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1.
Virus Res ; 261: 1-8, 2019 02.
Artigo em Inglês | MEDLINE | ID: mdl-30543874

RESUMO

Cellular proteins have been identified to participate in calicivirus replication in association with viral proteins and/or viral RNAs. By mass spectrometry from pull-down assays, we identified several cellular proteins bound to the feline calicivirus (FCV) genomic RNA; among them the lipid raft-associated scaffold protein Annexin (Anx) A2. AnxA2 colocalizes with FCV NS6/7 protein and with the dsRNA in infected cells; moreover, it was found associated with the viral RNA in the membrane fraction corresponding to the replication complexes (RCs), suggesting its role during FCV replication. AnxA2-knockdown from CrFK cells prior to infection with FCV caused a delay in the cytopathic effect, a strong reduction of viral non-structural proteins and dsRNA production, and a decrease of FCV yield in both cell-associated and supernatant fractions. Taken together, these results indicate that AnxA2 associates to the genomic RNA of FCV and is required for an efficient FCV replication.


Assuntos
Anexina A2/metabolismo , Calicivirus Felino/fisiologia , Interações Hospedeiro-Patógeno , RNA Viral/metabolismo , Replicação Viral , Animais , Calicivirus Felino/crescimento & desenvolvimento , Gatos , Linhagem Celular , Efeito Citopatogênico Viral , Espectrometria de Massas , Ligação Proteica , RNA de Cadeia Dupla/metabolismo , Carga Viral , Proteínas não Estruturais Virais/metabolismo
2.
Virus Res ; 198: 44-52, 2015 Feb 16.
Artigo em Inglês | MEDLINE | ID: mdl-25599602

RESUMO

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.


Assuntos
Apoptose/efeitos da radiação , Calicivirus Felino/fisiologia , Calicivirus Felino/efeitos da radiação , Temperatura Alta , Liberação de Vírus/efeitos da radiação , Animais , Caspase 3/metabolismo , Gatos , Linhagem Celular , Efeito Citopatogênico Viral
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