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Lymphopenia and increasing viral load in the first 10 days of severe acute respiratory syndrome (SARS) suggested immune evasion by SARS-coronavirus (CoV). In this study, we focused on dendritic cells (DCs) which play important roles in linking the innate and adaptive immunity. SARS-CoV was shown to infect both immature and mature human monocyte-derived DCs by electron microscopy and immunofluorescence. The detection of negative strands of SARS-CoV RNA in DCs suggested viral replication. However, no increase in viral RNA was observed. Using cytopathic assays, no increase in virus titer was detected in infected DCs and cell-culture supernatant, confirming that virus replication was incomplete. No induction of apoptosis or maturation was detected in SARS-CoV-infected DCs. The SARS-CoV-infected DCs showed low expression of antiviral cytokines (interferon alpha IFN-alpha, IFN-beta, IFN-gamma, and interleukin 12p40 IL-12p40), moderate up-regulation of proinflammatory cytokines (tumor necrosis factor alpha TNF-alpha and IL-6) but significant up-regulation of inflammatory chemokines (macrophage inflammatory protein 1alpha MIP-1alpha, regulated on activation normal T cell expressed and secreted RANTES), interferon-inducible protein of 10 kDa IP-10, and monocyte chemoattractant protein 1 MCP-1). The lack of antiviral cytokine response against a background of intense chemokine up-regulation could represent a mechanism of immune evasion by SARS-CoV.
Law et al. (2005) studied this question.