Survay about medical research

Department of Hygiene,
Epidemiology and Medical
Statistics, Medical School,
University of Athens, Athens,
Greece, 2 Centre for
Macroevolution and
Macroecology, Research School
of Biology, Australian National
University, Canberra, Australia, 3
Department of Biology, The
Pennsylvania State University,
University Park, Pennsylvania,
United States of America, 4
Department of Zoology,
University of Oxford, Oxford,
United Kingdom, 5 Department
of Haematology, School of
Clinical Medicine, University of
Cambridge, Cambridge, United
Kingdom
Abstract Top
Background
Hepatitis C virus (HCV) is
estimated to affect 130 –180
million people worldwide.
Although its origin is unknown,
patterns of viral diversity suggest
that HCV genotype 1 probably
originated from West Africa.
Previous attempts to estimate the
spatiotemporal parameters of
the virus, both globally and
regionally, have suggested that
epidemic HCV transmission
began in 1900 and grew steadily
until the late 1980s. However,
epidemiological data suggest that
the expansion of HCV may have
occurred after the Second World
War. The aim of our study was
to elucidate the timescale and
route of the global spread of
HCV.
Methods and Findings
We show that the rarely
sequenced HCV region
(E2P7NS2) is more informative
for molecular epidemiology
studies than the more commonly
used NS5B region. We applied
phylodynamic methods to a
substantial set of new E2P7NS2
and NS5B sequences, together
with all available global HCV
sequences with information in
both of these genomic regions,
in order to estimate the
timescale and nature of the
global expansion of the most
prevalent HCV subtypes, 1a and
1b. We showed that transmission
of subtypes 1a and 1b
“exploded” between 1940 and
1980, with the spread of 1b
preceding that of 1a by at least
16 y (95% confidence interval 15–
17). Phylogeographic analysis of
all available NS5B sequences
suggests that HCV subtypes 1a
and 1b disseminated from the
developed world to the
developing countries.
Conclusions
The evolutionary rate of HCV
appears faster than previously
suggested. The global spread of
HCV coincided with the
widespread use of transfused
blood and blood products and
with the expansion of
intravenous drug use but slowed
prior to the wide implementation
of anti-HCV screening.
Differences in the transmission
routes associated with subtypes
1a and 1b provide an
explanation of the relatively
earlier expansion of 1b. Our data
show that the most plausible
route of the HCV dispersal was
from developed countries to the
developing world.