medigraphic.com
Órgano Oficial del Instituto Nacional de Pediatría

2020, Número S1

<< Anterior Siguiente >>

Acta Pediatr Mex 2020; 41 (S1)


Fisiopatología del daño multiorgánico en la infección por SARS-CoV-2

López-Pérez GT, Ramírez-Sandoval MLP, Torres-Altamirano MS

Idioma: Español
Referencias bibliográficas: 71
Paginas: 27-41
Archivo PDF: 738.41 Kb.


RESUMEN

La glucoproteína S del SARS-CoV-2 se une a la enzima convertidora de la angiotensina 2 (ACE2). El genoma del virus codifica cuatro proteínas estructurales esenciales: glucoproteína espiga, proteína de envoltura pequeña, proteínas matrices y proteína de nucleocápside. Se expresa más en hombres, quizá por el estradiol y la testosterona. En la viremia pasa de las glándulas salivales y membranas mucosas, especialmente nasal y laringe, a los pulmones y a otros órganos con los mismos receptores ACE2: corazón, hígado e, incluso, al sistema nervioso central; llega a los intestinos, lo que puede explicar los síntomas ; se detecta en las heces desde el inicio de la infección. La coexistencia de hipertensión arterial sistémica, diabetes mellitus o neumopatías crónicas, obesidad o tabaquismo, inmunodeficiencias y la senescencia son clave en la patogénesis viral. Cuando el sistema inmunológico es ineficiente en controlar efectivamente al virus en la fase aguda, puede evolucionar a un síndrome de activación de macrófagos que da pie a la temida tormenta de citocinas que pone al paciente en un estado crítico.
Entender la fisiopatogenia de la infección por SARS-CoV-2 es la piedra angular para establecer el diagnóstico oportuno e implementar el tratamiento adecuado y limitar la propagación del virus y, en última instancia, eliminarlo.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Haibo Zhang H, et al. Angiotensin‑converting enzyme 2(ACE2) as a SARS‑CoV‑2 receptor: molecular mechanisms and potential therapeutic target. Intensive Care Med 2020; 46: 586-90. https://doi.org/10.1007/s00134-020-05985-9

  2. Guo Y et al. The origin, transmission and clinical therapies on coronavirus disease 2019(COVID-19). outbreak – an update on the Status. Military Medical Research 2020; 7: 11. https:// doi.org/10.1186/s40779-020-00240-0)

  3. Soler MJ, et al. Enzima conversiva de la angiotensina 2 y su papel emergente en la regulación del sistema reninaangiotensina. Med Clin (Barc) 2008;131(6): 230-36.

  4. Malavazos A, et al. Targeting the adipose tissue in COVID 19. Obesity. doi: 10.1002 / oby.22844

  5. Cai G. Bulk and single-cell transcriptomics identify tobacco-use disparity in lung gene expression of ACE2, the receptor of 2019-nCov. Med Rxiv. 2020; doi:10.1101/2020.02.05.20020107 (preprint).

  6. Wang JM, et al. the potential for antibody-dependent enhancement of SARS-CoV-2 Infection: Translational Implications for Vaccine Development. Journal of Clinical and Translational Science 2020. doi:10.1017/cts.2020.39

  7. Watkins J. Preventingacovid-19 pandemics. BMJ 2020; 368. doi: https://doi.org/10.1136/bmj.m810

  8. Landazuri P, et al. Diferencias entre los sexos en la actividad de la enzima conversora de la angiotensina y en la presión arterial en niños: un estudio observacional. Arq Bras Cardiol 2008; 91(6):.17-23.

  9. Bouman, A, et al. Sex hormones and the immune response in humans. Human Reproduction Update 2005; 11(4), 411- 23. https://doi.org/10.1093/humupd/dmi008

  10. Zhang H, et al. Angiotensin converting enzyme 2 (ACE2) as a SARS-CoV2 receptor: molecular mechanisms and potential therapeutic target. Intensive Care Med 2020: 46: 586-90. https://doi.org/10.1007/s00134-020-05985-9

  11. Channappanavar R, et al. T cell-mediated immune response to respiratory coronaviruses. Immunol Res. 2014; 59:118-28.

  12. Cervantes B, et al. Type I IFN-mediated protection of macrophages and dendritic cells secures control of murine coronavirus infection. J Immunol. 2009; 182: 1099-106.

