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

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VETERINARY QUARTERLY
卷 43, 期 1, 页码 1-18

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TAYLOR & FRANCIS LTD
DOI: 10.1080/01652176.2023.2234430

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Pig; porcine; circovirus; PCV2; immunosuppression; pathogenesis; review

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In this review, the mechanisms by which circoviruses trigger their own replication and confound the hosts' immune response are summarized. These viruses significantly influence cellular signaling pathways during different stages of infection, interfering with interferon and proinflammatory cytokine producing and responsive pathways, as well as apoptotic processes, altered cellular transport, and constraint of the mitotic phase, all supporting viral replication. The cytokine imbalance and lymphocyte depletion favor invasion of super- or co-infecting agents, resulting in illnesses with increased severity. The information summarized in this review highlights the diversity of host and viral factors involved in the mechanisms of disease progression during circovirus infections.
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.

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