Del covid-19 al poscovid-19: lecciones y desafíos
DOI:
https://doi.org/10.56050/01205498.1665Palabras clave:
SARS-CoV-2, Covid-19, sindrome poscovid, autoinmunidad, inflamaciónResumen
La enfermedad por el coronavirus (COVID-19) es causada por el nuevo coronavirus de tipo 2 del síndrome respiratorio agudo severo (SARS-CoV-2). Esta enfermedad es asintomática o leve en aproximadamente el 80 % de los casos, y severa o crítica en el 20 % restante. La COVID-19 fue considerada inicialmente una enfermedad pulmonar, pero ahora se reconoce como una enfermedad multiorgánica con un amplio espectro de manifestaciones clínicas. Algunos pacientes que sufren una infección aguda por SARS-CoV-2 desarrollan una amplia variedad de síntomas persistentes que no se resuelven en el transcurso de muchos meses. Esta condición es conocida como síndrome post-covid-19 (SPC). La respuesta inflamatoria persistente, la desregulación de la respuesta inmune innata y adaptativa, la presencia de autoinmunidad latente y autoinmunidad manifiesta y los reservorios persistentes de SARS-CoV-2 en ciertos tejidos pueden ser responsables de la severidad de la enfermedad en la infección aguda y de las secuelas del SPC. En este artículo presentamos la interacción del SARS-CoV-2 con el sistema inmune y la posterior contribución de las respuestas inmunes disfuncionales en la progresión de la enfermedad. Finalmente, destacamos las implicaciones de las intervenciones terapéuticas dirigidas para controlar la infección viral y regular la respuesta inmune.
Biografía del autor/a
Carolina Ramírez-Santana, Centro de Estudio de Enfermedades Autoinmunes (CREA)
Centro de Estudio de Enfermedades Autoinmunes (CREA), Escuela de Medicina y Ciencias de la Salud, Universidad del Rosario, Bogotá, Colombia.
Yeni Acosta-Ampudia, Centro de Estudio de Enfermedades Autoinmunes (CREA)
Centro de Estudio de Enfermedades Autoinmunes (CREA), Escuela de Medicina y Ciencias de la Salud, Universidad del Rosario, Bogotá, Colombia.
Diana M. Monsalve, Centro de Estudio de Enfermedades Autoinmunes (CREA)
Centro de Estudio de Enfermedades Autoinmunes (CREA), Escuela de Medicina y Ciencias de la Salud, Universidad del Rosario, Bogotá, Colombia.
Manuel Rojas, Centro de Estudio de Enfermedades Autoinmunes (CREA)
Centro de Estudio de Enfermedades Autoinmunes (CREA), Escuela de Medicina y Ciencias de la Salud, Universidad del Rosario, Bogotá, Colombia.
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4. Rodríguez Y, Novelli L, Rojas M, De Santis M, AcostaAmpudia Y, Monsalve DM, et al. Autoinflammatory and autoimmune conditions at the crossroad of COVID-19. J Autoimmun. 2020 ;114:102506.
5. Naqvi AAT, Fatima K, Mohammad T, Fatima U, Singh IK, Singh A, et al. Insights into SARS-CoV-2 genome, structure, evolution, pathogenesis and therapies: Structural genomics approach. Biochim Biophys Acta Mol Basis Dis. 2020;1866(10):165878.
6. Lu R, Zhao X, Li J, Niu P, Yang B, Wu H, et al. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet. 2020;395(10224):565–74.
7. Chan JF-W, Kok K-H, Zhu Z, Chu H, To KK-W, Yuan S, et al. Genomic characterization of the 2019 novel human-pathogenic coronavirus isolated from a patient with atypical pneumonia after visiting Wuhan. Emerg Microbes Infect. 2020;9(1):221–36.
8. Hu B, Guo H, Zhou P, Shi Z-L. Characteristics of SARS-CoV-2 and COVID-19. Nat Rev Microbiol. 2021;19(3):141–54.
9. Lan J, Ge J, Yu J, Shan S, Zhou H, Fan S, et al. Structure of the SARS-CoV-2 spike receptor-binding domain bound to the ACE2 receptor. Nature. 2020;581(7807):215–20.
10. Li M-Y, Li L, Zhang Y, Wang X-S. Expression of the SARS-CoV-2 cell receptor gene ACE2 in a wide variety of human tissues. Infect Dis poverty. 2020;9(1):45.
11. Vaduganathan M, Vardeny O, Michel T, McMurray JJ V, Pfeffer MA, Solomon SD. Renin-Angiotensin-Aldosterone System Inhibitors in Patients with Covid-19. N Engl J Med. 2020;382(17):1653–9.
