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Scientists Identify Protein Involved in HCV Infection
 

Researchers at The Rockefeller University in New York believe they have identified a
key protein necessary for the hepatitis C virus (HCV) to infect human cells. The protein,
claudin-1, supports “tight junctions,” which hold neighboring cells together and ensure
their structural integrity. These proteins are located in the body’s epithelial tissues, layers
of cells found on external and internal body surfaces. Claudin-1 is a protein that is
typically found in the liver.

Although it has already been established that two molecules – CD81 and SR-B1 – need to
be present on the surface of a cell for HCV to infect it, scientists have thought that at least
one other molecule must play a decisive role. Experiments on multiple human cell lines
using an HCV “pseudoparticle” (HIV particles modified to mimic authentic HCV)
showed that claudin-1 acts as a receptor and is critical in the virus’ ability to gain access
to cells. Additionally, investigators observed that in pseudoparticle cells lacking claudin-
1, HCV was not able to gain a foothold. “We did not see HCV enter any cell that did not
have claudin-1,” said Thomas von Hahn, PhD, postdoctoral associate in Rockefeller’s
Laboratory of Virology and Infectious Disease.

Although scientists recognize that there may be additional receptors that still need to be
identified, claudin-1 raises the hope that new, more effective HCV therapies could be
developed as a result. “Anti-HCV drugs currently under development are directed against
viral enzymes required for viral replication, to which the virus can readily evolve
resistance,” said Matthew Evans, PhD, postdoctoral associate in Rockefeller’s Laboratory
of Virology and Infectious Disease. “HCV may be less able to develop resistance to
drugs targeting receptors on the host cell.”

The study report, “Claudin-1 is a Hepatitis C Virus Co-Receptor Required for a Late Step
in Entry,” was published in the February 25, 2007 online version of the journal Nature.

Source: Rockefeller University news release dated February 26, 2007

 

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