Abstract
Theextent of neuronal cell damage caused by West Nile virus (WNV) infection governs the disease severity ranging from mild, febrile illness to fatal encephalitis. Availability of naturally occurring genetic variants is helpful to study viral factors governing differential pathogenesis. During WNV infection, apoptosis serves as a virulence determinant positively contributing to viral pathogenesis. We investigated the levels of apoptosis induced by a low neurovirulent WNV lineage 5 strain 804994 and a high neurovirulent lineage 1 strain 68856 in human neuroblastoma cells, IMR-32. Our investigations clearly show the correlation between higher multiplication capacities of 68856 with higher levels of cytopathology induced by apoptosis. We observed activation of both the extrinsic and intrinsic apoptotic pathways during WNV infection. Infection with higher neurovirulent strain resulted in higher upregulation of pro-apoptotic proteins including death receptors (DR), adaptor protein, BH3-only regulatory proteins and higher cleavage of initiator caspases of both pathways. These results suggest that the virulence of a WNV strain may correlate with its higher replication fitness and ability to cause more cellular damage.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
