The Hepatitis C
virus
transmitted for
63 days after
the virus dried
when the
contents of
syringes and
surfaces were
analyzed.
"Dried
droplets of
serum (blood)
contaminated
with HCV may be
inconspicuous
and, therefore,
more likely than
a liquid
droplets to
cause accidental
exposures to
HCV."
November 23,
2013
Hepatitis
C Virus
Maintains
Infectivity for
Weeks after
Drying on
Inanimate
Surfaces at Room
Temperature:
Implications for
Risks of
Transmission
Posted by
Hepatitis C
Research and
News
Journal of
Infectious
Diseases
Advance Access
published
November 23,
2013
Elijah
Paintsil1,
Mawuena Binka2,
Amisha Patel2,
Brett D.
Lindenbach3, and
Robert Heimer2
1 Departments of
Pediatrics &
Pharmacology,
Yale School of
Medicine, New
Haven, CT
2 Department of
the Epidemiology
of Microbial
Diseases, Yale
School of Public
Health,
New Haven, CT
3 Microbial
Pathogenesis,
Yale School of
Medicine, New
Haven, CT
Correspondence
to: Elijah
Paintsil, MD.,
Departments of
Pediatrics and
Pharmacology,
Yale School of
Medicine, 464
Congress Avenue,
New Haven,
Connecticut
06520, USA.
Phone:
203-785-6101
Fax:
203-785-6961;
email:
elijah.paintsil@yale.edu
ABSTRACT
Background:
Healthcare
workers may come
into contact
with fomites
containing
infectious HCV
during
preparation of
plasma, or
following
placement or
removal of
venous lines.
Similarly,
injection drugs
users may come
into contact
with fomites.
Hypothesizing
that prolonged
viability of HCV
in fomites may
contribute
significantly to
incidence; we
determined the
longevity of
virus
infectivity and
the
effectiveness of
antiseptics.
Methods: We
determined the
volume of drops
misplaced during
transfer of
serum or plasma.
Aliquots
equivalent to
the maximum drop
volume of plasma
spiked with 2a
HCV reporter
virus were
loaded into
24-well plates.
Plates were
stored uncovered
at three
temperatures:
4°, 22°, and
37°C for up to 6
weeks before
viral
infectivity was
determined in a
microculture
assay.
Results: The
mean volume of
an accidental
drop was 29 µl
(min - max of 20
- 33 µl). At
storage
temperatures 4°
and 22°C, we
recovered viable
HCV from the low
titer spots for
up to 6 weeks of
storage. The
rank order of
HCV virucidal
activity of
commonly used
antiseptics was
bleach (1:10) >
cavicide (1:10)
> ethanol (70%).
Conclusions: The
hypothesis of
potential
transmission
from fomites was
supported by the
experimental
results. The
anti-HCV
activity of
commercial
antiseptics
varied.
INTRODUCTION
The global
burden of
morbidity and
mortality from
hepatitis C
virus (HCV)
infection is
truly pandemic
with more than
170 million
people currently
infected 1
_ENREF_1. Since
there is
currently no
vaccine for HCV
and available
treatment
regimens are
limited by
efficacy, cost,
and side
effects,
prevention of
HCV transmission
remains the
primary strategy
for curbing the
HCV epidemic.
HCV is
transmitted
primarily
through
parenteral
exposure to
blood or body
fluids
contaminated
with HCV.
Injecting drug
use (IDU),
mother-to-child
transmission,
multiple
heterosexual
partners,
accidental
needle injuries,
and transfusion
of blood or
blood products
are among the
most relevant
risk factors for
HCV
acquisition2-4
The epidemiology
of HCV has
changed in the
last decade.
Transmission
from blood
transfusions and
surgical
procedures have
all but
disappeared in
developed
countries 5 .
There have been
modest but
insufficient
declines in
incidence among
IDUs in
locations with
broad
implementation
of syringe
exchange
programs6-12.
Nosocomial
transmissions of
HCV increasingly
account for a
large proportion
of new HCV
infections
(i.e., 20% to
50%) in
developed
countries13-17.