12. van Lier D, Kox M, Santos K, van der Hoeven H, Pillay J, Pickkers P. Increased blood angiotensin converting enzyme 2 activity in critically ill COVID-19 patients. ERJ open Res. 2021;7(1):00848-2020.
13. Rojas M, Acosta-Ampudia Y, Monsalve DM, Ramírez-Santana C, Anaya J-M. How Important Is the Assessment of Soluble ACE-2 in COVID-19? Am J Hypertens. 2021;34(3):296–7.
14. Rieder M, Wirth L, Pollmeier L, Jeserich M, Goller I, Baldus N, et al. Serum ACE2, Angiotensin II, and Aldosterone Levels Are Unchanged in Patients With COVID-19. Am J Hypertens. 2021;34(3):278–81.
15. Kyrou I, Randeva HS, Spandidos DA, Karteris E. Not only ACE2-the quest for additional host cell mediators of SARS-CoV-2 infection: Neuropilin-1 (NRP1) as a novel SARS-CoV-2 host cell entry mediator implicated in COVID-19. Signal Transduct Target Ther. 2021;6(1):21.
16. 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.e8.
17. Diamond MS, Kanneganti T-D. Innate immunity: the first line of defense against SARS-CoV-2. Nat Immunol. 2022;23(2):165–76.
18. Zheng M, Karki R, Williams EP, Yang D, Fitzpatrick E, Vogel P, et al. TLR2 senses the SARS-CoV-2 envelope protein to produce inflammatory cytokines. Nat Immunol. 2021;22(7):829–38.
19. Choudhury A, Mukherjee S. In silico studies on the comparative characterization of the interactions of SARSCoV-2 spike glycoprotein with ACE-2 receptor homologs and human TLRs. J Med Virol. 2020;92(10):2105–13.
20. Karki R, Sharma BR, Tuladhar S, Williams EP, Zalduondo L, Samir P, et al. Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes. Cell. 2021;184(1):149-168.e17.
21. Sette A, Crotty S. Adaptive immunity to SARS-CoV-2 and COVID-19. Cell. 2021;184(4):861–80.
22. Zhao J, Yuan Q, Wang H, Liu W, Liao X, Su Y, et al. Antibody Responses to SARS-CoV-2 in Patients With Novel Coronavirus Disease 2019. Clin Infect Dis . 2020;71(16):2027–34.
23. Guo L, Ren L, Yang S, Xiao M, Chang D, Yang F, et al. Profiling Early Humoral Response to Diagnose Novel Coronavirus Disease (COVID-19). Clin Infect Dis . 2020;71(15):778–85.
24. Yan X, Chen G, Jin Z, Zhang Z, Zhang B, He J, et al. Anti-SARS-CoV-2 IgG levels in relation to disease severity of COVID-19. J Med Virol. 2022;94(1):380–3.
25. Ibarrondo FJ, Fulcher JA, Goodman-Meza D, Elliott J, Hofmann C, Hausner MA, et al. Rapid Decay of AntiSARS-CoV-2 Antibodies in Persons with Mild Covid-19. N Engl J Med. 2020;383(11):1085–7.
26. Long Q-X, Tang X-J, Shi Q-L, Li Q, Deng H-J, Yuan J, et al. Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections. Nat Med. 2020;26(8):1200–4.
27. Tea F, Ospina Stella A, Aggarwal A, Ross Darley D, Pilli D, Vitale D, et al. SARS-CoV-2 neutralizing antibodies: Longevity, breadth, and evasion by emerging viral variants. PLoS Med. 2021;18(7):e1003656.
28. Sekine T, Perez-Potti A, Rivera-Ballesteros O, Strålin K, Gorin J-B, Olsson A, et al. Robust T Cell Immunity in Convalescent Individuals with Asymptomatic or Mild COVID-19. Cell. 2020;183(1):158-168.e14.
29. Anaya J-M, Rojas M, Salinas ML, Rodríguez Y, Roa G, Lozano M, et al. Post-COVID syndrome. A case series and comprehensive review. Autoimmun Rev. 2021;20(11):102947.
30. Halpert G, Shoenfeld Y. SARS-CoV-2, the autoimmune virus. Autoimmun Rev . 2020;19(12):102695.
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Cómo citar
[1]
Ramírez-Santana, C. et al. 2022. Del covid-19 al poscovid-19: lecciones y desafíos. Medicina. 44, 1 (abr. 2022), 99–113. DOI:https://doi.org/10.56050/01205498.1665.
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