Review Article

Hepatitis C virus: Screening, diagnosis,

and interpretation of laboratory
assays
Ekta Gupta, Meenu Bajpai, Aashish Choudhary

Department of Virology Abstract

and Transfusion An estimated 3% of the world population is infected with Hepatitis C virus (HCV), a hepatotropic RNA virus, transmitted
Medicine, Institute primarily via the blood route. The major modes of transmission of the virus include injection drug use, unsafe injection
of Liver and Biliary practices, blood transfusion etc. HCV causes chronic hepatitis in about 80% of those infected by it. The mainstay in
Sciences, New Delhi, diagnosing infection with HCV is to initially screen high risk groups for antibodies to HCV (anti-HCV). The inclusion of
India serum to cut-off ratio (S/CO) in recent guidelines is helpful in deciding the supplemental assay to be used to confirm initially
reactive screening results. Nucleic acid amplification tests (NAT) are used as confirmatory tools, and also to determine viral
load prior to initiating treatment. Quantitative NAT has replaced qualitative assays. Genotyping is an important tool in
clinical management to predict the likelihood of response and determine the optimal duration of therapy. The impact of
this infection has begun to emerge in India. The problem of professional blood donation despite an existing law against
it, and flourishing unsafe injection practices, are potential sources for the spread of hepatitis C in our country. All health
care practitioners need to understand how to establish or exclude a diagnosis of HCV infection and to interpret the
tests correctly. In the absence of a preventive or therapeutic vaccine, and also of post-exposure prophylaxis against the
virus, it is imperative to diagnose infection by HCV so as to prevent hepatic insult and the ensuing complications that
follow, including primary hepatocellular carcinoma (HCC). This review aims to help blood bank staff regarding options
for diagnosis and management of donors positive for HCV.
Key words:
Blood borne virus, hepatitis C virus diagnosis, nucleic acid test

Introduction potential sources for the spread of hepatitis C in

the country. It is imperative to screen and diagnose
Hepatitis C virus (HCV) is a hepatotropic virus HCV infection in high risk populations so that those
which is one of the major causes of liver disease and a at risk of progressive liver disease may benefit from
potential cause of substantial morbidity and mortality antiviral therapy and counseling. All health care
worldwide. The virus, estimated to infect about 3% practitioners need to understand how to establish or
of the world population, is primarily transmitted via exclude a diagnosis of HCV infection and to interpret
the parentral route which includes injection drug the tests correctly. This review aims to give an
use, blood transfusion, unsafe injection practices, overview of this emerging viral infection, enumerate
Access this article online
and other healthcare related procedures. HCV the transmission patterns discussing the screening,
Website: www.ajts.org
causes acute hepatitis which is mostly subclinical, diagnosis, and interpretation of available assays.
DOI: 10.4103/0973-6247.126683
Quick Response Code: but which gradually evolves into chronic hepatitis in
about 80% of those infected.[1] HCV infected people The Virus
are at risk for developing chronic liver disease (CLD),
cirrhosis, and primary hepatocellular carcinoma In the 1970s, it became apparent that most cases
(HCC). It has been estimated that HCV accounts of posttransfusion hepatitis were not attributable to
for 27% of cirrhosis and 25% of HCC worldwide.[2] either hepatitis A virus (HAV) or hepatitis B virus
The US Center for Disease Control and Prevention (HBV) infection, and a new disease entity, termed
(CDC) recommends screening all individuals with ‘‘non-A, non-B’’ hepatitis (NANBH) was described
risk factors for HCV infection for antibodies to HCV for the first time.[5] It took over a decade to identify
Correspondence to:
Dr. Meenu Bajpai,
(anti-HCV), or in specific situations, with molecular the etiological agent of NANBH owing to the inability
Department of Transfusion assays to demonstrate HCV ribonucleic acid (RNA) of the virus to propagate efficiently in cell culture.[6]
Medicine, Institute of Liver by reverse transcriptase polymerase chain reaction Finally, HCV was discovered in 1989 and established
and Biliary Sciences, (RT-PCR).[3,4] The impact of this infection has begun as an important etiological agent of transfusion
Sector D-1, Vasant Kunj,
New Delhi-110 070, India.
to emerge in India. The problem of professional associated hepatitis. HCV is a RNA virus belonging
E-mail: meenubajpai@ blood donation despite an existing law against to the family Flaviviridae, genus Hepacivirus.[1] The
hotmail.com it, and flourishing unsafe injection practices, are HCV virion is 55-65 nm in diameter containing in it

