Publicado

2009-04-01

Un modelo del mecanismo de entrada de los rotavirus a la célular hospedera

A model for the mechanism of entry of rotaviruses into the host cell

Palabras clave:

rotavirus, integrinas, proteína de choque térmico, disulfuros, isomerasas. (es)
rotavirus, integrins, heat-shock cognate protein 70, disulfides, isomerases. (en)

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Autores/as

  • Orlando Acosta Losada Departamento de Ciencias Fisiológicas, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá.
  • Martha N. Calderón Departamento de Química, Facultad de Ciencias, Universidad Nacional de Colombia, Bogotá.
  • Liz P. Moreno Sección de Fisiología y Producción de Cultivos, Facultad de Agronomía, Universidad Nacional de Colombia, Bogotá.
  • Carlos Arturo Guerrero Fonseca Departamento de Ciencias Fisiológicas, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá.

Antecedentes. La infección rotaviral es causa principal de gastroenteritis aguda severa en niños menores de cinco años. La capa protéica externa de la partícula viral está implicada en las interacciones iniciales virus-superficie celular. El mecanismo rotaviral de unión y entrada a la célula parece ser un proceso de múltiples pasos donde las proteínas rotavirales VP4 y VP7 interaccionan con diferentes moléculas de la superficie celular.

Objetivo. Proponer un mecanismo de entrada de rotavirus a la célula que incorpore la actividad de la proteína disulfuro isomerasa (PDI).

Material y métodos. Utilizando bases de datos electrónicas, se realizó una búsqueda de literatura original y de revisión publicada entre 1990 y 2009 sobre moléculas de la superficie rotaviral o celular participantes en el proceso de entrada del virus. El análisis de los resultados enfatizó las bases moleculares y celulares de las interacciones temporo-espaciales de las proteínas virales y las moléculas de unión/receptoras de la célula.

Resultados. Se encontró fundamentos moleculares y celulares para incorporar la actividad de PDI a un mecanismo coherente de vías secuenciales o alternativas previas a la penetración viral.

Se propone un mecanismo en que interaccionan las proteínas virales VP4, VP6 y VP7 con las moléculas de la superficie celular ácido siálico, integrinas, Hsc70 y PDI en un proceso endocítico caveola/"raft"-dependiente, caveolina/clatrina-independiente, dinamina-dependiente y sensible a depleción de colesterol.

Conclusión. Se amplía el concepto de múltiples pasos en el proceso de entrada de rotavirus, donde la participación de PDI podría ser un blanco potencial de la acción de inhibidores de grupos tiol/disulfuro.

Background. Rotavirus infection is the leading single cause of severe acute gastroenteritis in children under five years of age. The outermost layer of the triple-layered protein capsid of the non-enveloped virus particle has been involved in initial interactions between virus and host cell surface. The rotavirus mechanism for cell attachment and entry seems to be a multistep process in which outermost layer virus proteins VP4 and VP7 interact with different cell surface molecules.

Objective. To propose a mechanism for rotavirus entry to the host cell incorporating the protein disulfide isomerase (PDI) activity.

Materials and methods. A systematic search for original and review literature published from 1990 to 2009 on rotavirus and cell surface molecules participating in virus entry process was conducted through the use of electronic Databases. The analysis of the published results emphasized the molecular and cellular bases of time and space interactions between virus proteins and cell surface attachment and receptor molecules.

Results. We found molecular and cellular bases for incorporating PDI within a coherent mechanism involving sequential or alternative paths previous to virus penetration. A mechanism is proposed in which virus proteins VP4, VP6 and VP7, and cell surface sialico acid, integrins, Hsc70, and PDI interact as part of a caveola/ raft-mediated endocytic process that is characterized by its caveolin and clathrin independence, dynamin dependence, and sensitivity to cholesterol depletion.

Conclusions. The rotavirus entry mechanism appears to be a complex multistep process in which the path using PDI could be a potential target for antiviral agents reacting with thiol/disulfide groups.

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Cómo citar

APA

Acosta Losada, O., Calderón, M. N., Moreno, L. P. y Guerrero Fonseca, C. A. (2009). Un modelo del mecanismo de entrada de los rotavirus a la célular hospedera. Revista de la Facultad de Medicina, 57(2), 124–148. https://revistas.unal.edu.co/index.php/revfacmed/article/view/14438

ACM

[1]
Acosta Losada, O., Calderón, M.N., Moreno, L.P. y Guerrero Fonseca, C.A. 2009. Un modelo del mecanismo de entrada de los rotavirus a la célular hospedera. Revista de la Facultad de Medicina. 57, 2 (abr. 2009), 124–148.

ACS

(1)
Acosta Losada, O.; Calderón, M. N.; Moreno, L. P.; Guerrero Fonseca, C. A. Un modelo del mecanismo de entrada de los rotavirus a la célular hospedera. Rev. Fac. Med. 2009, 57, 124-148.

ABNT

ACOSTA LOSADA, O.; CALDERÓN, M. N.; MORENO, L. P.; GUERRERO FONSECA, C. A. Un modelo del mecanismo de entrada de los rotavirus a la célular hospedera. Revista de la Facultad de Medicina, [S. l.], v. 57, n. 2, p. 124–148, 2009. Disponível em: https://revistas.unal.edu.co/index.php/revfacmed/article/view/14438. Acesso em: 28 mar. 2024.

Chicago

Acosta Losada, Orlando, Martha N. Calderón, Liz P. Moreno, y Carlos Arturo Guerrero Fonseca. 2009. «Un modelo del mecanismo de entrada de los rotavirus a la célular hospedera». Revista De La Facultad De Medicina 57 (2):124-48. https://revistas.unal.edu.co/index.php/revfacmed/article/view/14438.

Harvard

Acosta Losada, O., Calderón, M. N., Moreno, L. P. y Guerrero Fonseca, C. A. (2009) «Un modelo del mecanismo de entrada de los rotavirus a la célular hospedera», Revista de la Facultad de Medicina, 57(2), pp. 124–148. Disponible en: https://revistas.unal.edu.co/index.php/revfacmed/article/view/14438 (Accedido: 28 marzo 2024).

IEEE

[1]
O. Acosta Losada, M. N. Calderón, L. P. Moreno, y C. A. Guerrero Fonseca, «Un modelo del mecanismo de entrada de los rotavirus a la célular hospedera», Rev. Fac. Med., vol. 57, n.º 2, pp. 124–148, abr. 2009.

MLA

Acosta Losada, O., M. N. Calderón, L. P. Moreno, y C. A. Guerrero Fonseca. «Un modelo del mecanismo de entrada de los rotavirus a la célular hospedera». Revista de la Facultad de Medicina, vol. 57, n.º 2, abril de 2009, pp. 124-48, https://revistas.unal.edu.co/index.php/revfacmed/article/view/14438.

Turabian

Acosta Losada, Orlando, Martha N. Calderón, Liz P. Moreno, y Carlos Arturo Guerrero Fonseca. «Un modelo del mecanismo de entrada de los rotavirus a la célular hospedera». Revista de la Facultad de Medicina 57, no. 2 (abril 1, 2009): 124–148. Accedido marzo 28, 2024. https://revistas.unal.edu.co/index.php/revfacmed/article/view/14438.

Vancouver

1.
Acosta Losada O, Calderón MN, Moreno LP, Guerrero Fonseca CA. Un modelo del mecanismo de entrada de los rotavirus a la célular hospedera. Rev. Fac. Med. [Internet]. 1 de abril de 2009 [citado 28 de marzo de 2024];57(2):124-48. Disponible en: https://revistas.unal.edu.co/index.php/revfacmed/article/view/14438

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