Humoral immune response in Japanese acute hepatitis patients with hepatitis C virus infection.

The humoral immune response to acute infection by hepatitis C virus (HCV) is not yet perfectly clear in terms of immunoglobulin (Ig) response, diversity of HCV antigen, and the relation with hepatitis severity and antibody response. Serum IgM and IgG anti-HCV levels in patients with HCV and either acute hepatitis (AH) or fulminant hepatitis (FH) were investigated; the diversity of HCV antigen was investigated by RIBA test III. Of 22 AH patients, 12 (54.5%) were positive for IgM anti-HCV, mainly reacting to HCV core protein. The mean interval until the appearance of IgM anti-HCV after onset was 24.1+/-26.2 days. IgG anti-HCV mainly reacted to both core and NS-3 antigen, appearing 42.6+/-42.1 days after onset. From a serial study of 15 AH patients, it was considered that in seven AH patients (46. 7%), the IgM response would precede the IgG response. In another two AH patients, IgM anti-HCV was not detected during the acute disease phase. Of 48 chronic hepatitis patients with HCV-RNA, 40 patients were positive for IgM anti-HCV. Therefore, IgM anti-HCV was useful for diagnosis in some of the AH patients, but it was difficult to use for distinguishing between acute and chronic infection. All four FH patients with HCV-RNA were positive for both IgM and IgG antibody to HCV at onset. Their antibody titres were higher than those of AH patients. These results suggested that, as in FH due to HBV, FH due to HCV could induce strong and rapid humoral immunity.     

Marrow transplantation from hepatitis C virus seropositive donors: transmission rate and clinical course

Bone marrow transplant recipients are at risk for acquiring hepatitis C infection from the donated marrow. Twelve patients who were hepatitis C virus (HCV) RNA-negative pretransplant received marrow from anti-HCV seropositive donors. HCV RNA was present in the sera of seven of these donors. After transplant, serial serum specimens were obtained from all marrow recipients for determination of HCV RNA and aminotransferase levels. All seven recipients of marrow from HCV RNA-positive donors were HCV RNA-positive after marrow infusion; none cleared virus from the serum. All five recipients of marrow from anti-HCV seropositive, HCV RNA-negative donors remained free of HCV RNA in serum up to day 100. Abnormal serum aminotransferases were common in both HCV RNA- negative and HCV RNA-positive marrow recipients. One HCV-infected recipient developed marked elevation in aminotransferases after immunosuppressive drugs were stopped. We conclude that the presence of HCV RNA in the serum of marrow donors is an accurate predictor of HCV infection in marrow recipients. The acute infection was subclinical in all patients. The long-term risk of chronic hepatitis C virus infection in these patients remains to be determined.     

Anti-HCV in post-transfusion hepatitis: deductions from a prospective study

Stored sera from 52 patients who developed post-transfusion hepatitis (PTH) during a prospective study of PTH in Toronto in 1984/85, sera from 111 donors whose blood was transfused into these patients and sera from 50 patients with chronic active hepatitis with a remote history of blood transfusion were tested for anti-HCV. In patients with PTH seroconversion occurred relatively early. Ten converted in less than 14 weeks after transfusion. Only three of the 34 patients (9%) whose hepatitis resolved developed anti-HCV compared to 11 of 18 (61%) whose hepatitis became chronic. Patients who seroconverted had higher alanine aminotransferase (ALT) values during the phase of acute hepatitis than those who did not seroconvert. Most of the patients who developed PTH received blood that was negative for anti-HCV. Four donors whose blood was positive for anti-HCV transmitted hepatitis. Three of the patients developed anti-HCV and chronic hepatitis. One of the recipients did not seroconvert and the hepatitis resolved. Forty-two of the 50 patients (84%) with chronic hepatitis and a remote history of blood transfusion were positive for anti-HCV. We conclude that anti-HCV-positive donors may transmit hepatitis C; that if anti-HCV is diagnostic of hepatitis C, most cases of acute PTH are either not due to hepatitis C or may represent cases of hepatitis C in which the anti-HCV test was undetectable. On the other hand, most cases of PTH which progress to chronic hepatitis are caused by HCV.(ABSTRACT TRUNCATED AT 250 WORDS)     