Asian Journal of Transfusion Science - Vol 8, Issue 1, January - June 2014 19

 Gupta, et al.: Hepatitis C virus screening assays

a 9.6 kb positive sense single-stranded RNA genome composed of assays used and differences in the population and practices between
a long open reading frame (ORF) flanked by untranslated regions different regions of the country. Studies in different population
(UTR’s) at both the ends. The precursor is cleaved into at least 10 groups found varying prevalence rates [Table 1].[10-19]
different proteins: the structural proteins: Core, E1, E2, and p7; as
well as the nonstructural (NS) proteins: NS2, NS3, NS4A, NS4B, Parenteral transmission through blood transfusion and
NS5A, and NS5B. An important feature of the HCV genome is its infected needles and syringes remain the most significant route
high degree of genetic variability. The E1 and E2 regions are the of transmission for HCV in our country. Blood transfusion is
most variable, while the 5’UTR and terminal segment of the 3’UTR an effective mode of transmission as it allows a large quantum
are highly conserved.[6] HCV has a high propensity for establishing of infective virions into the susceptible patient. In developed
chronic infection. It has been estimated that in chronically infected countries, numerous corrective measures have reduced the spread
people approximately 1012 viral particles are generated every day. of infection through this route. This has been documented in
This remarkable replicative rate in combination with the highly Japan where HCV prevalence dropped from 4.9 to 1.9% after
error prone polymerase activity of the virus results in tremendous mandatory screening was introduced in 1990, and in the US where
genetic diversity and existence of various quasispecies within an the prevalence dropped from 3.84 to 0.57%.[20] In India, mandatory
infected individual.[6] HCV has been classified into six genotypes[1-6] screening for HCV was introduced in 2002. Many of the more
with multiple subtypes. Genotyping is recognized as the primary recent blood donor studies report prevalence of <1.0%, indicating
tool for assessing the course of infection and determining treatment that increased screening and education of donors is working.
duration and response.[7] Replacement donors typically have higher HCV infection rates
than voluntary donors.[21]
Epidemiology of HCV Infection
HCV genotypes predominant in India are genotypes 3 and 1,
Global constituting approximately 60 and 30% of the six genotypes,
The estimated global prevalence of HCV infection is 3% respectively. Genotype 4 constitutes about 4%, the remaining
which translates to over 180 million people worldwide. High genotypes contributing to <2% each. Most of the reported studies
seroprevalence is observed in Asian and African countries, from India have shown that genotype 3 predominates in the north,
whereas the developed world including North America, northern east, and west India; whereas genotype 1 is commoner in south India.
and western Europe, and Australia have a low prevalence.[2,6] The reason for this difference between these regions is yet to be
In developing countries, the seroprevalence of HCV displays a explained. Various HCV genotypes prevalent across different regions
high range of variability, ranging from 0.9% in India to higher in India, as observed in select recent studies are shown in Table 2.[22-27]
prevalence from 2.1-6.5% in many countries. Egypt has a reported
seroprevalence of about 22% and is the highest in the world.[2] Natural history following infection with HCV
Substantial regional differences exist in the distribution of HCV Hepatitis C can present as acute or chronic hepatitis.
genotypes in the world. Genotypes 1, 2, and 3 have a worldwide Most of the cases of acute hepatitis C are asymptomatic.
distribution and HCV subtypes 1a and 1b are the most common Symptomatic acute hepatitis with jaundice is seen in 10-15%
genotypes prevalent.[7] of patients only and can be severe, but fulminant liver failure
is rare. Spontaneous clearance is observed in 25-50% of those
Epidemiology: India with symptomatic infection and in 10-15% of those with
HCV is considered an emerging infection in India. There is a lack asymptomatic infection. [1,28] The natural history following
of existing literature on the true prevalence in general population exposure to HCV is summarized in Figure 1.
due to paucity of well-designed population-based studies from the
country. Data available is mostly derived from isolated hospital- Chronic hepatitis C is marked by the persistence of HCV RNA in
based studies and blood banks. The estimates thus obtained have the blood for at least 6 months after the onset of acute infection.
been then extrapolated onto the general population. The estimated The risk of progression to chronic infection[28] by HCV is influenced
HCV prevalence at present is 1-1.9%.[8] Only one systematic study by various factors including:
from West Bengal determined a prevalence of 0.87%.[9] The majority • Age at the time of infection (more if infection occurs at age
of the studies in blood donors report prevalence from 0.3-1.85%. >25 years)
The differences can be due to different generations of the anti-HCV • Gender (males > females)