Thus, the
relative impact
and burden of
nosocomial HCV
transmission
might be greater
now than a
decade ago. In
an Italian study
of 214 patients
with acute HCV
infections18,
the most
relevant
associated risk
factors were:
history of
medical
procedures (32%)
(e.g.,
hospitalization,
surgery,
endoscopy,
dialysis, blood
transfusion,
dental
treatment, or
other invasive
procedures) and
intravenous drug
use (30%).
Interestingly,
among the
patients
classified under
medical
procedures
almost half of
them did not
have surgery or
any invasive
procedures while
on admission.
This has been
corroborated by
a study from
Spain where the
investigators
found that the
only documented
risk factor
among patients
with acute HCV
infection was
hospital
admission19. One
can speculate
that these
patients might
have been
exposed to
HCV-contaminated
surfaces during
hospitalization.
We hypothesized
that
occupational and
iatrogenic HCV
infections may
be due in part
to the ability
of the virus to
remain viable on
fomites and
other hospital
equipment for
prolonged
periods.
We recently
established a
microculture
assay for
propagation of
cell culture
derived HCV (HCVcc)
in small volumes
by using a
genetically
engineered
reporter virus
derived from the
HCVcc
clone20,21.
Using our
microculture
assay system, we
performed a set
of experiments
to replicate the
circumstances in
which healthcare
workers or
patients may
come into
contact with HCV
dried upon
surfaces that
include
preparation of
plasma, handling
of hemodialysis
equipment, and
following
placement or
removal of
venous lines. To
our knowledge
this constitutes
the first study
to closely
simulate
conditions
leading to
nosocomial
transmission of
HCV
MATERIALS AND
METHODS
Plasmids and
Viruses
The construction
of the
Jc1/GLuc2A
reporter virus,
a derivative of
the chimeric
genotype 2a
FL-J6/JFH with a
luciferase gene
from Gaussia
princeps
inserted between
the p7 and NS2
genes, has been
reported
previously
21,22. Viral
stocks of
Jc1/GLuc2A
reporter virus
were prepared by
RNA transfection
of Huh-7.5
cells. The titer
of HCVcc was
quantified by
infecting cells
with serial
dilutions of the
stock virus and
determining the
dilution that
will infect 50%
(TCID50) of the
wells by using
the method of
Reed and Muench
23
Cell Culture
Human hepatoma
cells highly
permissive for
HCVcc (Huh-7.5
subline)24 were
maintained as
subconfluent,
adherent
monolayers in
Dulbecco’s
Modified Eagle’s
Medium (DMEM)
supplemented
with 10%
heat-inactivated
fetal calf serum
and 1 mM
non-essential
amino acids (Invitrogen,
Carlsbad, CA) at
37°C and 5% CO2
Determination of
the volume of
accidentally
misplaced HCVcc-contaminated
plasma on
surfaces
The most likely
circumstances in
which healthcare
workers or
patients may
come into
contact with HCV
dried upon
surfaces are
following
spillage of
HCV-contaminated
blood, serum, or
plasma during
the course of
preparing a
blood sample for
analysis or
removing a
venous line. To
simulate such
accidents, we
obtained
ethylenediaminetetraacetic
acid (EDTA)-anticoagulated
blood from HIV
and HCV
seronegative
donors. The tube
was centrifuged
at 2000 rpm for
15 minutes and a
rubber dropper
was used to
aspirate and
transfer the
plasma into
several vials
for storage as
per practice and
recommendation
of the clinical
microbiology
laboratory at
Yale-New Haven
Hospital. The
procedure was
done in a
biosafety
cabinet with a
foil mat to
collect
accidental drops
of plasma. The
experiment was
done on two
occasions and at
each occasion 10
accidental drops
were weighed.
The volume of
the drop was
calculated based
on the formula
that 1 ml weighs
1 gram. The
mean, with
standard
deviation of the
mean, and
maximum volumes
were calculated.