New perspectives in occult hepatitis C virus infection

Occult hepatitis C virus (HCV) infection, defined as the presence of HCV RNA in liver and in peripheral blood mononuclear cells (PBMCs) in the absence of detectable viral RNA in serum by standard assays, can be found in anti-HCV positive patients with normal serum levels of liver enzymes and in anti-HCV negative patients with persistently elevated liver enzymes of unknown etiology. Occult HCV infection is distributed worldwide and all HCV genotypes seem to be involved in this infection. Occult hepatitis C has been found not only in anti-HCV positive subjects with normal values of liver enzymes or in chronic hepatitis of unknown origin but also in several groups at risk for HCV infection such as hemodialysis patients or family members of patients with occult HCV. This occult infection has been reported also in healthy populations without evidence of liver disease. Occult HCV infection seems to be less aggressive than chronic hepatitis C although patients affected by occult HCV may develop liver cirrhosis and even hepatocellular carcinoma. Thus, anti-HCV negative patients with occult HCV may benefit from antiviral therapy with pegylated-interferon plus ribavirin. The persistence of very low levels of HCV RNA in serum and in PBMCs, along with the maintenance of specific T-cell responses against HCV-antigens observed during a long-term follow-up of patients with occult hepatitis C, indicate that occult HCV is a persistent infection that is not spontaneously eradicated. This is an updated report on diagnosis, epidemiology and clinical implications of occult HCV with special emphasis on anti-HCV negative cases.     

Is it possible to diagnose acute hepatitis C virus (HCV) infection by a rising anti‐HCV titre rather than by seroconversion?

The diagnosis of acute hepatitis C virus (HCV) infection relies on documented positive-seroconversion of HCV antibody (anti-HCV). Because of the detection of seroconversion at an earlier stage by second or third generation anti-HCV enzyme immunoassays (EIA), the diagnosis of acute hepatitis C (AHC) may be underestimated. The aim of this study was to evaluate whether rising anti-HCV titre could be used to diagnose AHC or not. Eighteen patients with a clinical diagnosis of acute hepatitis C were enrolled, including eight cases with documented seroconversion to anti-HCV and 10 cases with clinically suspected acute hepatitis C. Four chronic hepatitis C patients with acute exacerbation were selected as a control group. Serial sera were assayed with a third generation anti-HCV (AxSYM, version 3.0; Abbott, Chicago, IL, USA) and recombinant immunoblot assays (RIBA; Chiron HCV 3.0 Strip; Immunoblot, Emeryville, CA, USA) and the titre of anti-HCV expressed as signal/cutoff (S/CO) ratio and the RIBA patterns were correlated. Seven of eight documented AHC (one lacking the initial serum) and five of 10 clinically suspected AHC showed a rising pattern of S/CO values. The initial S/CO values on the first visit were less than 40 in 14 of 18 cases. The RIBA pattern shifted from negative/indeterminate to positive in five of seven documented AHC and 4 of 10 clinically suspected AHC cases. Fifteen of 18 cases had seroconversions of at least one antibody, whilst 85.7% showed a rising S/CO ratio. On the contrary, the S/CO ratio and RIBA pattern remained unaltered in chronic hepatitis C with acute exacerbation. The rise in S/CO was usually accompanied with an increase in the number of RIBA reactive bands and their intensity in acute hepatitis C patients. The rise in S/CO ratios using a third generation anti-HCV assay and the RIBA pattern might be used as a supplemental diagnostic criterion for acute HCV infection.     

HCV HBV感染与肝细胞性肝癌

调查了肝癌高发地区不同肝病患者中丙型肝炎病毒(HCV)感染率。慢性肝病患者绝大多数已被乙型肝炎病毒(HBV)感染。HCV第二代抗体阳性率,肝癌7.3％,肝硬化6.6％,慢性肝炎6.6％和急性肝炎3.4％。两种病毒的复合感染率,肝癌5.1％,肝硬化1.7％,慢性肝炎3.9％和急性肝炎1.1％。在38例HCV抗体阳性的慢性肝病患者中,ALT异常84.2％,有输血史者占57.9％,HCV-RNA阳性率为71.1％。本研究的资料分析提示,在肝癌高发地区尽管HCV抗体阳性率较低,但HCV感染也是肝癌发生的重要病因之一。     

