title: Negative effect of heat shock on feline calicivirus release from infected cells is associated with the control of apoptosis.
abstract: FCV infection causes rapid cytopathic effects, and its replication results in the induction of apoptosis changes in cultured cells. It is well established that the survival of apoptotic cells can be enhanced by the expression of heat-shock proteins (Hsp) to prevent damage or facilitate recovery. Hsps can act as molecular chaperones, but they can also have anti-apoptotic roles by binding to apoptotic proteins and inhibiting the activation of caspases, the primary mediators of apoptosis. Because apoptosis occurs during FCV infection and heat shock (HS) treatment has a cytoprotective role due to the expression of Hsps, we studied the effect of the HS response to hyperthermia during FCV infection in cultured cells. We found that FCV infection does not inhibit the expression of Hsp70 induced by HS and that non-structural and structural protein synthesis was not modified during HS treatment. However, HS caused a delay in the appearance of a cytopathic effect in infected cells, as well as a reduction in the extracellular but not in the cell-associated viral yield. This antiviral effect of HS correlates with the inhibition of caspase-3 activation. Thus, the HS-induced reduction in virus production appeared to be associated with the control of apoptosis, supporting previous data that indicate that apoptosis is necessary for FCV release.
authors.affiliation: Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del IPN, México City, Mexico.
authors.forename: Cristal
authors.initials: C
authors.lastname: Alvarez-Sanchez
authors.affiliation: Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del IPN, México City, Mexico.
authors.forename: Clotilde
authors.initials: C
authors.lastname: Cancio-Lonches
authors.affiliation: Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del IPN, México City, Mexico.
authors.forename: José Eduardo
authors.initials: JE
authors.lastname: Mora-Heredia
authors.affiliation: Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del IPN, México City, Mexico.
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: Santos-Valencia
authors.affiliation: Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del IPN, México City, Mexico.
authors.forename: Oscar Salvador
authors.initials: OS
authors.lastname: Barrera-Vázquez
authors.affiliation: Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, México City, Mexico.
authors.forename: Martha
authors.initials: M
authors.lastname: Yocupicio-Monroy
authors.affiliation: Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del IPN, México City, Mexico. Electronic address: alonso@cinvestav.mx.
authors.forename: Ana Lorena
authors.initials: AL
authors.lastname: Gutiérrez-Escolano
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000528:radiation effects*; D017927:Calicivirus, Feline / Q000502:physiology* / Q000528:radiation effects*; D053148:Caspase 3 / Q000378:metabolism; D002415:Cats; D002460:Cell Line; D003588:Cytopathogenic Effect, Viral; D006358:Hot Temperature; D057074:Virus Release / Q000528:radiation effects*
chemical_list: D053148:Caspase 3
keywords: Apoptosis; Feline calicivirus; Heat shock