of Cervical Cancer Cells" (2019). Electronic Theses and Dissertations. 6383.