IMSc Webinar

Effect of Cholesterol on interactions, partitioning of Hepatitis A Virus peptide with cell model membranes

Samapan Sikdar

IMSc

Understanding the viral peptide detection, partitioning and subsequent host membrane composition-based response is required for gaining insights into viral mechanism. Here, we probe the crucial role of presence of membrane lipid packing defects, depending on the membrane composition, in allowing the viral peptide belonging to C-terminal Hepatitis A Virus- 2B (HAV-2B) to detect, attach and subsequently partition into the host cell membrane mimics. Using molecular dynamics simulations, we conclusively show that the hydrophobic residues in the viral peptide detect the transiently present lipid packing defects, insert themselves into such defects, form anchor points and facilitate the partitioning of the peptide, thereby inducing membrane disruption. We also show that the presence of cholesterol significantly alters such lipid packing defects, both in size and in number, thus mitigating the partitioning of the membrane active viral peptide into cholesterol-rich membranes. Our results are in much agreement with the previously published experimental data. These results show differential ways in which presence and absence of cholesterol can alter the permeability of the host membranes to the membrane active peptide component of HAV-2B virus, via lipid packing defects, and can possibly be a part of general membrane detection mechanism for the viroporins.
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Google Meet link: meet.google.com/xhu-qrsn-cwu
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