Hong Kong Med J 2009;15(Suppl 6):S21-5
The macrophage in the pathogenesis of severe acute respiratory syndrome coronavirus infection
JSM Peiris, CY Cheung
Department of Microbiology, The University of Hong Kong
1. Severe acute respiratory syndrome (SARS) coronavirus (SCoV) initiates virus replication in macrophages with the production of negative sense viral ribonucleic acid and viral protein, but such viral replication is abortive and no infectious virus is produced.
2. In contrast to influenza A virus, infection with SCoV fails to induce type-1 interferons (eg IFN-_), which are key mediators of innate immune defence, but does lead to a strong induction of proinflammatory chemokines (eg IP10).
3. Sub-neutralising antibody to SCoV does not lead to the mediation of antibody-dependent enhancement of SCoV viral replication in macrophages.
4. Microarray analysis of SCoV infected cells identifies novel pathways including cytokines and chemokines and apoptotic pathways that are differentially activated by SCoV, which may be important in the pathogenesis of SARS, and deserve further studies.
2. In contrast to influenza A virus, infection with SCoV fails to induce type-1 interferons (eg IFN-_), which are key mediators of innate immune defence, but does lead to a strong induction of proinflammatory chemokines (eg IP10).
3. Sub-neutralising antibody to SCoV does not lead to the mediation of antibody-dependent enhancement of SCoV viral replication in macrophages.
4. Microarray analysis of SCoV infected cells identifies novel pathways including cytokines and chemokines and apoptotic pathways that are differentially activated by SCoV, which may be important in the pathogenesis of SARS, and deserve further studies.