Hepatitis B and hepatitis C virus and chronic kidney disease

The most common cause of liver disease in patients with chronic kidney disease (CKD) remains infection by hepatitis B virus (HBV) and/or hepatitis C virus (HCV). The adverse effects of HBV and/or HCV infections upon survival in patients with CKD have been repeatedly confirmed. An excess risk of death in HBsAg positive or anti-HCV antibody-positive patients may be at least partially attributed to chronic liver disease with its attendant complications. A negative impact of HCV infection on survival after renal transplantation has been linked to extrahepatic complications, including chronic glomerulonephritis, sepsis, chronic allograft nephropathy, post-transplantation diabetes mellitus, and abnormal metabolism of calcineurin-inhibitors. Transmission of HCV infection by grafts from HCV-infected donors has been unequivocally demonstrated. Registry analyses suggest that recipients of kidneys from anti-HCV antibody positive donors are at increased risk of mortality. Renal grafts from HCV-infected donors should be restricted to viremic anti-HCV positive recipients. Several drugs have been recently licensed for therapy of HBV infection but availabledata in patients with CKD is mostly limited to experience with lamivudine. The standard of care for hepatitis C infection in patients on regular dialysis is monotherapy with conventional interferon, according to recent guidelines. Only dire circumstances justify interferon use after renal transplantation.     

A comparison of hepatitis C virus (HCV) RNA and – antibody as markers of infection and predictors of infectivity

Background: The diagnosis of hepatitis C virus (HCV) infection currently relies on the detection of antibody to HCV (anti-HCV). However, anti-HCV positivity may indicate past infection, current infection or possibly non-specific reactivity. For confirmation of current infection the virus needs to be assayed directly and this is possible by the polymerase chain reaction (PCR). Aims: The aims were to compare HCV RNA and anti-HCV as markers of infection in two groups of individuals: (i) a heterogeneous group with suspected HCV infection and (ii) a small group of blood and bone marrow donors, and their respective recipients. Methods: Serum samples were tested for alanine aminotransferase (ALT) as part of a liver function screen, for anti-HCV by ELISAII, and HCV RNA was detected by PCR. Single round and nested PCR was performed using primers designed from the sequence of the 5′-untranslated region of the HCV genome. Results: Of the 36 subjects in the heterogeneous group, 19/22 anti-HCV-positive patients with chronic non-A non-B hepatitis (NANBH) were viraemic, and the majority (17/19) demonstrated elevated ALT. However, HCV RNA was undetected in seven anti-HCV-positive patients, four of whom suffered autoimmune hepatitis Type I and three were low risk blood donors. Of the remaining subjects (seven/36) who were anti-HCV-negative, three/seven were HCV-RNA-positive and included two with acute post-transfusion (PT) NANBH and a recent needlestick victim who contracted HCV. In the second group, four individuals (donors), including a mother with a history of drug use, were implicated in transmission to three recipients. ALT levels were normal in all donors but raised in two of the recipients. PCR determined which of two anti-HCV-negative blood donors was infectious, confirmed transmission between a bone marrow donor and recipient, and indicated that anti-HCV detected in a newborn child represented passive transfer of antibody. Conclusions: Anti-HCV detected by ELISA II is a useful marker of chronic HCV infection, particularly in association with raised ALT. However, HCV RNA is a superior marker of acute HCV infection, a more reliable predictor of infectivity and is more specific.     

Incidence, prevalence, and clinical course of hepatitis C following liver transplantation.

Hepatitis C virus (HCV) is the agent responsible for posttransfusion hepatitis. The incidence, timing, and clinical course of HCV positive hepatitis in liver transplant recipients are unknown. Three hundred and seventeen donor-recipient liver transplant pairs were grouped on the basis of their pretransplant HCV antibody status. The biopsy findings were examined. Four distinct groups were identified on the basis of HCV serology: group I, both were negative; group II, donor was negative and recipient was positive; group III, donor was positive and recipient was negative; group IV, both were positive. The prevalence of anti-HCV positivity in recipients was 13.6%. The rate of seroconversion was 9.2%. Histologic hepatitis not ascribable to any specific cause other than non-A, non-B (NANB) hepatitis occurred in 13.8%. The incidence of histologic chronic active hepatitis was 1.6%, and none progressed to cirrhosis. The concordance rate for a positive anti-HCV serology and NANB hepatitis was 2.8%. Of the 35 patients (group II and IV) with positive anti-HCV serology pretransplant, only 17 were positive posttransplantation. Based on these data it can be concluded that posttransplant NANB hepatitis occurred in 13.8% of liver recipients. Twenty percent of these were anti-HCV positive. Progression to histologic chronic active hepatitis occurs over a period of 1-5 years in 1.6% of cases.     

