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Shewale, D. J.

Publications and source records attributed to Shewale, D. J..

2 recordsLinked to original sources

Single Chain Fragment Variable (scFv) corresponding to a novel epitope within HCV envelope protein restricts virus entry into hepatocytes

Hepatitis C virus (HCV) is a leading cause of chronic viral hepatitis. The use of neutralizing antibodies could be a more effective therapeutic option. Previously we reported the discovery of a novel epitope at the C terminus of HCV-E2 protein, that induced potent neutralizing antibodies in the infected patients. Furthermore, monoclonal antibodies generated against this epitope could also significantly reduce virus replication in a cell culture system. In this study, we have focused on the generation of single chain variable fragments of this unique neutralizing monoclonal antibody A8A11 raised against the conserved epitope. The nucleotide sequence of the neutralizing monoclonal antibody A8A11 was determined and the scFv gene was constructed followed by cloning into the expression plasmid for recombinant protein expression. The scFv mimicked the antibody in binding to the hepatitis C virus like particles (HCV-LP). As expected, the scFv inhibited HCV-LP binding to hepatocytes and could effectively reduce viral replication in the cell culture system. More importantly, scFv A8A11 could restrict serum HCV RNA levels in HCV-infected chimeric mice harboring human hepatocytes. Results provide a basis for developing a promising scFv-based entry inhibitor, which could be more effective against viruses refractory to drugs targeting viral enzymes.

microbiology↗

KIF1A neurodegenerative disease mutations modulate motor motility and force generation

KIF1A is involved in fast axonal transport of synaptic vesicle precursor, neurofilament, and dense-core vesicle, essential for neuronal development and maintenance. Several point mutations in the KIF1A motor domain have been identified in patients with various motor neuron diseases. Recent studies have shown that these mutations affected the motor and cargo localization in cultured hippocampal and C.elegans neurons. However, a detailed analysis of these mutations on KIF1A motility, force generation, and cargo transport is largely unexplored. Here, we have analyzed the effect of 16 point mutations and showed that these mutations significantly decreased the motor velocity and landing rates compared to wild-type motors. Except for A255V, mutations V144F, V220I, and E233D mildly affected motor mechanical outputs. S58L, A202P, R216P, R216H, L249Q, T312M, and R316W mutants exhibited drastic impairments in the motility properties, force generation, and cargo transport. Notably, T46M, T99M, G102D, S215R, and E253K mutants showed strong microtubule binding, resulting in complete disruption of cargo transport. Our study provides the first comprehensive demonstration of KIF1A disease mutations at the molecular level. The observed changes in motility properties and cargo transport align with the severity of disease phenotype observed in KIF1A-associated neurological disorders)

biophysics↗