Desiccation of
displaced HCVcc-contaminated
plasma drops on
work surfaces
To determine how
quickly the
plasma dried on
the surface we
seeded the wells
in uncovered
24-well tissue
culture plates
with the maximum
accidentally
dropped volume
(33 µl). The
24-well plates
were stored in a
refrigerator at
4°C, on a
benchtop at
22°C, or in an
incubator at
37°C, and
observed every
60 minutes until
all replicates
(20 drops) had
dried. The time
to dryness in
these storage
conditions was
recorded. To
determine the
effect of
humidity on time
to dryness, we,
in a separate
experiment,
recorded the
temperature and
humidity using
an analog
thermo-hygrometer
instrument
(General Tools,
New York, NY,
USA) three times
a day (7 - 9 am;
12 noon - 1 pm;
and 3 -5 pm) for
a week. The mean
humidity, with
standard
deviation of the
mean was
calculated.
Viability of
dried HCVcc on
surfaces
We spotted 33 µl
of plasma spiked
with HCVcc on
the 24-well
plates. They
were either
immediately
tested for
viable virus or
stored at 4°C,
22°C, and 37°C
for up to 6
weeks before
testing. Twenty
replicates were
tested per
condition and
the experiment
was repeated on
two separate
occasions.
Negative
controls
comprised of
plasma without
virus. The day
before each time
point, 96-well
plates were
seeded with 6.4
x 103 Huh-7.5
cells/well in
100 µl of medium
and incubated at
37°C in 5% CO2.
To test for
infectivity, the
dried spots were
rehydrated and
reconstituted
with 100 µl of
culture medium.
The medium from
the wells was
gently aspirated
from the cells
and replaced
with 100 μl of
the
reconstituted
virus mixture.
After 5 h of
incubation, the
cells were
washed with
sterile PBS to
remove the input
virus; fresh
medium was added
and incubated
for 3 days.
After 3 days,
culture
supernatant was
harvested and
mixed with 20 μl
of lysis buffer
before
luciferase
activity was
measured by
using luciferase
assay reagent
kit (Promega,
Madison, WI) and
a luminometer
(Synergy HT,
BioTek,
Winooski, VT).
The relative
luciferase
activity (RLA)
was determined
to be linearly
related to HCV
infectivity16.
Virucidal effect
of antiseptics
on viability of
contaminated
HCVcc on
surfaces
We used three
antiseptics –
bleach (Clorox),
ethanol, and
cavicide (Metrex)
- to determine
the effect of
antiseptics on
infectivity of
HCVcc
contaminated
spots by using a
culture media
without virus as
negative
control.
Positive
controls
consisted of
cell culture
media with
virus. These
antiseptics are
readily
available in
hospitals and
research
laboratories.
Bleach is
available as 6%
sodium
hypochlorite and
is diluted 1:10
in tap water
before use,
while ethanol is
available for
use as 70%
ethanol 25-27.
Cavicide is
ready-to-use
without dilution
as per product
insert. Prior to
testing
virucidal
activity, it was
necessary to
determine the
cytotoxic
effects of the
antiseptics on
the Huh-7.5
cells. Briefly,
33 μl of test
antiseptic was
pipetted onto a
24-well plate.
The antiseptic
was combined
with 297 μl of
culture media
(i.e., 1:10
dilution) and
the mixture was
passed through
MicroSpin S-400
HR columns (GE
Healthcare,
Freiburg,
Germany)
according to the
manufacturer’s
instructions.
300 μl of column
eluate or
mixture not
passed through
the columns was
added to Huh-7.5
cells seeded the
previous day in
a 48-well plate
at 3.0 x104
cells/well in
300 μl of
medium, to make
a final volume
of 600 μl and
then incubated
overnight at
37°C. After a
day of further
incubation, cell
growth was
determined with
the alamarBlue®
assay (Invitrogen)
as
manufacturer’s
instructions.
Cell growth was
determined as a
function of
relative
fluorescence
measured at 530
nm excitation
and 590 nm
emission
(Synergy HT
Plate Reader,
BioTek,
Winooski, VT).
Five replicates
were tested per
condition and
the experiment
was repeated
twice.
