Hepatitis C virus entry into the hepatocyte

Belouzard, Sandrine; Cocquerel, Laurence; Dubuisson, Jean

doi:10.2478/s11535-011-0076-y

Cited by 9 publications

(13 citation statements)

References 84 publications

(124 reference statements)

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“…At least, four cellular entry factors and two specific receptors are required for a successful virus entry (Figure 4 ). Since many interactions should take place, the binding to the cell surface is a relatively slow process which should be well coordinated[ 135 - 141 ]. The initiation of HCV entry seems to be similar to that of many other viruses, that utilize for attachment the glycosaminoglycans (GAGs)[ 141 ].…”

Section: Hcv Life Cyclementioning

confidence: 99%

“…Since many interactions should take place, the binding to the cell surface is a relatively slow process which should be well coordinated[ 135 - 141 ]. The initiation of HCV entry seems to be similar to that of many other viruses, that utilize for attachment the glycosaminoglycans (GAGs)[ 141 ]. Earlier, it was proposed that E1 and E2 are involved in these interactions[ 141 ].…”

Section: Hcv Life Cyclementioning

confidence: 99%

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Hepatitis C virus: Morphogenesis, infection and therapy

Morozov¹,

Lagaye²

2018

WJH

129

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Hepatitis C virus (HCV) is a major cause of liver diseases including liver cirrhosis and hepatocellular carcinoma. Approximately 3% of the world population is infected with HCV. Thus, HCV infection is considered a public healthy challenge. It is worth mentioning, that the HCV prevalence is dependent on the countries with infection rates around 20% in high endemic countries. The review summarizes recent data on HCV molecular biology, the physiopathology of infection (immune-mediated liver damage, liver fibrosis and lipid metabolism), virus diagnostic and treatment. In addition, currently available in vitro, ex vivo and animal models to study the virus life cycle, virus pathogenesis and therapy are described. Understanding of both host and viral factors may in the future lead to creation of new approaches in generation of an efficient therapeutic vaccine.

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Section: Hcv Life Cyclementioning

confidence: 99%

Section: Hcv Life Cyclementioning

confidence: 99%

Hepatitis C virus: Morphogenesis, infection and therapy

Morozov¹,

Lagaye²

2018

WJH

129

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“…Hepatitis C virus entry is a very complex process, which involves a series of host entry factors [37]. On the viral particle, envelope glycoproteins E1E2 play a major role during entry.…”

Section: Hepatitis C Virusmentioning

confidence: 99%

Hepatitis C Virus and Natural Compounds: A New Antiviral Approach?

Calland

Dubuisson

Rouillé

et al. 2012

Viruses

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124

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Hepatitis C is a major global health burden with an estimated 160 million infected individuals worldwide. This long-term disease evolves slowly, often leading to chronicity and potentially to liver failure. There is no anti-HCV vaccine, and, until recently, the only treatment available, based on pegylated interferon and ribavirin, was partially effective, and had considerable side effects. With recent advances in the understanding of the HCV life cycle, the development of promising direct acting antivirals (DAAs) has been achieved. Their use in combination with the current treatment has led to encouraging results for HCV genotype 1 patients. However, this therapy is quite expensive and will probably not be accessible for all patients worldwide. For this reason, constant efforts are being made to identify new antiviral molecules. Recent reports about natural compounds highlight their antiviral activity against HCV. Here, we aim to review the natural molecules that interfere with the HCV life cycle and discuss their potential use in HCV therapy.

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“…HCV entry is currently viewed as a complex multistep process, because a series of specific cellular entry factors have been shown to be essential in the early steps of the HCV life cycle. 7 These molecules include the scavenger receptor class B type 1 (SRB1), the tetraspanin CD81, tight-junction proteins claudin 1 (CLDN1) and occludin (OCLN), and receptor tyrosine kinase-like epidermal growth factor receptor. After its interaction with entry factors at the cell surface, HCV particle is internalized by clathrinmediated endocytosis.…”

mentioning

confidence: 99%

The antimalarial ferroquine is an inhibitor of hepatitis C virus

et al. 2013

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Hepatitis C virus (HCV) is a major cause of chronic liver disease. Despite recent success in improving anti-HCV therapy, additional progress is still needed to develop cheaper and interferon (IFN)-free treatments. Here, we report that ferroquine (FQ), an antimalarial ferrocenic analog of chloroquine, is a novel inhibitor of HCV. FQ potently inhibited HCV infection of hepatoma cell lines by affecting an early step of the viral life cycle. The antiviral activity of FQ on HCV entry was confirmed with pseudoparticles expressing HCV envelope glycoproteins E1 and E2 from six different genotypes. In addition to its effect on HCV entry, FQ also inhibited HCV RNA replication, albeit at a higher concentration. We also showed that FQ has no effect on viral assembly and virion secretion. Using a binding assay at 48C, we showed that FQ does not prevent attachment of the virus to the cell surface. Furthermore, virus internalization was not affected by FQ, whereas the fusion process was impaired in the presence of FQ as shown in a cell-cell fusion assay. Finally, virus with resistance to FQ was selected by sequential passage in the presence of the drug, and resistance was shown to be conferred by a single mutation in E1 glycoprotein (S327A). By inhibiting cell-free virus transmission using a neutralizing antibody, we also showed that FQ inhibits HCV cell-to-cell spread between neighboring cells. Combinations of FQ with IFN, or an inhibitor of HCV NS3/4A protease, also resulted in additive to synergistic activity. Conclusion: FQ is a novel, interesting anti-HCV molecule that could be used in combination with other direct-acting antivirals. (HEPATOLOGY 2013;58:86-97) H epatitis C virus (HCV) is a major cause of chronic liver disease (CLD). Approximately 160 million individuals suffer from chronic hepatitis C, putting them at risk to develop cirrhosis and hepatocellular carcinoma. 1 Recent improvements in the standard-of-care therapy, currently a combination of pegylated interferon (IFN) alpha (Peg-IFN-a), ribavirin (RBV), and one of two drugs interfering with the virally encoded NS3/4A protease, have raised the hope that HCV infection can be managed efficiently in countries with adequate medical infrastructure. 2 However, the current mode of treatment is not equally effective for all HCV genotypes and significant side effects are still observed. Efforts are currently being

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Hepatitis C virus entry into the hepatocyte

Cited by 9 publications

References 84 publications

Hepatitis C virus: Morphogenesis, infection and therapy

Hepatitis C virus: Morphogenesis, infection and therapy

Hepatitis C Virus and Natural Compounds: A New Antiviral Approach?

The antimalarial ferroquine is an inhibitor of hepatitis C virus

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