S ARS coronavirus (SARS-CoV), the causative agent of severe acute respiratory syndrome, is a versatile pathogen armed with a host of factors countering the antiviral type I interferon (IFN) system. Hence, tissue cells infected with SARS-CoV are unable to launch an IFN response. Plasmacytoid dendritic cells, however, produce high levels of IFN after infection. We recently demonstrated that minute amounts of IFN applied before infection (IFN priming) can ameliorate the IFN response of tissue

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... to SARS-CoV. IFN priming of SARS-CoVinfected cells activated genes for IFN transcription, IFN signaling, antiviral effector proteins, ubiquitinylation and ISGylation, antigen presentation, and other cytokines and chemokines, whereas IFN treatment or infection alone had no major effect. Thus, the IFN which is produced by plasmacytoid dendritic cells could enable tissue cells to at least partially overturn the SARS-CoV-induced block in innate immune activation. In 2002, the first epidemic of the new millenium was provoked by an emerging virus which caused severe acute respiratory syndrome (SARS). The outbreak quickly spread in 28 countries around the globe and resulted in 8,000 infected people of which approximately 10% had a fatal course. 1 The causative agent was found to be a coronavirus subsequently named SARS-CoV. [2] [3] [4] [5] There is evidence that bats are the reservoir host of this virus, since sequences of closely related viruses were found in these animals. 6-8 Most probably, SARS-CoV initially spilled over from bats to humans via an intermediate host like palm civets.