We modified a
previously
described
protocol to test
for the
infectivity of
HCVcc after
exposure to test
antiseptic28. In
brief, an equal
volume of test
antiseptic was
pipetted onto 33
µl HCVcc
contaminated
spots for an
exposure period
of one minute,
whereafter, 264
μl of culture
media was added
to the
virus-antiseptic
mixture (i.e.,
1:10 dilution)
and
reconstituted.
To reduce the
cytotoxicity of
antiseptics,
each mixture was
passed through a
MicroSpin S-400
HR column
according to the
manufacturer’s
instructions.
Then 300 μl of
eluate passed
through the
column or
mixture without
column
purification was
added to Huh-7.5
cells in a
48-well plate at
3 x 104
cells/well in
300 μl of medium
to make a final
volume of 600 μl.
The cells were
washed with
sterile PBS
after 4 h to
remove input
virus and
incubated in 200
µl fresh media
for 3 days. The
infectivity of
HCVcc was
determined by
luciferase assay
as described
above. Ten
replicates were
tested per
condition and
the experiment
conducted on
three occasions.
RESULTS
Volume of
accidentally
misplaced HCVcc
contaminated
plasma
The experiment
was done on
three occasions,
and on each
occasion 10
drops were
weighed. The
mean volume of
the drops,
calculated on
the basis that 1
ml weighs 1
gram, was 29 ± 5
μl and the range
was 18 to 33 μl.
Since the
maximum drop
volume of 33 μl
presents the
most risk of
transmission, we
used 33 μl
throughout our
study.
Time to drying
of HCVcc
contaminated
drops at
different
temperatures
Dried droplets
of serum
contaminated
with HCV may be
inconspicuous
and, therefore,
more likely than
a liquid droplet
to cause
accidental
exposures to
HCV. We
determined how
long it took a
drop of HCVcc
contaminated
plasma to dry at
4°, 22° and
37°C. We
determined the
mean temperature
and relative
humidity in the
refrigerator,
the benchtop,
and the
incubator over a
week. The
temperature was
4 ± 1°, 22 ± 0°,
and 37 ± 0°C in
the
refrigerator,
the benchtop,
and the
incubator,
respectively.
The humidity was
53 ± 10%, 44 ±
5%, and 82 ± 1%
at 4°, 22° and
37°C,
respectively.
The order of
time to dryness
was 4, 24, and
28 hrs at 22° (benchtop),
4°
(refrigerator),
and 37°C
(incubator),
respectively.
Thus time to
dryness
correlated
positively with
the humidity of
the storage
condition.
Infectivity of
dried HCVcc on
surfaces at
different
temperatures
We investigated
the infectivity
of HCVcc after
drying on
surfaces at
different
temperatures.
Aliquots of 33
µl of HCVcc
contaminated
serum were
pipetted into
24-well plates
and stored for
up to six weeks.
Twenty spots of
dried HCVcc for
each combination
of storage time
and temperature
were
reconstituted
with culture
media after
storage and
introduced into
our assay system
20. The
proportion of
HCVcc positive
dried spots and
the infectivity
per HCVcc dried
spot were
determined. The
results
presented here
came from at
least three
independent
experiments.
First, we used a
low titer stock
of HCVcc, (i.e.,
equivalent to
104 infectious
units/mL) to
determine the
infectivity of
HCVcc after
drying and
storage for up
to 6 weeks. We
observed a
negative
correlation
between storage
temperature and
HCVcc
infectivity
(Figure 1A).
With an assay
detection limit
of 1000 RLA (2-3
times over the
background
luciferase
activity), we
recovered viable
HCVcc from dried
spots stored at
37°C until day 7
of storage. In
contrast, at
storage
temperatures 4°
and 22C°, we
recovered
replicating
HCVcc from all
the spots for up
to 6 weeks of
storage. The
infectivity,
measured by RLA
of the
reconstituted
spots, declined
rapidly over
time inversely
to the storage
temperature
(Figure 1B). At
storage
temperatures of
4° and 22°C, we
observed a sharp
decline in
infectivity over
the first two
weeks followed
by persistent
but lower
infectivity
through week six
(Figure 1B).