Table 1: HCV prevalence in different population groups

Population studied State, region Assay for HCV Sample size % age HCV Reference
diagnosis detected
Blood donors Delhi Anti-HCV 94,716 0.57 10
Blood donors Nagpur, Maharashtra Anti-HCV, RT-PCR 68,000 0.2 11
Blood donors Kolkata, West Bengal Anti-HCV, RT-PCR 51,023 0.27 12
Blood donors Mysore, Karnataka Anti-HCV 39,060 0.23 13
Pregnant women Ludhiana, Punjab Anti-HCV, RT-PCR 488 1.6 14
HIV infected individuals Delhi Anti-HCV 1,953 1.69 15
HIV infected individuals Kolkata RT-PCR 204 7.35 16
Injection drug users Nagaland, Mizoram (northeast India) Anti-HCV 400 47.8 17
Hemodialysis patients Delhi RT-PCR 119 27.7 18
Health care workers Delhi Anti-HCV 100 4 19
HIV: Human immunodeficiency virus; anti-HCV: antibodies to HCV; RT-PCR: reverse transcriptase polymerase chain reaction

20 Asian Journal of Transfusion Science - Vol 8, Issue 1, January - June 2014

 Gupta, et al.: Hepatitis C virus screening assays

Table 2: HCV genotype distribution in India

State/region Population studied Method/assay used Sample HCV genotype Reference
size (approximate %)
Delhi Chronic hepatitis C RT-PCR 102 3 (59), 1 (21), 4 (12) 22
Delhi Chronic hepatitis C RFLP, direct sequencing (core region) 71 3 (63), 1 (31%), 2 (6) 23
Northeast India Chronic hepatitis C Direct sequencing (NS5b region) 75 4 (31), 3 (20), 1 (15), 24
6 (14), 2 (7)
All India patient cohort Chronic hepatitis C Sequencing (core envelope 1 region) 2,118 3 (62), 1 (31), 4 (5), 25
6 (2), 2 and 5 (<1)
Andhra Pradesh HIV-HCV RFLP 45 1 (69), 3 (31) 26
(Hyderabad) coinfection
Chennai CLD Line probe assay 23 1 (83), 3 and 4 (13), 27
1 and 4 (4)
HIV: Human immunodeficiency virus; HCV: hepatitis C virus; CLD: chronic liver disease; RT-PCR: reverse transcriptase polymerase chain reaction;
RFLP: restriction fragment length polymorphism

as the persistent absence of HCV RNA in serum for 6 months or

more after completing antiviral treatment. The second goal is to
prevent progression to cirrhosis, HCC, and decompensated liver
disease requiring liver transplantation.

Modes of transmission
HCV is transmitted from one person to another principally by
parenteral route. The major routes of transmission are:
• Injection drug use,
• blood transfusion, and
• unsafe therapeutic injections.

Other routes of transmissions include;

• healthcare related procedures (occupational exposures like
needle stick injuries),
• tattooing,
• perinatal transmission, and
• sexual transmission

Transmission through occupational, perinatal, and sexual routes

is less efficient as compared to transmission through large or
repeated percutaneous exposures. Hence, these routes are not
considered to be major sources of new HCV infection regardless
of the population or geographic area.[29]

