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1.
J Virol ; 93(1)2019 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-30333168

RESUMO

Type I interferon (IFN) inhibits viruses by inducing the expression of antiviral proteins. The IFN-induced myxovirus resistance B (MxB) protein has been reported to inhibit a limited number of viruses, including HIV-1 and herpesviruses, but its antiviral coverage remains to be explored further. Here we show that MxB interferes with RNA replication of hepatitis C virus (HCV) and significantly inhibits viral replication in a cyclophilin A (CypA)-dependent manner. Our data further show that MxB interacts with the HCV protein NS5A, thereby impairing NS5A interaction with CypA and NS5A localization to the endoplasmic reticulum, two events essential for HCV RNA replication. Interestingly, we found that MxB significantly inhibits two additional CypA-dependent viruses of the Flaviviridae family, namely, Japanese encephalitis virus and dengue virus, suggesting a potential link between virus dependence on CypA and virus susceptibility to MxB inhibition. Collectively, these data have identified MxB as a key factor behind IFN-mediated suppression of HCV infection, and they suggest that other CypA-dependent viruses may also be subjected to MxB restriction.IMPORTANCE Viruses of the Flaviviridae family cause major illness and death around the world and thus pose a great threat to human health. Here we show that IFN-inducible MxB restricts several members of the Flaviviridae, including HCV, Japanese encephalitis virus, and dengue virus. This finding not only suggests an active role of MxB in combating these major pathogenic human viruses but also significantly expands the antiviral spectrum of MxB. Our study further strengthens the link between virus dependence on CypA and susceptibility to MxB restriction and also suggests that MxB may employ a common mechanism to inhibit different viruses. Elucidating the antiviral functions of MxB advances our understanding of IFN-mediated host antiviral defense and may open new avenues to the development of novel antiviral therapeutics.


Assuntos
Ciclofilina A/farmacologia , Hepacivirus/fisiologia , Interferons/farmacologia , Proteínas de Resistência a Myxovirus/metabolismo , Proteínas não Estruturais Virais/metabolismo , Replicação Viral/efeitos dos fármacos , Animais , Linhagem Celular , Chlorocebus aethiops , Ciclosporina/farmacologia , Retículo Endoplasmático/metabolismo , Técnicas de Silenciamento de Genes , Células HEK293 , Hepacivirus/efeitos dos fármacos , Humanos , Proteínas de Resistência a Myxovirus/genética , Ligação Proteica/efeitos dos fármacos , Células Vero
2.
World J Gastroenterol ; 22(4): 1477-86, 2016 Jan 28.
Artigo em Inglês | MEDLINE | ID: mdl-26819515

RESUMO

Host-hepatitis C virus (HCV) interactions have both informed fundamental concepts of viral replication and pathogenesis and provided novel insights into host cell biology. These findings are illustrated by the recent discovery of host-encoded factors that restrict HCV infection. In this review, we briefly discuss these restriction factors in different steps of HCV infection. In each case, we discuss how these restriction factors were identified, the mechanisms by which they inhibit HCV infection and their potential contribution to viral pathogenesis.


Assuntos
Hepacivirus/patogenicidade , Hepatite C/virologia , Animais , Progressão da Doença , Hepacivirus/crescimento & desenvolvimento , Hepacivirus/metabolismo , Hepatite C/metabolismo , Interações Hospedeiro-Patógeno , Humanos , Transdução de Sinais , Internalização do Vírus , Replicação Viral
3.
Bing Du Xue Bao ; 30(1): 91-7, 2014 Jan.
Artigo em Chinês | MEDLINE | ID: mdl-24772905

RESUMO

Lipid droplets are the main storage organelles for intracellular neutral lipids. Many recent studies have found that lipid droplets are closely related to hepatitis C virus (HCV). Lipid droplets play important roles in the multiple processes of HCV life cycle, such as infection, replication, assembly, and secretion. In this review, we summarize the recent research progress in the roles of lipid droplets in HCV life cycle.


Assuntos
Hepacivirus/fisiologia , Metabolismo dos Lipídeos , Organelas/virologia , Animais , Hepacivirus/metabolismo , Interações Hospedeiro-Patógeno , Humanos , Proteínas Virais/metabolismo
4.
Bing Du Xue Bao ; 30(5): 594-8, 2014 Sep.
Artigo em Chinês | MEDLINE | ID: mdl-25562972

RESUMO

Infection with the hepatitis C virus (HCV) frequently causes chronic viral hepatitis, a major risk factor for the development of cirrhosis and hepatocellular carcinoma or primary liver cancer. The origin of the HCV remains obscure because no closely related animal virus homolog has been identified. Also, efforts to understand the pathogenesis of the HCV have been hampered by the absence of small animal models for this human disease. Since 2011, with application of new sequencing technologies, various non-primate HCV homologs have been identified that will play an important part in understanding the origin and evolution of HCV, as well as establishment of related animal models.


Assuntos
Hepacivirus/genética , Hepatite C/virologia , Animais , Modelos Animais de Doenças , Hepatite C/etiologia , Humanos
5.
Bing Du Xue Bao ; 28(2): 185-9, 2012 Mar.
Artigo em Chinês | MEDLINE | ID: mdl-22519182

RESUMO

COPI is a protein complex that transports vesicles from the Golgi complex back to endoplasmic reticulum. Many viruses such as RNA viruses, DNA viruses and retroviruses, hijack or adapt COPI related proteins including coatomer, ARF1 and GBF1 for their own benefits. Here, we summarize the current progress of the roles of COPI related proteins in virus replication.


Assuntos
Complexo I de Proteína do Envoltório/metabolismo , Viroses/metabolismo , Replicação Viral , Animais , Complexo I de Proteína do Envoltório/genética , Humanos , Viroses/genética , Viroses/virologia , Fenômenos Fisiológicos Virais
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