Regulation of Apoptosis by Enteroviruses

Abstract

Enterovirus infection can cause a variety of diseases and severely impair the health of humans, animals, poultry, and other organisms. To resist viral infection, host organisms clear infected cells and viruses via apoptosis. However, throughout their long-term competition with host cells, enteroviruses have evolved a series of mechanisms to regulate the balance of apoptosis in order to replicate and proliferate. In the early stage of infection, enteroviruses mainly inhibit apoptosis by regulating the PI3K/ Akt pathway and the autophagy pathway and by impairing cell sensors, thereby delaying viral replication. In the late stage of infection, enteroviruses mainly regulate apoptotic pathways and the host translation process via various viral proteins, ultimately inducing apoptosis. This paper discusses the means by which these two phenomena are balanced in enteroviruses to produce virus-favoring conditions-in a temporal sequence or through competition with each other. This information is important for further elucidation of the relevant mechanisms of acute infection by enteroviruses and other members of the picornavirus family.

Effects of Deformed Wing Virus Infection on Expressions of Immune- and Apoptosis-Related Genes in Western Honeybees (Apis mellifera)

“…Enteroviruses (EV) are positive-sense RNA viruses in the order Picornavirales [ 68 ] that have been well studied in relation to apoptosis. EV can inhibit apoptotic pathways in the early stage of infection but induce apoptosis to release viral progeny in the late stage of infection [ 69 ]. Therefore, it is reasonable to suggest that the apoptosis mechanism may be used to destroy the cell and release DWV virus particles in newly emerged adult bees and further induce immune responses within the host [ 59 ].…”

Myocardial Damage by SARS-CoV-2: Emerging Mechanisms and Therapies

“…To efficiently replicate, cardiogenic viruses such as enteroviruses inhibit apoptosis signaling at the beginning of viral infection. In later stages, the focus shifts to viral release, so enteroviruses manipulate the host cell towards apoptosis [ 113 ]. PVB19 utilizes its nonstructural protein NS1 to trigger cell-cycle arrest to induce apoptosis in endothelial cells in the late viral cycle [ 33 , 114 ].…”

Virus-Host Interactions of Enteroviruses and Parvovirus B19 in Myocarditis

“…by inhibiting apoptosis in order to efficiently replicate inside the host cells in early stage of infection. In later infection phases enteroviruses induce apoptosis to facilitate the release of the virus via cell lysis [123,124].…”

“…Agol et al observed a pro-apoptotic phase at the very early stage of infection, followed by an anti-apoptotic stage and another switch to pro-apoptotic signaling in the late stage of infection [165]. By sequentially inhibiting or activating cell signaling, viruses can regulate apoptosis at different stages of infection [123]. One way to control this is by gradually increasing cytosolic Ca 2+ levels through the expression of viroporins, which is initially pro-survival at moderate Ca 2+ levels, but promotes apoptosis at later stages with high cytosolic Ca 2+ concentrations.…”