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J Gen Virol. The ORF4b-encoded accessory proteins of MERS-Coronavirus and two related bat coronaviruses localize to the nucleus and inhibit innate immune signaling.
[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]
J Gen Virol. 2014 Jan 17. doi: 10.1099/vir.0.062059-0. [Epub ahead of print]
The ORF4b-encoded accessory proteins of MERS-Coronavirus and two related bat coronaviruses localize to the nucleus and inhibit innate immune signaling.
Matthews KL, Coleman CM, van der Meer Y, Snijder EJ, Frieman MB.
Author information: University of Maryland;
Abstract
The recently emerged Middle East respiratory syndrome coronavirus or MERS-CoV, a beta-coronavirus, is associated with severe pneumonia and renal failure. The environmental origin of MERS-CoV is yet unknown, however, its genome sequence is closely related to those of two bat coronaviruses, named BtCoV-HKU4 and BtCoV-HKU5, which were derived from Chinese bat samples. A hallmark of highly pathogenic respiratory viruses is their ability to evade the innate immune response of the host. Coronavirus accessory proteins, for example those from severe acute respiratory syndrome coronavirus (SARS-CoV), have been shown to block innate anti-viral signaling pathways. MERS-CoV, similar to SARS-CoV, has been shown to inhibit type I interferon induction in a variety of cell types in vitro. We therefore hypothesized that MERS-CoV and the phylogenetically related coronaviruses BtCoV-HKU4 and BtCoV-HKU5 may encode proteins with similar capabilities. In this study, we demonstrate that the ORF4b-encoded accessory proteins (p4b) of MERS-CoV, BtCoV-HKU4, and BtCoV-HKU5 may indeed facilitate innate immune evasion by inhibiting the type I IFN and NF-kB signaling pathways. We also analyzed the subcellular localization of p4b from MERS-CoV, BtCoV-HKU4, and BtCoV-HKU5 and demonstrate that all are localized to the nucleus.
KEYWORDS: accessory protein, innate immune evasion, innate immunity, nuclear transport
PMID: 24443473 [PubMed - as supplied by publisher]
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J Gen Virol. 2014 Jan 17. doi: 10.1099/vir.0.062059-0. [Epub ahead of print]
The ORF4b-encoded accessory proteins of MERS-Coronavirus and two related bat coronaviruses localize to the nucleus and inhibit innate immune signaling.
Matthews KL, Coleman CM, van der Meer Y, Snijder EJ, Frieman MB.
Author information: University of Maryland;
Abstract
The recently emerged Middle East respiratory syndrome coronavirus or MERS-CoV, a beta-coronavirus, is associated with severe pneumonia and renal failure. The environmental origin of MERS-CoV is yet unknown, however, its genome sequence is closely related to those of two bat coronaviruses, named BtCoV-HKU4 and BtCoV-HKU5, which were derived from Chinese bat samples. A hallmark of highly pathogenic respiratory viruses is their ability to evade the innate immune response of the host. Coronavirus accessory proteins, for example those from severe acute respiratory syndrome coronavirus (SARS-CoV), have been shown to block innate anti-viral signaling pathways. MERS-CoV, similar to SARS-CoV, has been shown to inhibit type I interferon induction in a variety of cell types in vitro. We therefore hypothesized that MERS-CoV and the phylogenetically related coronaviruses BtCoV-HKU4 and BtCoV-HKU5 may encode proteins with similar capabilities. In this study, we demonstrate that the ORF4b-encoded accessory proteins (p4b) of MERS-CoV, BtCoV-HKU4, and BtCoV-HKU5 may indeed facilitate innate immune evasion by inhibiting the type I IFN and NF-kB signaling pathways. We also analyzed the subcellular localization of p4b from MERS-CoV, BtCoV-HKU4, and BtCoV-HKU5 and demonstrate that all are localized to the nucleus.
KEYWORDS: accessory protein, innate immune evasion, innate immunity, nuclear transport
PMID: 24443473 [PubMed - as supplied by publisher]
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