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11th World Congress on Virology and Infectious Diseases

Tokyo, Japan

Muhammad Awais

Muhammad Awais

University of Veterinary and Animal ,Pakistan

Title: The influence of TLR7 deficiency on central nervous system pathology and TLR8 expression in JEV infection


Biography: Muhammad Awais


Japanese encephalitis virus (JEV) is an emerging highly fatal pathogen which could induce zoonose. JEV is generally transmitted by infection carrying mosquitoes, inducing Japanese encephalitis (JE). It’s the first critical step in the initiation of innate antiviral responses to effectively recognize JEV. Toll Like Receptor 7 (TLR7) and Toll Like Receptor 8 (TLR8) are the members of the family of Toll-like receptor, which can recognize single-stranded RNA (ssRNA) and activate immune cells that can produce downstream cytokines for immune clearance. As a single - stranded positive sense RNA virus, the relation between JEV infection and TLR7/8 remain unclear. In previous study, it was found that the expression of TLR7 in the brains of C57BL/6 mice observably increased after JEV-infection. However, we found that the survival ship of TLR7 deficient mice was not significantly changed as compared to C57BL/6 mice after JEV infection. And the expression of TLR8 observably increased in the brains. Thus, further study was done on TLR7 deficient mice to explore whether the expression of TLR8 played a role in the TLR7 deficient mice during innate antiviral responses after JEV-infection and detect the expression of TLR8 in CNS. Brain tissues were embedded as paraffin sections after that the mice were infected with vaccine strain SA14 -14 -2 or virulent strain P3. The pathological changes were observed in the brain of JEV-infected brain tissue with hematoxylin eosin staining (HE staining), and viral load and expression of TLR8 in the barin of JEV-infected TLR7 deficient mice were detected by Immunofluorescence. The results demonstrated that there was plentiful co-localization of TLR8 and JEV E-protein in the brains of JEV-infected TLR7 deficient mice without disease symptoms, but there was little co-localization in the brains of JEV-uninfected TLR7 deficient mice. Since the TLR8 is highly homologous to TLR7, it’s possible that TLR8 plays a role as compensative function to recognize ssRNA of JEV and activate downstream signal pathway to produce a series of inflammatory and type I interferon for immune clearance in the absence of TLR7.