Researchers identify breakthrough in hepatitis C virus infection
From: An Metet (anmetet_at_freedom.gmsociety.org)
Date: 10/16/04
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Date: Sat, 16 Oct 2004 07:49:42 -0400
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Researchers have made a significant advance in the understanding of the
hepatitis C virus (HCV) by identifying new genetic factors associated with
clearing the virus spontaneously without the necessity for additional
treatment. Their findings are set out in a paper published in Science magazine
today (6 August 2004).
Hepatitis C virus infects the liver and leads to serious permanent liver
damage. The infection affects about 170 million people worldwide and up to
500,000 people in the UK. Most people who come into contact with HCV contract
a long-term or chronic infection and, as a consequence, run a significant risk
of liver failure - necessitating liver transplantation - or liver cancer.
The new multi-centre study was jointly led by researchers from the University
of Southampton's School of Medicine, the National Genetics Institute, USA, and
the Johns Hopkins Hospital, USA. The findings demonstrate that natural killer
(NK) cells provide a central defence against HCV infection and that this
defence is mediated by specific inhibitory receptors expressed on NK cells and
the partners or ligands for these receptors on liver cells.
Over 1,000 patients from the UK and the USA were involved in the study, some of
whom were chronically infected and some who had cleared the virus. Researchers
identified a specific combination of genes in these individuals that directly
confers protection against HCV. The genes are killer cell immunoglobulin-like
receptors (KIR) and HLA class I genes and the favourable genes identified in
the study are KIR2DL3 and group 1 HLA-C alleles.
Dr Salim Khakoo of Southampton's Infection, Inflammation and Repair Division,
who co-authored the paper with Professor Mary Carrington of the National
Genetics Institute in the USA, commented: 'These favourable genes control the
functions of NK cells. NK cells are part of the innate immune system, a branch
of immunity that has not been well-studied in HCV to date.
'KIR2DL3 on NK cells binds group 1 HLA-C alleles on liver cells and our work
suggests that this interaction is more easily disturbed in HCV infection than
other
KIR-HLA interactions. Simply put, as an analogy to a car, it is like taking
your foot off the brake of the natural killer cell rather than pressing the
accelerator in order to get it going. This may then kick-start the rest of the
immune response to HCV'
By studying how people acquired HCV infection, the findings also suggest that
the amount of virus they received is an important factor. Data suggests that
the mechanism that researchers have discovered is more important in people
receiving lower infectious amounts of HCV. The protective effect of genes on
the virus was observed in Caucasians and African Americans with expected low
infectious doses of HCV, but not in those with high-dose exposure, in whom the
innate immune response is probably overwhelmed.
Dr Khakoo continued: 'We believe that this study is a significant advance in
the understanding of hepatitis C virus infection. There are other interesting
outcomes from our research. It implicates NK cells, and the innate immune
system in general, in clearing HCV infection and this has not previously been
clearly documented. It also suggests that the more NK cells of the protective
type that an individual has the more likely they are to clear HCV.'
The researchers believe that the findings could eventually lead to new
treatment strategies for HCV based around NK cells in general and KIR2DL3/HLA-C
in particular.
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