دورية أكاديمية

MERS-CoV endoribonuclease and accessory proteins jointly evade host innate immunity during infection of lung and nasal epithelial cells.

التفاصيل البيبلوغرافية
العنوان: MERS-CoV endoribonuclease and accessory proteins jointly evade host innate immunity during infection of lung and nasal epithelial cells.
المؤلفون: Comar CE; Department of Microbiology, University of Pennsylvania, Philadelphia, PA 19104.; Penn Center for Research on Coronaviruses and Other Emerging Pathogens, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Otter CJ; Department of Microbiology, University of Pennsylvania, Philadelphia, PA 19104.; Penn Center for Research on Coronaviruses and Other Emerging Pathogens, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Pfannenstiel J; Department of Molecular Biosciences, University of Kansas, Lawrence, KS 66045., Doerger E; Department of Molecular Biosciences, University of Kansas, Lawrence, KS 66045., Renner DM; Department of Microbiology, University of Pennsylvania, Philadelphia, PA 19104.; Penn Center for Research on Coronaviruses and Other Emerging Pathogens, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104., Tan LH; Otorhinolaryngology-Head and Neck Surgery, University of Pennsylvania, Philadelphia, PA 19104., Perlman S; Department of Microbiology and Immunology, University of Iowa, Iowa City, IA 52242., Cohen NA; Otorhinolaryngology-Head and Neck Surgery, University of Pennsylvania, Philadelphia, PA 19104.; Department of Surgery, Corporal Michael J. Crescenz VA Medical Center, Philadelphia, PA 19104., Fehr AR; Department of Molecular Biosciences, University of Kansas, Lawrence, KS 66045.; Department of Microbiology and Immunology, University of Iowa, Iowa City, IA 52242., Weiss SR; Department of Microbiology, University of Pennsylvania, Philadelphia, PA 19104.; Penn Center for Research on Coronaviruses and Other Emerging Pathogens, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.
المصدر: Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2022 May 24; Vol. 119 (21), pp. e2123208119. Date of Electronic Publication: 2022 May 20.
نوع المنشور: Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: National Academy of Sciences Country of Publication: United States NLM ID: 7505876 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1091-6490 (Electronic) Linking ISSN: 00278424 NLM ISO Abbreviation: Proc Natl Acad Sci U S A Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Washington, DC : National Academy of Sciences
مواضيع طبية MeSH: COVID-19* , Coronavirus Infections*/immunology , Middle East Respiratory Syndrome Coronavirus*/genetics , Middle East Respiratory Syndrome Coronavirus*/pathogenicity, Endoribonucleases/genetics ; Endoribonucleases/metabolism ; Epithelial Cells/metabolism ; Humans ; Immunity, Innate ; Lung/metabolism ; Nasal Mucosa ; SARS-CoV-2/pathogenicity ; Uridylate-Specific Endoribonucleases
مستخلص: Middle East respiratory syndrome coronavirus (MERS-CoV) emerged into humans in 2012, causing highly lethal respiratory disease. The severity of disease may be, in part, because MERS-CoV is adept at antagonizing early innate immune pathways—interferon (IFN) production and signaling, protein kinase R (PKR), and oligoadenylate synthetase/ribonuclease L (OAS/RNase L)—activated in response to viral double-stranded RNA (dsRNA) generated during genome replication. This is in contrast to severe acute respiratory syndrome CoV-2 (SARS-CoV-2), which we recently reported to activate PKR and RNase L and, to some extent, IFN signaling. We previously found that MERS-CoV accessory proteins NS4a (dsRNA binding protein) and NS4b (phosphodiesterase) could weakly suppress these pathways, but ablation of each had minimal effect on virus replication. Here we investigated the antagonist effects of the conserved coronavirus endoribonuclease (EndoU), in combination with NS4a or NS4b. Inactivation of EndoU catalytic activity alone in a recombinant MERS-CoV caused little if any effect on activation of the innate immune pathways during infection. However, infection with recombinant viruses containing combined mutations with inactivation of EndoU and deletion of NS4a or inactivation of the NS4b phosphodiesterase promoted robust activation of dsRNA-induced innate immune pathways. This resulted in at least tenfold attenuation of replication in human lung–derived A549 and primary nasal cells. Furthermore, replication of these recombinant viruses could be rescued to the level of wild-type MERS-CoV by knockout of host immune mediators MAVS, PKR, or RNase L. Thus, EndoU and accessory proteins NS4a and NS4b together suppress dsRNA-induced innate immunity during MERS-CoV infection in order to optimize viral replication.