Figure 1: Natural history following infection with hepatitis C virus Screening for HCV infection
HCV screening has several potential benefits. By detecting HCV
infection early, antiviral treatment can be offered earlier in the
• Ethnicity (higher in Africans than in Caucasians and Hispanic
course of the disease which is more effective than starting at a
whites)
• Coinfection with human immunodeficiency virus (HIV), HBV later stage.[30] Further, early detection together with counseling
• Concomitant alcohol consumption and lifestyle modifications may reduce the risk of transmission
• Comorbid conditions like cancer, immunosuppression, insulin of HCV infection to other people. The optimal approach to
resistance, nonalcoholic steatohepatitis, obesity, etc. screen for HCV is to test the individuals having risk factors for
exposure to the virus. The American Association for the Study
Treatment for HCV infection of Liver Diseases (AASLD) recommends[4] screening for HCV for
Treatment for HCV infection is available. The role of treatment the following individuals:
in acute infection is being evaluated and currently the existing • Recipient of blood or blood components (red cells, platelets,
data shows that response to 6 months of standard therapy fresh frozen plasma).
with interferon (IFN) in terms of absence of HCV RNA from • Recipient of blood from a HCV-positive donor.
serum is excellent and progression to chronicity is reduced. • Injection drug user (past or present).
The recommended treatment for chronic HCV infection is • Persons with following associated conditions;
a combination of a pegylated IFN alpha and ribavirin. The • persons with HIV infection,
treatment duration depends on the genotype of the virus and • persons with hemophilia,
it has two goals. The first is to achieve sustained eradication of • persons who have ever been on hemodialysis, and
HCV, that is, sustained virologic response (SVR), which is defined • persons with unexplained abnormal aminotransferase
levels.

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 Gupta, et al.: Hepatitis C virus screening assays

• Children born to HCV-infected mothers. The window period has been documented to decrease from
• Healthcare workers after a needle stick injury or mucosal approximately 16 weeks to 10 weeks and finally to 8 weeks with the
exposure to HCV-positive blood. introduction of first-, second-, and third-generation anti-HCV ELISAs,
• Current sexual partners of HCV-infected persons. respectively. The newest generation of immunoassays available, that
is, fourth generation of tests is those that simultaneously detect HCV
Risk of HCV infection in recipients of blood transfusion capsid antigen as well as antibodies to the core, NS3, NS4, and NS5
Prior to 1992, blood transfusions carried a high risk of HCV regions of the virus. These assays have further reduced the window
infection, approximately 15-20% with each unit transfused.[31] In period of HCV detection by 17 days to already existing assays. But the
1988, 90% of cases of posttransfusion hepatitis were due to NANBH literature supporting the inclusion of these assays as 4th generation on
viruses which was later found out to be due to HCV. The move to the basis of improved sensitivity, specificity is limited.[1,36]
all-volunteer blood donors instead of paid donors had significantly
reduced the risk of posttransfusion hepatitis to 10%. Screening Supplemental anti-HCV test and significance of signal-to-cut off
of blood further reduced the rate of posttransfusion hepatitis C (S/CO) ratio
by a factor of about 10,000; to a current rate of 1 per million Recombinant immunoblot assays (RIBA) were used in the past
transfusions.[32] The few cases that still occur are due to newly infected as supplemental assays to confirm serological reactivity by ELISA,
people donating blood before they have developed antibodies but are now clinically obsolete with the availability of molecular
(window period) to the virus, which can take up to 6-8 weeks. tests.[37] Confirmation of serological reactive tests may be done
by a nucleic acid test (NAT) for detection of HCV RNA. Recent
studies have also suggested that higher the anti-HCV antibody titer
Virological Tools for Diagnosis
in patient’s serum; more are the chances of it being true positive
than false positive. This was the basis of inclusion of measurement
Virological diagnosis of HCV infection is based on two categories of
of anti-HCV S/CO ratio that indirectly represents higher
laboratory tests, namely serologic assays detecting specific antibody to
antibody levels in patient’s sample, as a marker for confirmation
HCV (anti-HCV) (indirect tests) and assays that can detect, quantify,
of serological reactive results. CDC in 2003 expanded the earlier
or characterize the components of HCV viral particles, such as HCV
guidelines to recommend an option for inclusion of S/CO ratio to
RNA and core antigen (direct tests). Direct and indirect virological
determine the need for supplementary testing.[38]
tests play a key role in the diagnosis of infection, therapeutic decision-
making, and assessment of virological response to therapy.
This was based on the analysis of many thousands of repeatedly
reactive samples screened for anti-HCV, and their results compared
Anti-HCV Antibodies to those generated by a supplemental assay. It was estimated that
for ELISA, a S/CO of 3.8, and for chemiluminescence immunoassay
The “serologic window” between HCV infection and the detection (CLIA) a S/CO of 8, predicted true viremia in 95-98% cases. Since then,
of specific antibodies varies from patient to patient. With current various studies have also confirmed the usefulness of S/CO in predicting
assays, seroconversion occurs on an average at 6-8 weeks after true positive anti-HCV results.[1,39-41] This should be limited to only
the onset of infection. In patients with spontaneously resolving diagnostic tests as this criteria does not hold true for screening assays.
infection, anti-HCV may persist throughout life, or decrease slightly
while remaining detectable, or gradually disappear after several HCV core antigen (HCV Ag) detection
years.[33] Anti-HCV persists indefinitely in patients who develop During the past decade, several assays for the detection of the
chronic infection, although antibodies may become undetectable in core antigen of HCV by ELISA or CLIA have been developed.[42]
hemodialysis patients or in cases of profound immunosuppression. These assays were envisioned as alternatives to NAT to be used
in resource-limited settings, where molecular laboratory services
Anti-HCV detection are either not available or not widely utilized owing to cost issues.
Serological assays for detecting anti-HCV were developed and Since these assays are either ELISA or CLIA based, they are user
improved following the initial discovery of the virus because of friendly, require less technical expertise and are less expensive
the urgent need to screen blood donors and prevent transmission. compared to molecular techniques. Evaluations in transfusion
Anti-HCV is typically identified by using enzyme-linked settings have shown that the HCVcore Ag assay detects HCV
immunosorbent assay (ELISA). Three generations of ELISAs infection as effective as NAT, about 40-50 days earlier than the
[Table 3] have been developed since 1989. The first generation current third generation anti-HCV screening assays. HCV core
assays, which incorporated the recombinant c100-3 epitope from antigen levels closely follow HCV RNA dynamics, and allow
the NS4 region, were used until 1992, when they were replaced clinical monitoring of a patient’s therapy, independently of HCV
by second generation assays, which additionally incorporated genotype.[42,43] The major limitation of the HCV core Ag assay is its
epitopes c22-3 and c33c from the HCV core and NS3 regions, lower sensitivity limiting its utility. A new generation CLIA based
respectively. The third generation assays contained reconfigured quantitative test (Architect HCV Ag Test, Abbot, Germany) with
core and NS3 antigens and in addition a newly incorporated sensitivity comparable to that of end point PCR (~1,000 IU/ml) but
antigen from the NS5 region.[34-36] less than that of real time RT-PCR has been reported.[44,45]

