National Institute of Virology Pune, National AIDS Research Institute, Pune, India.
Abstracts of the papers presented at the International Conference of Indian Virological Society on “Emerging and Re-emerging viral Diseases of the Tropics and Subtropics” at Indian Agricultural Research Institute, New Delhi, India, December 11–14, 2007.
Critical understanding of the ways in which viruses modulate and manipulate the host immune defense system and the host response towards the virus remains pivotal in predicting the outcome of infection. A mouse model was used to understand the kinetics of viral spread, cytokine secretion and the role of cell mediated immune response in protection against a non-neuroinvasive West Nile virus (WNV) E101 strain and the neuroinvasive Indian strain, WNV 68856. Lethal infection by both the neuroinvasive strain (i.p) and non-neuroinvasive strain (i.p virus + i.c starch) showed no distinct differences in growth kinetics patterns in the brain as determined by RT PCR. ex-pression of pro- and antiinflammatory cytokines IL-2, IL-6, TNF-fN, IFN-fx and IL-10 followed a pattern similar to the kinetics of virus multiplication in the brain. Induction of Cell Mediated Immunity in the periphery was analyzed by determining the CD8+: CD4+ cell ratio in the spleen after infection. WNV E101 showed an increase in CD8+ T cell proliferation while the ratio remained unchanged in response to WNV 68856 infection. Adoptive transfer of CD4+ and CD8+ subsets of immune T cells also reinforced the role of CD8+ T cells in protection against a lethal challenge of WNV E101 indicating that cellular immunity on its own can protect mice from lethal challenge against a non-neuroinvasive strain of WNV. This protective effect of cellular immunity was however, ineffective in protection against neuroinvasive WNV 68856.
