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Comment
. 2009 Aug 4;106(31):12567-8.
doi: 10.1073/pnas.0906760106. Epub 2009 Jul 28.

Plugging the holes in hepatitis C virus antiviral therapy

Affiliations
Comment

Plugging the holes in hepatitis C virus antiviral therapy

Stephen D C Griffin. Proc Natl Acad Sci U S A. .
No abstract available

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Conflict of interest statement

The author declares no conflict of interest.

Figures

Fig. 1.
Fig. 1.
Potential sites of action for p7 inhibitors in the HCV life cycle. p7 could function during multiple stages of HCV particle production and may also play a role during infection. As such, inhibitors could block HCV at multiple stages of the life cycle. At early stages (stage 1) p7 may interact with NS2 to promote efficient virion assembly. p7 channels in secretory vesicles can prevent their acidification (stage 2), which could protect viral glycoproteins from premature fusogenic change or alter vesicle trafficking during exocytosis. The effect of p7 inhibitors on virus entry suggests that the ion channel is incorporated into secreted virions (stage 3). After virus entry (stage 4; for simplicity, only the CD81 receptor is shown), endosome acidification (stage 5) induces fusogenic change in the viral glycoproteins and p7 potentially permits the passage of protons into the viral core, destabilizing the structure and promoting efficient uncoating (stage 6).

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