Getting on the right track: Interactions between viruses and the cytoskeletal motor proteins

Abstract

The cytoskeleton is an essential component of the cell and it is involved in multiple physiological functions, including intracellular organization and transport. It is composed of three main families of proteinaceous filaments; microtubules, actin filaments and intermediate filaments and their accessory proteins. Motor proteins, which comprise the dynein, kinesin and myosin superfamilies, are a remarkable group of accessory proteins that mainly mediate the intracellular transport of cargoes along with the cytoskeleton.Like other cellular structures and pathways, viruses can exploit the cytoskeleton to promote different steps of their life cycle through associations with motor proteins. The complexity of the cytoskeleton and the differences among viruses, however, has led to a wide diversity of interactions, which in most cases remain poorly understood. Unveiling the details of these interactions is necessary not only for a better comprehension of specific infections, but may also reveal new potential drug targets to fight dreadful diseases such as rabies disease and acquired immunodeficiency syndrome (AIDS). In this review, we describe a few examples of the mechanisms that some human viruses, that is, rabies virus, adenovirus, herpes simplex virus, human immunodeficiency virus, influenza A virus and papillomavirus, have developed to hijack dyneins, kinesins and myosins.

The Transient Receptor Potential Vanilloid 2 (TRPV2) Channel Facilitates Virus Infection Through the Ca2+‐LRMDA Axis in Myeloid Cells

“…[ 7 ] The small GTPase RhoA functions downstream of IAV‐induced Ca 2+ oscillations to trigger the internalization of cell membrane for IAV endocytosis. [ 7 ] Recent studies have demonstrated that the entry of IAV substantially induces the cytoskeletal remodeling and the formation of filopodia, [ 8 ] indicating that the immediate Ca 2+ influx triggered by viral infection induces cytoskeleton‐dependent cell membrane dynamics for the entry of viruses. Accordingly, the entry of IAV is substantially hampered by Ca 2+ channel blockers (CCBs) or by knockdown of Ca v 1.2 in various cell lines, [ 9 ] indicating that blocking Ca 2+ influx by targeting Ca 2+ channels would provide plausible therapeutic strategies for virus‐related diseases.…”

A TRAFFIC themed series ‐ Host membrane trafficking subversion by pathogens

“…Fulvio Reggiori and colleagues review the literature highlighting the ability of some human viruses (including rabies virus, adenovirus, herpes simplex virus, human immunodeficiency virus, influenza A virus and papillomavirus) to exploit dynein and kinesin‐driven centripetal and centrifugal movements along microtubules to promote cell invasion and replication or virus assembly and egression from the host cells, respectively. This ability is mainly due to the property of some viral components to directly bind the molecular motors, but also, in selected cases, to trigger signalling cascades that boost the motor activity 5 …”