ArticleJournal of virology2008
Severe acute respiratory syndrome coronavirus protein 6 accelerates murine hepatitis virus infections by more than one mechanism.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Article
- SARS-CoV-2 nsp13, nsp14, nsp15 and orf6 function as potent interferon antagonists.Emerging microbes & infections · 2020Article
- The molecular virology of coronaviruses.The Journal of biological chemistry · 2020Review
- The multifarious roles of heterogeneous ribonucleoprotein A1 in viral infections.Reviews in medical virology · 2020Review
- Prospects for RNAi Therapy of COVID-19.Frontiers in bioengineering and biotechnology · 2020Review
- Article
- A review of genetic methods and models for analysis of coronavirus-induced severe pneumonitis.The Journal of general virology · 2015Review
- Components and regulation of nuclear transport processes.The FEBS journal · 2015Review
- Coronavirus virulence genes with main focus on SARS-CoV envelope gene.Virus research · 2014Review
- Accessory proteins of SARS-CoV and other coronaviruses.Antiviral research · 2014Review
- Viral subversion of nucleocytoplasmic trafficking.Traffic (Copenhagen, Denmark) · 2014Review
- MERS-coronavirus replication induces severe in vitro cytopathology and is strongly inhibited by cyclosporin A or interferon-α treatment.The Journal of general virology · 2013Article
- Induction of alternatively activated macrophages enhances pathogenesis during severe acute respiratory syndrome coronavirus infection.Journal of virology · 2012Article
- The role of severe acute respiratory syndrome (SARS)-coronavirus accessory proteins in virus pathogenesis.Viruses · 2012Review
- SARS coronavirus pathogenesis: host innate immune responses and viral antagonism of interferon.Current opinion in virology · 2012Review
- A putative diacidic motif in the SARS-CoV ORF6 protein influences its subcellular localization and suppression of expression of co-transfected expression constructs.BMC research notes · 2011Article
- Coronavirus pathogenesis.Advances in virus research · 2011Review
- SARS-coronavirus protein 6 conformations required to impede protein import into the nucleus.Virus research · 2010Article
- The N-terminal region of severe acute respiratory syndrome coronavirus protein 6 induces membrane rearrangement and enhances virus replication.Journal of virology · 2010Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The severe acute respiratory syndrome coronavirus (SARS-CoV) encodes numerous accessory proteins whose importance in the natural infection process is currently unclear. One of these accessory proteins is set apart by its function in the context of a related murine hepatitis virus (MHV) infection. SARS-CoV protein 6 increases MHV neurovirulence and accelerates MHV infection kinetics in tissue culture. Protein 6 also blocks nuclear import of macromolecules from the cytoplasm, a process known to involve its C-terminal residues interacting with cellular importins. In this study, protein 6 was expressed from plasmid DNAs and accumulated in cells prior to infection by wild-type MHV. Output of MHV progeny was significantly increased by preexisting protein 6. Protein 6 with C-terminal deletion mutations no longer interfered with nuclear import processes but still retained much of the capacity to augment MHV infections. However, some virus growth-enhancing activity could be ascribed to the C-terminal end of protein 6. To determine whether this augmentation provided by the C terminus was derived from interference with nuclear import, we evaluated the virus-modulating effects of small interfering RNAs (siRNAs) directed against importin-beta mRNAs, which down-regulated classical nuclear import pathways. The siRNAs did indeed prime cells for enhanced MHV infection. Our findings indicated that protein 6-mediated nuclear import blocks augmented MHV infections but is clearly not the only way that this accessory protein operates to create a milieu conducive to robust virus growth. Thus, the SARS-CoV protein 6 accelerates MHV infections by more than one mechanism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.