التعليقات: Update of: bioRxiv. 2021 Dec 21:2021.12.20.473564. doi: 10.1101/2021.12.20.473564. (PMID: 34981054)
References: J Clin Invest. 2019 Jul 29;129(9):3625-3639. (PMID: 31355779)
Nucleic Acids Res. 2012 Feb;40(4):1737-47. (PMID: 22039154)
Proc Natl Acad Sci U S A. 2017 May 23;114(21):E4251-E4260. (PMID: 28484023)
J Virol. 2013 Nov;87(22):12489-95. (PMID: 24027320)
mBio. 2016 Mar 29;7(2):e00258. (PMID: 27025250)
Cell Host Microbe. 2015 Apr 8;17(4):466-77. (PMID: 25816776)
Proc Natl Acad Sci U S A. 2016 Feb 23;113(8):2241-6. (PMID: 26858407)
J Virol. 2007 Dec;81(23):12720-9. (PMID: 17804500)
PLoS Pathog. 2016 Oct 26;12(10):e1005982. (PMID: 27783669)
Proc Natl Acad Sci U S A. 2020 Apr 7;117(14):8094-8103. (PMID: 32198201)
Proc Natl Acad Sci U S A. 2020 Nov 10;117(45):28344-28354. (PMID: 33097660)
J Virol. 2021 Aug 10;95(17):e0040221. (PMID: 34133899)
Emerg Infect Dis. 2015 Jul;21(7):1153-8. (PMID: 26079346)
mBio. 2013 Sep 10;4(5):e00650-13. (PMID: 24023385)
Protein Cell. 2013 Dec;4(12):951-61. (PMID: 24318862)
RNA. 2020 Dec;26(12):1976-1999. (PMID: 32989044)
PLoS One. 2018 Mar 26;13(3):e0194527. (PMID: 29579103)
J Virol. 2017 Feb 14;91(5):. (PMID: 28003490)
Cell Host Microbe. 2012 Jun 14;11(6):607-16. (PMID: 22704621)
J Clin Invest. 2014 Mar;124(3):1393-405. (PMID: 24531552)
J Virol. 2016 Jan 06;90(6):3160-72. (PMID: 26739051)
J Virol. 2005 Apr;79(7):4219-28. (PMID: 15767423)
N Engl J Med. 2012 Nov 8;367(19):1814-20. (PMID: 23075143)
J Virol. 2013 Aug;87(15):8408-18. (PMID: 23698313)
PLoS Pathog. 2018 Jan 25;14(1):e1006838. (PMID: 29370303)
J Virol. 2014 Oct;88(19):11297-303. (PMID: 25031349)
Front Microbiol. 2021 Jul 14;12:682603. (PMID: 34335504)
Emerg Infect Dis. 2014 Aug;20(8):1370-4. (PMID: 25062254)
mBio. 2014 Jul 01;5(4):e01312-14. (PMID: 24987090)
J Virol. 2018 Sep 26;92(20):. (PMID: 30068649)
mBio. 2017 Apr 4;8(2):. (PMID: 28377531)
J Virol. 2019 Feb 5;93(4):. (PMID: 30463965)
Adv Virus Res. 2016;96:219-243. (PMID: 27712625)
J Clin Invest. 2012 Nov;122(11):4145-59. (PMID: 23041624)
Sci China Life Sci. 2022 Feb;65(2):280-294. (PMID: 34387838)
mBio. 2017 Aug 22;8(4):. (PMID: 28830941)
J Allergy Clin Immunol. 2018 Aug;142(2):460-469.e7. (PMID: 29778504)
J Virol. 2019 Apr 3;93(8):. (PMID: 30728254)
Elife. 2017 Mar 31;6:. (PMID: 28362255)
J Interferon Cytokine Res. 2014 Jun;34(6):455-63. (PMID: 24905202)
J Virol. 2008 Oct;82(20):9829-38. (PMID: 18667505)
Annu Rev Immunol. 2019 Apr 26;37:349-375. (PMID: 30673536)
mBio. 2019 Mar 26;10(2):. (PMID: 30914508)
EMBO J. 1997 Nov 3;16(21):6355-63. (PMID: 9351818)
J Virol. 2015 Feb;89(3):1523-36. (PMID: 25428866)
mBio. 2019 Nov 12;10(6):. (PMID: 31719180)
Proc Natl Acad Sci U S A. 2021 Apr 20;118(16):. (PMID: 33811184)
Methods Mol Biol. 2020;2099:53-68. (PMID: 31883087)
J Gen Virol. 2014 Apr;95(Pt 4):874-882. (PMID: 24443473)
Nature. 2007 Aug 16;448(7155):816-9. (PMID: 17653195)
Sci Rep. 2015 Dec 03;5:17554. (PMID: 26631542)
Emerg Microbes Infect. 2015 Dec 02;4(12):e74. (PMID: 26632876)
J Virol. 2014 May;88(9):4866-76. (PMID: 24522921)
Proc Natl Acad Sci U S A. 2018 Mar 20;115(12):3144-3149. (PMID: 29507189)
EBioMedicine. 2021 Oct;72:103629. (PMID: 34655949)
J Virol. 2007 Sep;81(18):9812-24. (PMID: 17596301)
PLoS Pathog. 2017 Feb 3;13(2):e1006195. (PMID: 28158275)
Sci Signal. 2012 Oct 23;5(247):pe47. (PMID: 23092889)
Nat Rev Immunol. 2020 Sep;20(9):537-551. (PMID: 32203325)
معلومات مُعتمدة: P20 GM113117 United States GM NIGMS NIH HHS; R35 GM138029 United States GM NIGMS NIH HHS; R01 AI129269 United States AI NIAID NIH HHS; P01 AI060699 United States AI NIAID NIH HHS; R01 AI140442 United States AI NIAID NIH HHS; T32 AI055400 United States AI NIAID NIH HHS; K22 AI134993 United States AI NIAID NIH HHS; I01 BX005432 United States BX BLRD VA
فهرسة مساهمة: Keywords: MERS-CoV; PKR; RNase L; endonuclease U; innate immune antagonism
المشرفين على المادة: EC 3.1.- (Endoribonucleases)
EC 3.1.- (Uridylate-Specific Endoribonucleases)
تواريخ الأحداث: Date Created: 20220520 Date Completed: 20220524 Latest Revision: 20240610
رمز التحديث: 20240610
مُعرف محوري في PubMed: PMC9173776
DOI: 10.1073/pnas.2123208119
PMID: 35594398
قاعدة البيانات: MEDLINE
الوصف
تدمد:1091-6490
DOI:10.1073/pnas.2123208119