Severe acute respiratory syndrome coronavirus nucleocapsid protein does not modulate transcription of the human FGL2 gene.

Abstract

Among the structural and nonstructural proteins of severe acute respiratory syndrome coronavirus (SARS-CoV), the nucleocapsid (N) protein plays pivotal roles in the biology and pathogenesis of viral infection. N protein is thought to dysregulate cell signalling and the transcription of cellular genes, including FGL2, which encodes a prothrombinase implicated in vascular thrombosis, fibrin deposition and pneumocyte necrosis. Here, we showed that N protein expressed in cultured human cells was predominantly found in the cytoplasm and was competent in repressing the transcriptional activity driven by interferon-stimulated response elements. However, the expression of N protein did not influence the transcription from the FGL2 promoter. More importantly, N protein did not modulate the expression of FGL2 mRNA or protein in transfected or SARS-CoV-infected cells. Taken together, our findings did not support the model in which SARS-CoV N protein specifically modulates transcription of the FGL2 gene to cause fibrosis and vascular thrombosis.

• Authors: Kam-Leung Siu, Ching-Ping Chan, Chris Chan, Bo-Jian Zheng, Dong-Yan Jin
• Journal: The Journal of general virology (J Gen Virol) Vol. 90 Issue Pt 9 Pg. 2107-13 (Sep 2009) ISSN: 0022-1317 [Print] England
• PMID: 19423547 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Coronavirus Nucleocapsid Proteins
• FGL2 protein, human
• Nucleocapsid Proteins
• Fibrinogen

Topics

• Cell Line
• Coronavirus Nucleocapsid Proteins
• Fibrinogen (genetics, metabolism)
• Humans
• Nucleocapsid Proteins (genetics, metabolism)
• Severe acute respiratory syndrome-related coronavirus (genetics, metabolism)
• Severe Acute Respiratory Syndrome (genetics, metabolism, virology)
• Transcription, Genetic