medigraphic.com
SPANISH

Revista Mexicana de Mastología

ISSN 1870-2821 (Print)
Organo Oficial de la Asociación Mexicana de Mastología
  • Contents
  • View Archive
  • Information
    • General Information        
    • Directory
  • Publish
    • Instructions for authors        
  • medigraphic.com
    • Home
    • Journals index            
    • Register / Login
  • Mi perfil

2021, Number 1

<< Back Next >>

Rev Mex Mastol 2021; 11 (1)

Spike glycoprotein

Vásquez MI
Full text How to cite this article 10.35366/99276

DOI

DOI: 10.35366/99276
URL: https://dx.doi.org/10.35366/99276

Language: Spanish
References: 8
Page: 18-21
PDF size: 224.56 Kb.


Key words:

Spike protein, ACE2 receptor, COVID-19, SARS-CoV-2.

ABSTRACT

The appearance of this new pathogenic virus has set off alarms in the health systems of all countries, becoming a challenge for biomedical research. The spike protein, or spike, is one of the four main structural proteins that cover the surface of each virion. Spike is a type I transmembrane protein, highly glycosylated and responsible for entry into the host cell. Structurally, there are two domains, S1 and S2, that play important roles in receptor binding and membrane fusion. Within the S1 N-terminal domain is the receptor-binding domain (called RBD). This domain binds to the host cell's receptor for angiotensin called ACE2 and initiates viral infection. The viral binding leads to conformational changes in the spike S2 ??domain that allow fusion between the membranes and, ultimately, transfer of the nucleocapsid into the cell. Due to its essential role during spike coronavirus infection, it is the main therapeutic target.


REFERENCES

  1. Du L, He Y, Zhou Y, Liu S, Zheng BJ, Jiang S. The spike protein of SARS-CoV--a target for vaccine and therapeutic development. Nat Rev Microbiol. 2009; 7 (3): 226-236.

  2. Belouzard S, Millet JK, Licitra BN, Whittaker GR. Mechanisms of coronavirus cell entry mediated by the viral spike protein. Viruses. 2012; 4 (6): 1011-1033.

  3. Li F. Structure, function, and evolution of coronavirus spike proteins. Annu Rev Virol. 2016; 3 (1): 237-261.

  4. Zhang H, Penninger JM, Li Y, Zhong N, Slutzky A. Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target. Intensive Care Med. 2020; 46 (4): 586-590.

  5. Verdecchia P, Cavallini C, Spanevello A, Angeli F. The pivotal link between ACE2 deficiency and SARS-CoV-2 infection. Eur J Intern Med. 2020; 76: 14-20.

  6. Glowacka I, Bertram S, Müller MA, Allen P, Soilleux E, Pfefferle S et al. Evidence that TMPRSS2 activates the severe acute respiratory syndrome coronavirus spike protein for membrane fusion and reduces viral control by the humoral immune. J Virol. 2011; 85 (9): 4122-4134.

  7. Hoffmann M, Kleine-Weber H, Schroeder S, Krüger N, Herrler T, Erichsen S et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell. 2020; 181 (2): 271-280.

  8. Delpino MV, Quarleri J. SARS-CoV-2 pathogenesis: imbalance in the renin-angiotensin system favors lung fibrosis. Front Cell Infect Microbiol. 2020; 10: 340.




Figure 1

2020     |     www.medigraphic.com

Mi perfil

C?MO CITAR (Vancouver)

Rev Mex Mastol. 2021;11