Abstract
Apoptosis, an indispensable innate immune mechanism, regulates cellular homeostasis by removing unnecessary or damaged cells. It contains three signaling pathways: the mitochondria-mediated pathway, the death receptor pathway and the endoplasmic reticulum pathway. The importance of apoptosis in host defenses is stressed by the observation that multiple viruses have evolved various strategies to inhibit apoptosis, thereby blunting the host immune responses and promoting viral propagation. Porcine Circovirus type 2 (PCV2) utilizes various strategies to induce or inhibit programmed cell death. In this article, we review the latest research progress of the apoptosis mechanisms during infection with PCV2, including several proteins of PCV2 regulate apoptosis via interacting with host proteins and multiple signaling pathways involved in PCV2-induced apoptosis, which provides scientific basis for the pathogenesis and prevention of PCV2.
Highlights
Porcine circovirus (PCV) from the genus Circovirus within the family Circoviridae is an icosahedral, small, non-enveloped DNA virus with a circular, single negative-stranded genome of approximately 1.76 kb (Tischer et al, 1982; Fauquet et al, 1995; Wei et al, 2016; Wang et al, 2018)
To cope with the apoptotic responses caused by viral infections, many viral proteins interact with apoptotic signals molecules to regulate apoptosis
There may be a discrepancy between induction and inhibition of apoptosis after Porcine Circovirus type 2 (PCV2) infection, as the experimental situation can be different, and close relationships between apoptosis and other factors that regulate cell fate, such as Ca2+, can make it more complicated and difficult
Summary
Porcine circovirus (PCV) from the genus Circovirus within the family Circoviridae is an icosahedral, small, non-enveloped DNA virus with a circular, single negative-stranded genome of approximately 1.76 kb (Tischer et al, 1982; Fauquet et al, 1995; Wei et al, 2016; Wang et al, 2018). A novel ORF5 protein has recently been discovered in PCV2-infected cells and may be involve in activation of NF-κB pathway (Lv et al, 2015a).
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