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Factors Affecting the Risk of Infection01:26

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Correction: de Melo et al. SARS-CoV-2 Spike Protein and Long COVID-Part 2: Understanding the Impact of Spike Protein and Cellular Receptor Interactions on the Pathophysiology of Long COVID Syndrome. <i>Viruses</i> 2025, <i>17</i>, 619.

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Correction: de Melo et al. SARS-CoV-2 Spike Protein and Long COVID-Part 1: Impact of Spike Protein in Pathophysiological Mechanisms of Long COVID Syndrome. <i>Viruses</i> 2025, <i>17</i>, 617.

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Alpha-1-antitrypsin: A possible host protective factor against Covid-19.

Mariana Braccialli de Loyola1, Thaís Tereza Aguiar Dos Reis1, Guilherme Xavier Lyra Malcher de Oliveira1

  • 1Laboratory of Molecular Neurovirology, Faculty of Health Science, University of Brasília, Brasilia, Brazil.

Reviews in Medical Virology
|August 27, 2020
PubMed
Summary

Alpha-1-antitrypsin (A1AT) inhibits SARS-CoV-2 infection by blocking key proteases like TMPRSS2 and ADAM17. This review explores A1AT

Keywords:
A1ATADAM17Covid-19SARS-CoV-2TMPRSS2

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Area of Science:

  • Immunology
  • Virology
  • Biochemistry

Background:

  • Understanding COVID-19 pathophysiology is critical for developing effective treatments.
  • Alpha-1-antitrypsin (A1AT) possesses known antiviral and anti-inflammatory properties.
  • A1AT is a natural tissue protector with potential roles in disease modulation.

Purpose of the Study:

  • To review the interplay between A1AT, key proteases (TMPRSS2, ADAM17), and immune molecules in COVID-19.
  • To elucidate the role of A1AT in the pathophysiology of COVID-19.
  • To explore A1AT as a potential therapeutic target for COVID-19.

Main Methods:

  • Literature review focusing on the molecular mechanisms of A1AT.
  • Analysis of A1AT's interactions with SARS-CoV-2 entry and replication factors.
  • Examination of A1AT's influence on inflammatory pathways relevant to COVID-19.

Main Results:

  • A1AT inhibits SARS-CoV-2 infection by blocking TMPRSS2 and ADAM17.
  • A1AT modulates inflammatory responses by inhibiting IL-8, TNF-α, and neutrophil elastase.
  • A1AT's interaction with ACE2 shedding and renin-angiotensin system balance is highlighted.
  • Clinical data suggests A1AT levels correlate with COVID-19 outcomes, potentially linking to air pollution and diabetes.

Conclusions:

  • A1AT plays a significant role in mitigating COVID-19 pathophysiology through multiple mechanisms.
  • A1AT's inhibitory effects on viral entry and inflammation present therapeutic potential.
  • Further investigation into A1AT-based therapies for COVID-19 is warranted.