Abstract
Many diverse viruses target a polarized epithelial monolayer during host invasion. The polarized epithelium is adept at restricting the movement of solutes, ions, macromolecules, and pathogens across the mucosa. This regulation can be attributed to the presence of a junctional complex between adjacent cells and to an intricate network of actin filaments that provides support to the subapical membrane and stabilizes intercellular junctions. It is therefore not surprising that many viruses have evolved highly varied strategies to dissolve or modulate the cortical actin meshwork to promote infection of polarized cells. In this review, we will discuss the cell biological properties of the actin cytoskeleton in polarized epithelial cells and review the known mechanisms utilized by viral pathogens to manipulate this system in order to facilitate their infection.
Highlights
IntroductionSeveral families of viruses target a polarized epithelial monolayer during their life cycles
Several families of viruses target a polarized epithelial monolayer during their life cycles. Airway pathogens such as rhinovirus, respiratory syncytial virus, and influenza virus invade via the polarized epithelia lining the airways, and enteric viruses such as enteroviruses and rotavirus require infection of the intestinal epithelial cells (IECs) lining the gastrointestinal (GI) tract
Microvilli localize to the apical surface and are anchored by interactions with actin-binding proteins ezrin, radixin, and moesin (ERM). (B) The highlighted area of the apical domain demonstrates the close interactions between actin and junctional complex proteins [zonula occludens (ZO)-1, ZO-2, ZO-3, Afadin, multi-PDZ domain protein 1 (MUPP1), MAGI, α- and β-catenin]
Summary
Several families of viruses target a polarized epithelial monolayer during their life cycles. The polarized epithelium of both the respiratory and gastrointestinal systems is adept at Viruses 2011, 3 restricting the movement of solutes, ions, macromolecules, and pathogens across the mucosa This regulation can be attributed to the junctional complex between adjacent cells [composed of the tight junction (TJ), adherens junction (AJ), and desmosomes (Figure 1)] and to an intricate association of actin filaments that provides support to the subapical membrane and junctional complex. Cortical actin filaments directly below the apical cell membrane form a multifaceted network that provides a physical barrier to the penetration of viruses and endocytic vesicles. This network must be modulated for a virus to gain entry from the apical surface into the cell cytoplasm, and to assist traffic from the cell periphery to deep within the cell. Microvilli localize to the apical surface and are anchored by interactions with actin-binding proteins ezrin, radixin, and moesin (ERM). (B) The highlighted area of the apical domain demonstrates the close interactions between actin and junctional complex proteins [ZO-1, ZO-2, ZO-3, Afadin, multi-PDZ domain protein 1 (MUPP1), MAGI, α- and β-catenin]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
