scholarly journals Potential cross-protection against SARS-CoV-2 from previous exposure to bovine coronavirus

2021 ◽  
Author(s):  
Lana B. P. Querne ◽  
Fernanda Z Bastos ◽  
Breno Castello Branco Beirao

Humans have long shared infectious agents with cattle, and the common cold OC-43 CoV is a not-so-distant example of cross-species viral spillover. Human exposure to BCoV is certainly common, as the virus is endemic in cattle-raising regions. This article shows an in silico investigation of shared viral epitopes between BCoV and SARS-CoV-2. HLA recognition and lymphocyte reactivity were assessed using freely-available resources. Several epitopes were shared between BCoV and SARS-CoV-2, both for B and T lymphocytes. These data demonstrate that possible cross-protection is being induced by human exposure to cattle.

Author(s):  
Ghotekar D S ◽  
Vishal N Kushare ◽  
Sagar V Ghotekar

Coronaviruses are a family of viruses that cause illness such as respiratory diseases or gastrointestinal diseases. Respiratory diseases can range from the common cold to more severe diseases. A novel coronavirus outbreak was first documented in Wuhan, Hubei Province, China in December 2019. The World Health Organization (WHO) has declared the coronavirus disease 2019 (COVID-19) a pandemic. A global coordinated effort is needed to stop the further spread of the virus. A novel coronavirus (nCoV) is a new strain that has not been identified in humans previously. Once scientists determine exactly what coronavirus it is, they give it a name (as in the case of COVID-19, the virus causing it is SARS-CoV-2).


BMJ ◽  
1925 ◽  
Vol 2 (3386) ◽  
pp. 980-980
Author(s):  
F. R. Walters
Keyword(s):  

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii511-iii511
Author(s):  
Jose Tarcisio Giffoni de Carvalho ◽  
Marion Schneider ◽  
Lilian Cuppari ◽  
Caren Cristina Grabulosa ◽  
Silvia Regina Manfredi ◽  
...  

2021 ◽  
Vol 33 (1) ◽  
Author(s):  
Emad M. El-Shebiny ◽  
Enas S. Zahran ◽  
Sabry A. Shoeib ◽  
Eman S. Habib

Abstract Background Autoimmunity is used to cause by impairment of adaptive immunity alone, whereas autoinflammatory was originally defined as a consequence of unregulated innate immunity. So, the pathogenetic mechanisms of autoimmune diseases were well-thought-out to be mediated by B and T lymphocytes. Whereas, autoinflammatory diseases were defined as unprovoked times of inflammation with the absence of a high titre of autoantibodies. Main body of the abstract Autoimmune and autoinflammatory diseases were split into two groups, but considering the similarities, it can be considered as only one group of diseases with a large immune pathological and clinical spectrum which involves at one end pure autoimmune diseases and the other pure autoinflammatory diseases. Conclusions We can safely conclude that there is bridging between autoinflammatory and autoimmune diseases.


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