  13. Cameron MJ, et al. Interferon-mediated immunopathological events are associated with atypical innate and adaptive immune responses in patients with severe acute respiratory syndrome. J Virol. 2007; 81: 8692-706.

  14. Fink SL, et al. Apoptosis, pyroptosis, and necrosis: mechanistic description of dead and dying eukaryotic cells. Infect Immun. 2005; 73: 1907-16.

  15. Mali SN, et al. The rise of new coronavirus infection (COVID-19): A recent update and potential therapeutic candidates. EJMO. 2020; 4 (1):35-41.

  16. Xu Z, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Medicin. 2020; 8 :420-22. https://doi.org/10.1016/ S2213-2600(20)30076-X

  17. Bonanad C, et al. Coronavirus: the geriatric emergency of 2020. Joint document of the Section on Geriatric Cardiology of the Spanish Society of Cardiology and the Spanish Society of Geriatrics and Gerontology. Rev Esp Cardiol (English Edition (2020). https://doi.org/10.1016/j. rec.2020.05.001

  18. Kam KQ–, et al. A well infant with coronavirus disease 2019 (COVID-19) with high viral load. –Clin Infect Dis. 2020;ciaa201. doi:10.1093/cid/ciaa201

  19. Dong Y, et al. Epidemiological characteristics of 2143 pediatric patients with 2019 coronavirus disease in China. Pediatrics 2020 Mar 16. pii: e20200702. doi: 10.1542/ peds.2020-0702.

  20. Gu J, et al. Multiple organ infection and the pathogenesis of SARS. J Exp Medicin. 2005; 202: 415-24.

  21. Cheung CY, et al. Cytokine responses in severe acute respiratory syndrome coronavirus-infected macrophages in vitro: Possible relevance to pathogenesis. J Virol. 2005; 79: 7819-26. DOI: 10.1128/JVI.79.12.7819-7826.2005

  22. Yilla M, et al. SARS-coronavirus replication in human peripheral monocytes-macrophages. Virus Res. 2005; 107: 93-101.

  23. Faraha GA, et al. Increased expression of CD8 marker on T-cells in COVID-19 patients. Blood Cells Mol Dis. 2020; 83:102437. doi: 10.1016/j.bcmd.2020.102437.

  24. García-Salido A. Revisión narrativa sobre la respuesta inmunitaria frente a coronavirus: descripción general, aplicabilidad para Sars-Cov2 e implicaciones terapéuticas. Anales de Pediatría (2020). https://doi.org/10.1016/j. anpedi.2020.04.

  25. Geng Li, et al. Coronavirus infections and immune responses. J Med Virol. 2020; 92:424-32. https://doi. org/10.1002/jmv.25685

  26. Wu D, et al. TH17 responses in cytokine storm of COVID-19: An emerging target of JAK2 inhibitor Fedratinib. Journal of Microbiology, Immunology and Infection. https://doi. org/10.1016/j.jmii.2020.03.005

  27. Maloir Q, et al. Acute respiratory distress revealing antisynthetase syndrome. Rev Med Liege. 2018; 73(7‐8): 370‐75.

  28. Ow Ng, et al. Memory T cell responses targeting the SARS coronavirus persist up to 11 years post‐infection. Vaccine. 2016; 34(17):2008‐2014.

  29. Zhao J, et al. Antibody responses to SARS-CoV-2 in patients of novel coronavirus disease 2019, Clinical Infectious Diseases. 2020, ciaa344. https://doi.org/10.1093/cid/ciaa344

  30. Xiao T, et al. Profile of specific antibodies to SARS-CoV-2: The First Report. J Infection 2020. doi: https://doi. org/10.1016/j.jinf.2020.03.012)

  31. Ho MS, et al. Neutralizing Antibody Response and SARS Severity. Emerg Infect Dis. 2005; 11: 1730-37.

  32. Lu R, et al. Genomic characterization and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet 2020; 20:30251-58. pii: S0140-6736.

