scholarly journals SARS-CoV-2 Nsp5 Demonstrates Two Distinct Mechanisms Targeting RIG-I and MAVS To Evade the Innate Immune Response

mBio ◽  
2021 ◽  
Author(s):  
Yongzhen Liu ◽  
Chao Qin ◽  
Youliang Rao ◽  
Chau Ngo ◽  
Joshua J. Feng ◽  
...  

The ongoing COVID-19 pandemic is caused by SARS-CoV-2, which is rapidly evolving with better transmissibility. Understanding the molecular basis of the SARS-CoV-2 interaction with host cells is of paramount significance, and development of antiviral agents provides new avenues to prevent and treat COVID-19 diseases. This study describes a molecular characterization of innate immune evasion mediated by the SARS-CoV-2 Nsp5 main protease and subsequent development of a small-molecule inhibitor.

Virology ◽  
2015 ◽  
Vol 479-480 ◽  
pp. 122-130 ◽  
Author(s):  
Christopher F. Basler

2019 ◽  
Vol 13 (1) ◽  
pp. 219-222 ◽  
Author(s):  
Alvaro I. Herrera ◽  
Abhinav Dubey ◽  
Brian V. Geisbrecht ◽  
Haribabu Arthanari ◽  
Om Prakash

2009 ◽  
Vol 53 (10) ◽  
pp. 4490-4494 ◽  
Author(s):  
Amit Sarkar ◽  
Kit Tilly ◽  
Philip Stewart ◽  
Aaron Bestor ◽  
James M. Battisti ◽  
...  

ABSTRACT We hypothesize a potential role for Borrelia burgdorferi OspC in innate immune evasion at the initial stage of mammalian infection. We demonstrate that B. burgdorferi is resistant to high levels (>200 μg/ml) of cathelicidin and that this antimicrobial peptide exhibits limited binding to the spirochetal outer membrane, irrespective of OspC or other abundant surface lipoproteins. We conclude that the essential role of OspC is unrelated to resistance to this component of innate immunity.


2018 ◽  
Vol 115 (16) ◽  
pp. E3788-E3797 ◽  
Author(s):  
Quentin Bernard ◽  
Alexis A. Smith ◽  
Xiuli Yang ◽  
Juraj Koci ◽  
Shelby D. Foor ◽  
...  

Borrelia burgdorferiis one of the few extracellular pathogens capable of establishing persistent infection in mammals. The mechanisms that sustain long-term survival of this bacterium are largely unknown. Here we report a unique innate immune evasion strategy ofB. burgdorferi, orchestrated by a surface protein annotated as BBA57, through its modulation of multiple spirochete virulent determinants. BBA57 function is critical for early infection but largely redundant for later stages of spirochetal persistence, either in mammals or in ticks. The protein influences host IFN responses as well as suppresses multiple host microbicidal activities involving serum complement, neutrophils, and antimicrobial peptides. We also discovered a remarkable plasticity in BBA57-mediated spirochete immune evasion strategy because its loss, although resulting in near clearance of pathogens at the inoculum site, triggers nonheritable adaptive changes that exclude detectable nucleotide alterations in the genome but incorporate transcriptional reprograming events. Understanding the malleability in spirochetal immune evasion mechanisms that ensures their host persistence is critical for the development of novel therapeutic and preventive approaches to combat long-term infections like Lyme borreliosis.


2020 ◽  
Vol 64 (2) ◽  
pp. 87-98 ◽  
Author(s):  
Pitchaipillai Sankar Ganesh ◽  
Sivakumar Vishnupriya ◽  
Jamuna Vadivelu ◽  
Vanitha Mariappan ◽  
Kumutha M. Vellasamy ◽  
...  

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