Table 3: The different generations of immunoassays for anti-HCV

Core E1/E2/NS1 NS2 NS3 NS4 NS5
1st generation — — — — c100-3 (recombinant) —
2nd generation c22-3 — — c33c C200, HC-31 —
3rd generation c22p — — c33c c100-3, 5-1-1p NS5
anti-HCV: antibodies to hepatitis C virus

22 Asian Journal of Transfusion Science - Vol 8, Issue 1, January - June 2014

 Gupta, et al.: Hepatitis C virus screening assays

NAT: Detection of HCV RNA as a globally recognized standard for calibration of quantitative
assays.[1] For monitoring purposes, it is important to use the same
Molecular virological techniques play a key role in diagnosis assay before and throughout during therapy.[4,49]
and monitoring of treatment for HCV. Because it is difficult to
cultivate the virus in cell culture, molecular techniques were Iatrogenic exposure and postexposure prophylaxis
instrumental in first identifying HCV, making it one of the first The potential of health care delivery to transmit HCV to
pathogens to be identified by purely molecular methods. NAT is healthcare worker (HCW) is increasingly being recognized
considered the ‘gold standard’ for detecting active HCV replication. especially if infection control or disinfection practices are
HCV NAT is extremely useful in establishing the diagnosis of inadequate and contaminated equipment is shared among patients.
acute HCV infection, since RNA is detectable as early as 1 week The mechanisms of transmission in the healthcare setting are
after exposure via needle-stick or blood transfusion, and at least related to:[50]
4-6 weeks prior to seroconversion as demonstrated in a number • Improperly cleaned, disinfected, or sterilized equipment
of transmission settings.[46-48] The diagnosis of HCV infection is • Medication administration (e.g., direct syringe reuse,
established with antibody screening followed by NAT for HCV contamination of medication through syringe reuse, etc.)
RNA for confirmation as well as for follow-up of patients on • Blood sampling
treatment.[1] Viral load assessment at baseline is also critical for
determining response kinetics during therapy. Table 4 enumerates The CDC in collaboration with healthcare infection control practices
the role of NAT in HCV diagnosis. advisory committee (HICPAC) has issued recommendations following
occupational exposure to HCV.[51-53] These recommendations emphasize
Qualitative NAT that each institution should have its own policy regarding follow-up
Qualitative NAT have traditionally been considered as of personnel who sustain percutaneous or permucosal exposure to
confirmatory tools for HCV diagnosis. These assays commonly suspected HCV infected blood. They minimally recommend:
utilize conventional RT-PCR or transcription-mediated a. Baseline testing for anti-HCV in source.
amplification (TMA). The present indication of qualitative NAT b. Baseline and follow-up testing for anti-HCV and alanine
is to confirm viremia (especially low level viremia) in patients aminotransferase (ALT) levels in exposed at 6 months and
with reactive anti-HCV results, and to screen blood donations for 1 year postexposure.
evidence of infection with HCV.[1,49] With the availability of more c. Confirmation by NAT of all anti-HCV reactive results.
sensitive quantitative PCR that has a lower limit of detection (LOD) d. Education of workers about the risk for and prevention of
to as low as 30 copies/ml, qualitative assays have taken a back seat blood-borne infections.
especially in diagnostic laboratories.