This is
consistent with
our previous
report of
biphasic decay
rate of HCVcc20.
By using a high
titer stock of
HCVcc
(equivalent
to106 infectious
units/mL), we
observed a
prolonged
infectivity of
HCVcc at all
storage
temperatures.
Almost 100% of
the contaminated
spots stored at
4° and 22°C
remained
positive for
HCVcc through
three weeks of
storage (Figure
2A). At 37°C,
100% of the
spots were
positive till 10
days of storage
and then
declined to 40%
and 0% at days
14 and 21,
respectively
(Figure 2A). The
infectivity of
the HCVcc
recovered from
the high titer
HCVcc
contaminated
spots was in
general 2 to
3-fold higher
than the RLA of
the low titer
HCVcc at each
time point.
Infectivity was
inversely
proportional to
the storage
temperature. We
observed a 50%
reduction in
infectivity at
day 3, 14 and 21
for storage
temperatures
37°, 22°, and
4°, respectively
(Figure 2B).
Effect of
antiseptics on
infectivity of
HCVcc on
surfaces
To investigate
the virucidal
effect of
bleach, ethanol,
and cavicide, we
first determined
the effects of
these
antiseptics on
the growth of
Huh-7.5 cells by
using the
alamarBlue®
assay. When we
tried undiluted
bleach and
cavicide, which
were diluted
1:10 before
addition to the
tissue culture
system, we found
they were
uniformly
ctytotoxic to
Huh-7.5 cells
whereas 70%
ethanol had no
significant
effect on cell
growth (Figure
3A). Cell growth
was almost
restored to
control levels
with a 1:10
dilution of
bleach and a
1:20 dilution of
cavicide
following
passage of the
solution through
MicroSpin S-400
HR columns
(Figure 3A).
Cavicide at a
1:10 dilution
reduced growth
by 70% relative
to the control.
Based on the
cytotoxicity
results,
experiments
using bleach
diluted 1:10 and
1:100, cavicide
diluted 1:10 and
1:20, and
ethanol at 70%
and 7% were
conducted by
using MicroSpin
S-400 HR
columns29 prior
to adding eluate
to the
microculture
system. After 1
min exposure to
bleach (1:10
dilution),
cavicide (1:10),
and ethanol
(70%), the
percentage of
positive
contaminated
HCVcc spots were
0%, 3 ± 6%, and
13 ± 6%,
respectively
(Figure 3B).
Further
dilutions of
bleach (1:100),
cavicide (1:20),
and ethanol (7%)
resulted in 17 ±
6%, 43 ± 6%, and
90 ± 17%
positive spots,
respectively.
For certain
viruses, passage
through a
MicroSpin column
could reduce
viral
infectivity30,
therefore, we
performed a
control
experiment
comprising HCVcc
without exposure
to any
antiseptic and
with or without
passage through
a MicroSpin
column prior to
infection of Huh
7.5 cells. The
infectivity was
80 ± 10% and
100% for HCVcc
with and without
passage through
MicroSpin
column,
respectively
(Figure 3B). We
next tested the
infectivity of
HCVcc without
MicroSpin column
after exposure
to antiseptic at
concentrations
that are least
cytotoxic. After
1 min exposure
to bleach (1:100
dilution),
cavicide (1:20),
70% ethanol, and
7% ethanol, the
percentage of
positive
contaminated
HCVcc spots were
30 ± 10%, 60 ±
36%, 30 ± 35%,
and 93 ± 12%,
respectively
(Figure 3B). The
infectivity of
residual HCVcc
after passage
through
MicroSpin column
(Figure 3C) was
correlated with
the likelihood
of recovery of
viable HCVcc.
RLA was highest
for 7% ethanol
(with 27 of 30
spots yielding
viable HCVcc)
and lowest for
1:10 cavicide (1
of 30 spots
yielding viable
HCV).
DISCUSSION
In our
simulation of
real world risks
of HCV
transmission in
settings
conducive to
exposure to
HCV-contaminated
fomites, we
observed that
HCVcc could
maintain
infectivity for
up to 6 weeks at
4° and 22°C.
