Kinesin motor proteins as host factors regulating viral infection: Mechanisms of exploitation, emerging paradigms, and therapeutic horizons.

Intracellular transport via microtubules is integral to eukaryotic cell function, and viruses have developed intricate mechanisms to exploit this system at nearly every stage of their replication cycle. The mammalian kinesin superfamily, consisting of 14 distinct families, enables anterograde transport that is used by both DNA and RNA viruses. This review provides a comprehensive analysis of how a wide range of viral pathogens-including herpesviruses, human immunodeficiency virus type 1, vaccinia virus, hepatitis B virus (HBV), influenza virus, and severe acute respiratory syndrome coronavirus-interact with specific kinesin family members to promote viral entry, genome trafficking, organization of replication compartments, assembly, and egress. Recent findings underscore the role of the kinesin-4 family member KIF4A as a novel host factor for HBV. The therapeutic potential of modulating the surface expression of the HBV-entry receptor (NTCP) is discussed, either by suppressing KIF4 expression-necessary for anti-retrograde transport of NTCP to the cell surface-or by disrupting the NTCP-KIF4 interaction. Additionally, emerging pharmacological approaches targeting kinesin-dependent transport are evaluated. By establishing a unified framework that connects motor protein biology to virology, this review identifies key knowledge gaps and outlines future research directions for the development of broad-spectrum, host-targeted, antiviral therapies.