Infection of cultured intestinal epithelial cells with severe acute respiratory syndrome coronavirus

Cinatl, Jindrich; Hoever, Gerold; Morgenstern, Birgit; Preiser, Wolfgang; Vogel, Jens‐Uwe; Hofmann, W.-K.; Bauer, Gabriele; Michaelis, Martin; Rabenau, Holger F.; Doerr, Hans Wilhelm

doi:10.1007/s00018-004-4222-9

Cited by 79 publications

(100 citation statements)

References 41 publications

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“…However, SARS-CoV infection does not result in IFN production in many cell cultures and pretreatment of cells with IFN blocks SARS-CoV infection [13,[24][25][26]. The N protein of SARS-CoV was found to inhibit the activation of IRF-3 and NF-jB induced by SenV, resulting in inhibition of IFN synthesis [8].…”

Section: Discussionmentioning

confidence: 97%

SARS-CoV nucleocapsid protein antagonizes IFN-β response by targeting initial step of IFN-β induction pathway, and its C-terminal region is critical for the antagonism

et al. 2010

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Severe acute respiratory syndrome coronavirus (SARS-CoV) encodes a highly basic nucleocapsid (N) protein which can inhibit the synthesis of type I interferon (IFN), but the molecular mechanism of this antagonism remains to be identified. In this study, we demonstrated that the N protein of SARS-CoV could inhibit IFN-beta (IFN-β) induced by poly(I:C) or Sendai virus. However, we found that N protein could not inhibit IFN-β production induced by overexpression of downstream signaling molecules of two important IFN-β induction pathways, toll-like receptor 3 (TLR3)- and RIG-I-like receptors (RLR)-dependent pathways. These results indicate that SARS-CoV N protein targets the initial step, probably the cellular PRRs (pattern recognition receptors)-RNAs-recognition step in the innate immune pathways, to suppress IFN expression responses. In addition, co-immunoprecipitation assays revealed that N protein did not interact with RIG-I or MDA5. Further, an assay using truncated mutants revealed that the C-terminal domain of N protein was critical for its antagonism of IFN induction, and the N deletion mutant impaired for RNA-binding almost completely lost the IFN-β antagonist activity. These results contribute to our further understanding of the pathogenesis of SARS-CoV.

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Section: Discussionmentioning

confidence: 97%

SARS-CoV nucleocapsid protein antagonizes IFN-β response by targeting initial step of IFN-β induction pathway, and its C-terminal region is critical for the antagonism

et al. 2010

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“…It could therefore be expected that coronaviruses also suppress production of these chemokines (which are also termed CCL5 and CXCL10, respectively). Recent data indicate that RANTES transcripts are indeed absent in tissue cells productively infected with SARS-CoV [107,127] or MHV [103]. IP-10 transcription, however, is upregulated in some SARS-CoV-infected fibroblast cell lines [107,127] and in macrophages [105].…”

Section: Cytokines and Chemokines Induced By Sars-cov And Mhvmentioning

confidence: 99%

Interferon and cytokine responses to SARS-coronavirus infection

Thiel

Weber

2008

Cytokine & Growth Factor Reviews

144

147

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The sudden emergence of severe acute respiratory syndrome (SARS) has boosted research on innate immune responses to coronaviruses. It is now well established that the causative agent, a newly identified coronavirus termed SARS-CoV, employs multiple passive and active mechanisms to avoid induction of the antiviral type I interferons in tissue cells. By contrast, chemokines such as IP-10 or IL-8 are strongly upregulated. The imbalance in the IFN response is thought to contribute to the establishment of viremia early in infection, whereas the production of chemokines by infected organs may be responsible for (i) massive immune cell infiltrations found in the lungs of SARS victims, and (ii) the dysregulation of adaptive immunity. Here, we will review the most recent findings on the interaction of SARS-CoV and related Coronaviridae members with the type I interferon and cytokine responses and discuss implications for pathogenesis and therapy.

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“…However, in many instances, the expression of ISGs results from a direct response to virus infection, in addition to induction by IFNs (2,15,23). Therefore, often it is not clear whether the observed expression of ISGs is indeed induced by IFN or rather by other pathways, such as Toll-like receptor signaling or direct activation by specific virus components (14,38,81). Type I and type III IFNs are induced by viral infection and act through the JAK/STAT pathway (17,74).…”

mentioning

confidence: 99%

Induction of MxA Gene Expression by Influenza A Virus Requires Type I or Type III Interferon Signaling

Holzinger¹,

Jorns²,

Stertz³

et al. 2007

J Virol

206

155

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Infection of cultured intestinal epithelial cells with severe acute respiratory syndrome coronavirus

Cited by 79 publications

References 41 publications

SARS-CoV nucleocapsid protein antagonizes IFN-β response by targeting initial step of IFN-β induction pathway, and its C-terminal region is critical for the antagonism

SARS-CoV nucleocapsid protein antagonizes IFN-β response by targeting initial step of IFN-β induction pathway, and its C-terminal region is critical for the antagonism

Interferon and cytokine responses to SARS-coronavirus infection

Induction of MxA Gene Expression by Influenza A Virus Requires Type I or Type III Interferon Signaling

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