  33. Chen IY, et al. Severe acute respiratory syndrome coronavirus Viroporin 3a Activates the NLRP3 Inflammasome. Front Microbiol. 2019;10: 50. doi: 10.3389/fmicb.2019.00050. eCollection 2019.

  34. Metha P, et al. COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet. 2010; 395: 1033- 34. https://doi.org/10.1016/ S0140-6736(20)30630-9

  35. Chan JF, et al. A familial cluster of pneumonia associated with the 2019 novel coronavirus indicating person-toperson transmission: a study of a family cluster Lancet. 2020; 395: 514-23.

  36. Moore JB, et al. Cytokine release syndrome in severe COVID-19 Science 2020;368:473-474 DOI: 10.1126/science. abb8925

  37. Pacha O, et al. COVID-19: a case for inhibiting IL-17?. Nat Rev Immunol (2020). https://doi.org/10.1038/s41577- 020-0328-z

  38. Respuesta inmune trombótica asociada a COVID-19 Modificado de (RITAC) Gauna M https://fundacionio.com/ wp-content/uploads/2020/04/Si%CC%81ndrome RITAC. pdf.pdf.pdf.pdf.pdf.pdf.pdf

  39. McGonagle D, et al. Interleukin-6 use in COVID-19 pneumonia related macrophage activation syndrome Autoimmunity Reviews 2020. https://doi.org/10.1016/j. autrev.2020.102537

  40. Wang WK, et al. Detection of SARS-associated coronavirus in throat wash and saliva in early diagnosis. Emerg Infect Dis. 2004;10 (7): 1213-19.

  41. Sims AC, et al. Severe acute respiratory syndrome coronavirus infection of human ciliated airway epithelia: Role of ciliated cells in viral spread in the conducting airways of the lungs. J Virol. 2005; 79: 155111-24.

  42. Ling Lin, et al. Hypothesis for potential pathogenesis of SARS-CoV-2 infection–a review of immune changes in patients with viral pneumonia. Emerging Microbes & Infections 2020; 9: 727-32. doi: 10.1080/22221751.2020.1746199

  43. Zhou F, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort Study. Lancet 2020; 395: 1054-62.

  44. Liao M, et al. The landscape of lung bronchoalveolar immune cells in COVID-19 revealed by single-cell RNA sequencing. Preimpression en medRxiv 2020. https://doi. org/10.1101/2020.02.23.20026690.

  45. Zhou Y, et al. Pathogenic T cells and inflammatory monocytes incite inflammatory storm in severe COVID-19 patients. Natl Sci Rev 2020. https://doi.org/10.1093/nsr/ nwaa041.

  46. Carolyn M, et al. MD1 Viral Pathogens and Acute Lung Injury: Investigations Inspired by the SARS Epidemic and the 2009 H1N1 Influenza. Semin Respir Crit Care Med. 2013; 34:475-86.

  47. Gu J, et al. COVID-19: COVID-19: Gastrointestinal Manifestations and Potential Fecal-Oral Transmission. Gastroenterology 2020 Mar 3. doi: 10.1053/j.gastro.2020.02.054.

  48. Xiao F, et al. Evidence for gastrointestinal infection of SARS-CoV-2. Gastroenterology. 3 Mar 2020: S0016- 5085(20)30282-1. doi: 10.1053/j.gastro.2020.02.055. PMID: 3214277.

  49. Yeo C, et al. Enteric involvement of coronaviruses: is faecal–oral transmission of SARS CoV-2 possible? Lancet Gastroenterol Hepatol. 2020. doi: 10.1016/S2468- 1253(20)30048-0. published online Feb 19

  50. Chai X, et al. Specific ACE2 expression in cholangiocytes may cause liver damage after 2019-nCoV infection. bioRxiv. 2020 doi: 10.1101/2020.02.03.931766. published online Feb 4. (preprint)

  51. Xu Z, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med. 2020 doi: 10.1016/S2213-2600(20)30076-X. published online

  52. Zhang C, Shi L, Wang FS. Liver injury in COVID-19: Management and challenges. Lancet Gastroenterol Hepatol 2020 Mar 4. doi: 10.1016/S2468-1253(20)30057-1.

