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. 2022 Jan 24:1–18. [Article in Spanish] doi: 10.1159/000521507

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Copyright © 2022 by S. Karger AG, Basel

This article is licensed under the Creative Commons Attribution 4.0 International License (CC BY). Usage, derivative works and distribution are permitted provided that proper credit is given to the author and the original publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

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Fig. 2 — Esquema de la entrada del coronavirus tipo 2 del síndrome respiratorio agudo severo (SARS-CoV-2) en las células humanas. La entrada del SARS-CoV-2 en las células humanas es mediada por un receptor de superficie celular, la enzima convertidora de angiotensina-2 (ACE2). La ACE2 se une al dominio de unión al receptor (RBD) de la proteína spike (S) del SARS-CoV-2. Además, para que el virus entre en la célula huésped, la imprimación de la proteína «S» para su fusión con la membrana de la célula huésped se realiza mediante proteasas de la célula huésped, lo que implica la escisión de la proteína «S» por serina proteasas, la serina proteasa transmembrana 2 (TMPRSS2) o la catepsina B o L (CTS-B o -L), y la furina presente en la membrana de la célula huésped. La CTS-B o -L actúa principalmente en el interior de los endosomas. El sitio de corte de la furina (PRRAR), presente en la intersección de S1 y S2, se considera una adquisición evolutiva en el SARS-CoV-2.