Quantitative NAT Blood Transfusion Issues and Donor Counseling

Quantification of HCV RNA can be accomplished by many
methods. Commonly available formats include quantitative RT- Guidelines for donor notification for donors positive for
PCR (qRT-PCR) and branched deoxyribonucleic acid (bDNA) transfusion transmissible infections (TTIs) are outlined in
technology. Table 5 summarizes currently available quantitative ‘An Action Plan for Blood Safety’ by National AIDS Control
NAT’s for HCV. Organization (NACO) 2004.[54] A blood donor is offered an option
to know his TTI status at the time of registration for blood donation
Owing to its good sensitivity (99%) and specificity (98-99%) after due counseling and give consent for the same.
quantitative PCR has replaced qualitative PCR.[4,49] Prior to 1997,
the interpretation of quantitative NAT was hampered by the use of Notifying donors regarding a single positive screening test is
individual reporting units that were specific to individual assays. In fraught with the risk of causing undue anxiety and stress to a donor.
response to this, WHO established a preparation of HCV to be used If a screening test is positive, the blood unit should be immediately

Table 4: Role of NAT in HCV diagnosis

Situation Role of NAT
ELISA nonreactive Immunocompromised patients Actual virus detected, rather than immune response, which may not develop
Window phase prior to seroconversion Detection of virus within 1-2 weeks of infection
ELISA reactive As a confirmatory assay Positive result confirms current infection
NAT: Nucleic acid test; ELISA: Enzyme-linked immunosorbent assay; HCV: Hepatitis C virus

Table 5: Commercial HCV RNA quantification tests (RUO, Research use only; ASR, Analyte-specific reagents). Data
collected from the manufacturer’s website
Test (Manufacturer) Method Measurable IU/ml-to copies/ Status
range (IU/ml) ml conversion
Versant HCV RNA 3.0 (Siemens) bDNA 615-7.7 × 106 5.2 FDA approved
Cobas Amplicor Monitor HCV v2.0 (Roche) Semiautomated RT-PCR 600-5 × 105 2.7 RUO
Real Time HCV (Abbott) qRT-PCR 10-1 × 107 3.8 ASR
Cobas AmpliPrep/Cobas TaqMan (Roche) Automated q RT-PCR 43-6.9 × 107 3 FDA approved
High Pure/Cobas Taqman (Roche) qRT-PCR 25-3.9 × 108 3 FDA approved
HCV: Hepatitis C virus; RNA: ribonucleic acid; bDNA: branched deoxyribonucleic acid; qRT-PCR: quantitative reverse transcriptase polymerase chain reaction;
FDA: Food and Drug Administration

Asian Journal of Transfusion Science - Vol 8, Issue 1, January - June 2014 23

 Gupta, et al.: Hepatitis C virus screening assays

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evaluation of four automated chemiluminescence immunoassays
for hepatitis C virus antibody detection. J Clin Microbiol Cite this article as: Gupta E, Bajpai M, Choudhary A. Hepatitis C virus:
Screening, diagnosis, and interpretation of laboratory assays. Asian J Transfus
2008;46:3919-23.
Sci 2014;8:19-25.
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Source of Support: Nil , Conflicting Interest: None declared.
Significance of the signal-to-cutoff ratios of anti-hepatitis C enzyme

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