  53. Kang Y, Chen T,Mui D, et al. Heart Epub ahead of print: [please include Day Month Year]. doi:10.1136/heartjnl- 2020-317056

  54. Guo T, Fan Y, Chen M, et al. Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19). JAMA Cardiol 2020.

  55. Sugiura M, Hiraoka K, Ohkawa S, et al. A clinicopathological study on cardiac lesions in 64 cases of disseminated intravascular coagulation. Jpn Heart J. 1977; 18:57-69.

  56. Xu D, et al. Identification of a Potential Mechanism of Acute Kidney Injury During theCOVID-19 Outbreak: A Study Bas don Single Cell Transcriptome Analysis Preprints 2020 2020020331.

  57. Cheng Y, et al. Kidney impairment is associated with inhospital death of COVID-1 patients med Rxiv. 2020 https://doi. org/10.1101/2020.02.18.20023242.

  58. Wang T, et al. Comorbidities and multi-organ injuries in the treatment of COVID-19. Lancet 2020; 395:10228. https:// doi.org/101016/S0140- 6736(20)30558-4

  59. Diao B, et al. Human kidney is a target for novel severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) infection medRxiv 2020 Doi: https://doi. org/10.1101/2020.03.04.20031120

  60. Wu Y, et al. Nervous system involvement after infection with COVID-19 and other coronaviruses. Brain Behav Immun 2020; Mar 30. [Epub ahead of print].

  61. Bohmwald K, et al. Neurologic alterations due to respiratory virus infections. Front Cell Neurosci. 2018; 12: 386.

  62. Li Y, et al. Acute cerebrovascular disease following COVID-19: a single, retrospective, observational study. Lancet 2020. http://dx.doi.org/10.2139/ssrn.3550025. [03.03.2020].

  63. Baig AM, et al. Evidence of the COVID-19 virus targeting the CNS: Tissue distribution, host-virus interaction, and proposed neurotropic mechanisms. ACS Chem Neurosci 2020; 11: 995-8.

  64. Mannan BA, et al. Evidence of the COVID-19 virus targeting the CNS: Tissue distribution, host−virus interaction, and proposed neurotropic mechanisms. ACS Chem Neurosci 2020; 11: 995-98.

  65. Lechien JR, et al. Olfactory and gustatory dysfunctions as a clinical presentation of mild-to-moderate forms of the coronavirus disease (COVID-19): a multicenter European study. Eur Arch Otorhinolaryngol 2020. https://doi. org/10.1007/s00405-020-05999-5

  66. Xinhua.net. Beijing hospital confirms nervous system infections by novel coronavirus. URL: http://www. xinhuanet.com/english/2020-03/05/c_138846529.htm. [05.03.2020].

  67. Poyiadji N, et al. COVID-19-associated acute hemorrhagic necrotizing encephalopathy: CT and MRI features. Radiology 2020; Mar 31. [Epub ahead of print].

  68. Li YC, et al. The neuroinvasive potential of SARS-CoV2 may play a role in the respiratory failure of COVID-19 patients. J Med Virol 2020; Feb 27. [Epub ahead of print].

  69. Zhao H, et al. Guillain-Barré syndrome associated with SARS-CoV-2 infection: causality or coincidence? Lancet Neurol 2020; Apr 1. [Epub ahead of print]

  70. Carod-Artal FJ. Complicaciones neurológicas por coronavirus y COVID-19. Rev Neurol 2020;70 (09):311-322 doi: 10.33588/rn.7009.2020179

  71. Liu W, et al. COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism Chem Rxiv 2020. https://doi.org/10.26434/ chemrxiv.11938173.v7




2020     |     www.medigraphic.com