The initial event in viral infection is binding of the virus particle (virion) to specific receptors on the surface of the host cell. Bound virus is internalized and disassembled, exposing the genome to either the cytoplasm or the nucleus, depending on the type of virus. Once inside the cell, a combination of host and viral factors mediate transcription/reverse transcription, translation, and replication of the virus. During replication, new geometrically shaped, highly ordered protein capsid shells that compact and protect viral nucleic acid are formed. New virus particles are released from the cell (after membrane envelopment for specific viruses) that can initiate new rounds of infection.

    Capsid assembly has been a "black box" in the viral life cycle, with little mechanistic detail known. Virology has been dominated by the notion that capsids form spontaneously through 'self-assembly' of capsid proteins. In contrast, recent evidence suggests that capsid assembly is a complex, multi-step process catalyzed by host proteins acting as enzymes of assembly. We are developing novel anti-viral therapeutics targeting this capsid assembly process.


    1.Host–rabies virus protein–protein interactionsas druggable antiviral targets

    2.From COVID-19 to the Common Cold: Novel Host-Targeted, Pan-Respiratory Antiviral Small Molecule Therapeutics

    3.MksB, an alternate condensin from Mycobacterium smegmatis is involved in DNA binding and condensation

    4.Discovery of a Novel Class of Small Molecule with Potent In Vitro Activity Against MRSA and MDR S. aureus