Computational exploration of viral cell membrane structures for identifying novel therapeutic target.

Abstract

The membrane proteins of viruses play a critical role, and they shield viruses and takes biochemical mechanisms like sticking to the host cell membrane, merging with them, building new viruses, and breaking free. These steps make sure the virus can infect and multiply. But the membrane proteins of Nipah, Zika, SARS-CoV-2, and Hendra virus can cause special kinds of infections. Nipah and Hendra viruses use their fusion protein to join with the host cell membrane. Their glycoprotein interacts with host receptors. The matrix protein helps to build and support the virus structure. Zika virus relies on its envelope protein to attach and fuse with host cells. Its membrane protein keeps the viral envelope stable. SARS-CoV-2 uses its spike protein to enter host cells and its envelope protein helps assemble new viruses. The membrane protein gives structural stability whereas the nucleocapsid protein interacts with the RNA genome. These viral membranes contain various kinds of lipids and proteins and they make up about 30 % of the membrane area. Yet, scientists find it hard to predict their molecular structure and different biological characters. The coarse-grained molecular dynamics simulations, enhanced sampling methods, and various structural bioinformatics investigations on viral proteins provide reliable scientific data. These investigations reveal viral membrane proteins' structural features, movement patterns, and thermodynamic properties. These computer methods are vital for drug discovery because it allows researchers to find new compounds that target viral membrane proteins to prevent their functions.