Molecular Mechanisms Between Canine Parvovirus 2 and Host Interactions: From Viruses to Innate Immune Signaling Pathways
TL;DR
This review summarizes the innate immunity evasion tactics employed by CPV-2, focusing on the interactions of various viral proteins and host signaling pathways, and identifies the key mechanisms underlying the defective TLR activation.
Abstract
Canine parvovirus 2 (CPV-2) is a major pathogen causing acute haemorrhagic enteritis and myocarditis in dogs. Since the discovery in the late 1970s, the original CPV-2 strain has evolved through VP2 mutations into new subtypes CPV-2a, 2b, and 2c. The viruses pose a persistent threat to canine health worldwide. This review summarizes the innate immunity evasion tactics employed by CPV-2, focusing on the interactions of various viral proteins and host signaling pathways. CPV-2 regulates the activation and inhibition of Toll-like receptors (TLRs), thereby influencing the downstream MyD88/TRIF signaling pathway and modulating the activation of NF-κB and interferons. CPV-2 exerts bidirectional regulation of apoptosis, thereby modulating host innate immune responses and promoting viral replication. CPV-2 employs multiple strategies to evade the humoral and adaptive immune systems, including evolutionary escape through rapid replication and the accumulation of mutations. Clarifying the key mechanisms underlying the defective TLR activation, the immunomodulatory functions of CPV proteins, and cross-species transmission of CPV-2 among animals and the potential zoonotic risk to humans can provide a crucial theoretical basis for precise virus control, understanding immune evasion, and assessing zoonotic risks, with significant value for both vaccine development and basic research.