This finding
supports our
hypothesis that
the increasing
incidence of
nosocomial HCV
infections may
be due to
accidental
contact with
HCV-contaminated
fomites and
other hospital
equipment even
after prolonged
periods
following their
deposition.
Moreover, we
found that HCVcc
infectivity was
influenced by
HCVcc viral
titer and the
temperature and
humidity of the
storage
environment.
Furthermore, the
commercially
available
antiseptics
reduced the
infectivity of
HCVcc on
surfaces only
when used at the
recommended
concentrations
25,27, but not
when further
diluted.
Although there
have been two
previous studies
on infectivity
and stability of
HCV on
surfaces28,31,
to our
knowledge, this
is the first
study that
closely
simulates the
natural events
likely to cause
transmission of
HCV. First,
Kamili et al.
reported that
100 µl aliquots
of chimpanzee
plasma
contaminated
with HCV was
still infectious
when dried and
stored at room
temperature for
up to 16 hours
31. Transmission
of infection did
not occur after
16 hours to up 7
days of storage.
More recently,
Doerrbecker et
al. demonstrated
that 50 µl of
cell
culture-derived
HCV dried on
steel discs
remains
infectious for
up to 5 days at
room
temperature28.
The limitations
of these
previous studies
include
simulation of
HCV transmission
under artificial
drying
conditions.
Furthermore,
Doerrbecker et
al. found that
the infectivity
of the virus
recovered from
the carrier
system was
10-fold lower
than that stored
in liquid media.
Therefore, one
can speculate
that the
duration of
infectivity
observed in
their study
could be an
underestimation.
Moreover,
differences in
the three assay
systems (e.g.,
in vivo versus
in vitro assay;
artificial
versus passive
desiccation)
might account
for the
different
durations of
survival
reported. Our
study sought to
overcome some of
these
limitations by
determining the
exact size of
accidentally
misplaced HCVcc-contaminated
plasma and
allowing the
drops to dry
under natural
conditions. The
fact that under
these conditions
we found HCVcc
to be infectious
for up to 6
weeks,
consistent with
our previous
report that
HCVcc survived
in tuberculin
syringes for up
to 63 days 20,
is of public
health concern.
Taken together,
these studies
show that HCVcc
remains
potentially
infectious for
prolonged
periods of time,
ranging from 16
hours to 6 weeks
depending on the
assay system. We
previously
reported on the
biphasic decay
rate of our
genotype 2a
HCVcc at room
temperature; a
rapid decline of
infectivity
within the first
6 h followed by
a second phase
of a relatively
slow exponential
decay 20. This
is consistent
with recent
report on
thermostability
of 7 genotypes
including 2a
genotype 32.
Such prolonged
infectivity
could contribute
to the
increasing
incidence of
nosocomially
acquired HCV
infections.
Of infection
control
relevance is the
fact that all
the HCVcc-contaminated
spots dried at
room air within
4 hours,
becoming
inconspicuous
and therefore
more likely to
cause accidently
exposures to
HCV. HIV was
also reported to
dry at room
temperature
within 3 hours
and retain
infectivity for
up to 7 days
33,34. The
infectivity of
HCVcc and HIV
when stored at
room temperature
for several days
is consistent
with that of
other envelope
viruses 35,36.
The prolonged
infectivity of
these viruses
has been
attributed, in
part, to their
lipid envelope,
which resists
drying and
protects the
viral capsid
from the
deleterious
effects of
dehydration 37.
Hepatitis B
virus, another
lipid-enveloped
hepatotropic
virus, was
reported to
survive up to 7
days at room
temperature;
further time
points were not
available due to
a laboratory
mishap 38. The
resilience of
these viruses at
room temperature
raises the
possibility of
their being
transmitted
through fomites.
Our findings
support the
surveillance
data on
increasing
incidence of
nosocomial
transmissions of
HCV in developed
countries 13-17.
Interestingly,
most of the
patients who
acquired HCV in
the hospital had
no surgeries or
invasive
procedures;
their only risk
was hospital
admission18,19.
