Mechanisms of circovirus immunosuppression and pathogenesis with a focus on porcine circovirus 2: a review

• Published in: The Veterinary quarterly Vol. 43; no. 1; pp. 1 - 18
• Main Authors: Fehér, Enikő, Jakab, Ferenc, Bányai, Krisztián
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 01.12.2023; Taylor & Francis Ltd; Taylor & Francis Group
• Subjects: Adaptive immunity; Animals; Antigens; Apoptosis; Cell cycle; Circoviridae; Circoviridae Infections - veterinary; Circovirus; Cytokines; Cytokines - metabolism; Genes; Genomes; Immune response; Immune system; Immunosuppression; Immunosuppression Therapy - veterinary; Inflammation; Kinases; Lymphocytes; Mammals; Medical research; Pathogenesis; Pathogens; PCV2; Pig; porcine; Proteins; Replication; Review; Signal transduction; Swine; Swine Diseases; Transcription factors; Veterinary medicine; Virus Replication; Viruses; pathogenesis; circovirus; review; porcine; immunosuppression; PCV2; Pig
• ISSN: 0165-2176; 1875-5941; 1875-5941
• DOI: 10.1080/01652176.2023.2234430

Certain pathogens, due to their adverse effects on the immune reaction, aggravate the course of concomitant heterologous infections. Here we summarize mechanisms by which circoviruses, including the most studied porcine circovirus 2, and other mammalian and avian circoviruses, trigger their own replication and confound the hosts' immune response. At different stages of infection, from latent state to disease induction, these viruses markedly influence the cellular signaling pathways. Circoviruses have been found to interfere with interferon and proinflammatory cytokine producing and responsive pathways. Apoptotic processes, altered cellular transport and constraint of the mitotic phase all support the viral replication. The cytokine imbalance and lymphocyte depletion, thus the impaired immunity, favors invasion of super- or co-infecting agents, which in concert with circoviruses induce illnesses with increased severity. The information summarized in this review point out the diversity of host and viral factors involved in the mechanisms of disease progression during circovirus infections.