Echovirus 11 infection induces dramatic changes in the actin cytoskeleton of polarized Caco-2 cells

Abstract

Binding of echovirus 11 strain 207 (EV11-207) to Caco-2 monolayers results in rapid transfer of the virus to tight junctions prior to uptake. Using a confocal microscopy based-method, this study quantified the spatiotemporal distribution of actin during the time course of infection by EV11-207 in Caco-2 polarized cells. It was found that binding of EV11-207 to the apical surface resulted in rapid rearrangement of the actin cytoskeleton, concomitant with transport of the virus particles to tight junctions. By interfering with the actin network dynamics, the virus remained trapped at the cell surface, leading to abortion of infection. In addition, it was observed that at 4 h post-infection, concomitant with the detection of virus replication, actin filament was depolymerized and degraded. Finally, it was shown that the mechanisms leading to loss of actin were independent of viral genome synthesis, indicating a potential role for the viral protein synthesis seen in late infection. These data confirmed a previous study on the requirement for an intact actin cytoskeleton for EV11-207 to infect cells and reinforce the notion of actin cytoskeleton subversion by picornaviruses during infection in polarized epithelial cells

Label-free digital holo-tomographic microscopy reveals virus-induced cytopathic effects in live cells

“…The RIG of RV-A1a infected cells steadily increased at 10 to 16 h pi up to about 2.5-fold of the RIG of the uninfected controls. This coincided with the induction of apoptosis, virus-controlled necroptosis, and the loss of cytoskeletal elements, such as F-actin, as observed in picornavirus infections (21)(22)(23). Remarkably, RV-A1a-infected cells adopted a transient branched shape at 12 to 14 h pi, before rounding up at 16 h pi (Fig.…”

Transmissible gastroenteritis virus and porcine epidemic diarrhoea virus infection induces dramatic changes in the tight junctions and microfilaments of polarized IPEC-J2 cells

“…However, microfilament disorder, either stabilisation or depolymerisation, could inhibit the replication and release of viruses, and in particular the depolymerisation of microfilaments. These results were consistent with a requirement of dynamic microfilaments for other viruses, such as Echovirus 11 and herpesvirus, among others (Forest et al, 2005;Sobo et al, 2012). However, it was not clear how these stabilised or depolymerised microfilaments affected the viral production and budding.…”

Cellular proteome alterations in response to enterovirus 71 and coxsackievirus A16 infections in neuronal and intestinal cell lines

“…The rearrangement of microtubules is important for extracellular release of the poliovirus [62]. F-actin depolymerization and degradation were also induced in echovirus-infected Caco-2 cells [63].…”