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A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
Prediction of the post-translational modification sites on dengue virus E protein and deciphering their role in
M Ruhul Amin1, A H M Mahbub, Abdur R Sikder
1Department of Microbiology, University of Dhaka, Dhaka 1000, Bangladesh. ruhulmb@gmail.com
Abstract:
Dengue virus, a member of the flavivirus family, is a mosquito-borne viral pathogen for which any specific treatment or control of infection by vaccination is yet to be conclusive. The envelope glycoprotein, E, mediates viral entry by membrane fusion. Elucidation of post-translational modification sites in E protein followed by sequence alignment produced stretches of residues which are conserved in most of the members of flaviviruses. Presence of protein kinase A (PKA) and protein kinase G (PKG) phosphorylation sites predicts that E protein may activate PKA and PKG through phosphorylation which is responsible for inhibition of platelet activation, and thereby causing thrombocytopenia. Here, we attempt to decipher the novel role of Dengue virus E protein in pathogenesis.
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