AI Article Synopsis
- MERS-CoV is a respiratory virus with a high mortality rate that influences various host immune responses during infection.
- A monoclonal antibody was developed to study the nucleocapsid protein (MERS-N) and its role in regulating antiviral genes, particularly focusing on CXCL10.
- The study found that MERS-N can significantly up-regulate CXCL10, which has been linked to disease severity in infected patients, with specific regions of the MERS-N protein identified as critical for this effect.
Article Abstract
Middle East respiratory syndrome coronavirus (MERS-CoV) causes respiratory diseases in humans and has a high mortality rate. During infection, MERS-CoV regulates several host cellular processes including antiviral response genes. In order to determine if the nucleocapsid protein of MERS-CoV (MERS-N) plays a role in viral-host interactions, a murine monoclonal antibody was generated so as to allow detection of the protein in infected cells as well as in overexpression system. Then, MERS-N was stably overexpressed in A549 cells, and a PCR array containing 84 genes was used to screen for genes transcriptionally regulated by it. Several up-regulated antiviral genes, namely , and , were selected for independent validation in transiently transfected 293FT cells. Out of these, the overexpression of MERS-N was found to up-regulate CXCL10 at both transcriptional and translational levels. Interestingly, CXCL10 has been reported to be up-regulated in MERS-CoV infected airway epithelial cells and lung fibroblast cells, as well as monocyte-derived macrophages and dendritic cells. High secretions and persistent increase of CXCL10 in MERS-CoV patients have been also associated with severity of disease. To our knowledge, this is the first report showing that the MERS-N protein is one of the contributing factors for CXCL10 up-regulation during infection. In addition, our results showed that a fragment consisting of residues 196-413 in MERS-N is sufficient to up-regulate CXCL10, while the N-terminal domain and serine-arginine (SR)-rich motif of MERS-N do not play a role in this up-regulation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6200698 | PMC |
| http://dx.doi.org/10.1042/BSR20181059 | DOI Listing |
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