Actin in herpesvirus infection

Abstract

Actin is important for a variety of cellular processes, including uptake of extracellular material and intracellular transport. Several emerging lines of evidence indicate that herpesviruses exploit actin and actin-associated myosin motors for viral entry, intranuclear transport of capsids, and virion egress. The goal of this review is to explore these processes and to highlight potential future directions for this area of research.

Keywords: Rho GTPase; actin; herpes; myosin.

Figure 1.

Examples of Actin Networks. Filopodium, stress fiber, and lamellipodium structures are featured showing actin polarities.

Figure 2.

Model of herpesvirus entry, maturation and egress. (A) Herpes virion “surfing” towards the plasma membrane along membrane protrusions for entry. (B) Capsid trafficking toward the nuclear periphery for budding via a myosin motor on F-actin. (C) U_S3-mediated depolymerization of actin stess fibers. (D) U_S3-mediated generation of membrane projection and cell-to-cell spread of herpesvirus. (E) Myosin IIA- and Rab6-dependent fission of nascent vesicles from the Golgi body. (F) Enveloped virion within a TGN-derived vesicle trafficking through cortical actin via myosin Va toward the plasma membrane for secretion.