Fomites could,
therefore, be an
important
vehicle for
transmission of
HCV in the
hospital and
household
settings.
Finally, given
the infection
control
implications of
our findings, we
decided to
investigate if
commonly used
antiseptics are
effective
against HCV. We
demonstrated
that bleach,
cavicide, and
ethanol are
effective at
their
recommended
concentrations
25-27. It is
possible that
the efficacy of
cavicide at 1:10
is overestimated
because the
disinfectant
itself reduced
host cell
viability by
70%. Further
dilution of each
antiseptic
proved
sub-optimal
(Figures 3B and
C.The finding
for ethanol
paralleled that
of Ciesek et
al., who found
that HCV titers
decreased at
concentrations
of 30% and 40%
but complete
inactivation did
not occur at an
exposure time of
5 min29.
However,
undiluted
concentrations
of several hand
antiseptics
(based on
povidone-iodine,
chlorhexidine
digluconate, and
triclosan)
reduced HCV
infectivity to
undetectable
levels 29. Thus,
there are
several
commercially
available
antiseptics that
are effective
against HCV.
Our study, which
sought to
improve upon
prior studies,
still has some
limitations.
First, the assay
employs a
genetically
modified HCV
laboratory clone
derived from a
genotype 2a
virus that may
not reflect
survival
characteristics
of human
isolates.
However, the
thermostability
pattern of our
virus is similar
to that of other
genotypes 32.
Second, the
spiking of
HCVcc-seronegative
blood might not
sufficiently
replicate the
biological
factors present
in the blood of
HCV-infected
individuals that
could moderate
HCV transmission
and infectivity.
However, the
consistency of
our results with
previous in
vitro studies
and
epidemiologic
studies
reporting
transmission of
HCV in
healthcare
setting and
through sharing
of injection
paraphernalia39-43
support our
findings.
In conclusion,
we have
demonstrated
that HCVcc can
remain
infectious at
room temperature
for up to 6
weeks. Our
hypothesis of
potential
transmission
from fomites was
supported by the
experimental
results and
provides the
biological basis
for recent
observational
studies
reporting
increasing
incidence of
nosocomial HCV
infections and
continued high
incidence among
people who
inject drugs.
Acknowledgments
This study was
made possible by
grant from NIH/NIDA
(R01 DA030420 to
RH). EP is a
Yale CTSA
scholar and was
supported by
Clinical
Translational
Science Award (CTSA)
Grant Number UL1
RR024139 from
the National
Center for
Research
Resources (NCRR).
The development
of the
Jc1/GLuc2A
system involved
NIH funding
(1K01CA107092
and
1R01AI076259,
both to B.D.L).
Footnote:
(1) The authors
do not have a
commercial or
other
association that
might pose a
conflict of
interest.
(2) This study
was made
possible by
grant from NIH/NIDA
(R01 DA030420 to
RH). EP is a
Yale CTSA
scholar and was
supported by
Clinical
Translational
Science Award (CTSA)
Grant Number UL1
RR024139 from
the National
Center for
Research
Resources (NCRR).
The development
of the
Jc1/GLuc2A
system involved
NIH funding
(1K01CA107092
and
1R01AI076259,
both to B.D.L).
The content of
the paper is
solely the
responsibility
of the authors
and do not
necessarily
represent the
official view of
NIH or NCRR.
(3)
Correspondence
to: Elijah
Paintsil, MD.,
Departments of
Pediatrics and
Pharmacology,
Yale School of
Medicine, 464
Congress Avenue,
New Haven,
Connecticut
06520, USA.
Phone:
203-785-6101
Fax:
203-785-6961;
email:
elijah.paintsil@yale.edu
References pp.
17 - 22 of PDF
.....
Figure Legend
pp. 23 - 27 of
PDF .....
Source
- See more at:
http://hepatitiscresearchandnewsupdates.blogspot.com/2013/12/hepatitis-c-virus-maintains-infectivity.html#sthash.bOhvBeGJ.dpuf
More information
1999 Hepatitis C
Survives
2008 CDC
Infection
Control
Requirements
2008 CDC Review