A prospective study of hepatitis C virus infection after needlestick accidents

Abstract: There have been few prospective studies of hepatitis C virus (HCV) infection after needlestick accidents in hospital employees. In the present study, the prevalence and features of HCV infection after needlestick accidents were evaluated prospectively measuring serum HCV-RNA. Subjects were 56 employees who had HCV needlestick accidents. To monitor the development of hepatitis, the serum ALT levels and HCV-related seromarkers, such as first generation anti-HCV (RIA), second generation anti-HCV (PHA) and HCV-RNA (RT-PCR) were measured every month for at least 12 months after the accidents. Three of 56 (5.4%) recipients developed HCV infection. HCV-RNA was detected in all three recipients within 4 months after the exposure, and second-generation HCV antibody was detected in two of three recipients. The detection of HCV-RNA was earlier than that of HCV antibody. Two of three HCV-infected recipients developed type C acute hepatitis and one of two received interferon therapy; however, the other case received no medication. The detection of HCV-related seromarkers and the elevation of ALT levels were transient in these three recipients; thus, none developed chronic hepatitis. In conclusion, HCV infection developed in 5.4% of recipients within 4 months after HCV accidents. All of these HCV-infected recipients showed fair prognosis. HCV-RNA was a beneficial parameter for early detection of HCV infection.     

Serum hepatitis C virus sequences in posttransfusion non-A, non-B hepatitis.

We investigated 17 patients (12 males and 5 females, ages 2 to 57 years old) with posttransfusion non-A, non-B hepatitis to determine relationships between clinical courses and hepatitis C virus (HCV) markers. The patients were grouped according to time course of abnormal serum alanine aminotransferase (ALT) levels into three categories (chronic biochemical disease, biochemically resolved chronic disease, and acute disease). Latest serum samples (1.3 to 10.8 years after blood transfusion) were used to detect antibodies against C100-3 antigen (anti-HCV) by enzyme-linked immunosorbent assay and HCV sequences by polymerase chain reaction (PCR) assay. Of the 17 patients, 13 patients (76.5%) were anti-HCV positive and 8 patients (47.1%), including one anti-HCV negative case, were positive for HCV RNA. In total, 14 patients (82.4%) were positive for either HCV markers. With respect to clinical course, HCV RNA was detected in six of eight patients (75%) with chronic biochemical disease, and in two of five patients (40%) with biochemically resolved chronic disease. HCV RNA was not detectable in convalescent sera from four patients with acute disease. These results show that there is a relationship between clinical status and HCV viremia, but that normal liver function tests do not always represent the clearance of the virus. Viremia in two patients with normal ALT level suggests that hepatitis is not only caused by viral cytopathic effects, but also by immunologic reactions against virus-infected cells. Thus, PCR is useful in determining the persistence of HCV infection as well as to diagnose anti-HCV negative HCV infection.     

Hepatitis C virus infection in chronic liver disease in Bombay.

To find out the prevalence of antibody of hepatitis C virus (anti-HCV) in patients with chronic liver disease in Bombay, sera from 126 patients (93 men, 33 women; aged 9-70 years, mean 39.7) with chronic liver disease (cirrhosis 103, cirrhosis with hepatocellular carcinoma 3, chronic active hepatitis 20) were tested for HBsAg and anti-HCV antibody. HBsAg positive sera were tested for anti-delta antibody and IgM anti-HBc. All the tests were carried out by ELISA. Of 126 patients, 51 (40.5%) were HBsAg positive, 49 (38.8%) alcoholic and 21 (16.6%) anti-HCV positive. The prevalence of anti-HCV in HBsAg positive, alcoholic and cryptogenic (HBV negative and no alcohol) liver disease patients was 13.7%, 14.7% and 20.5% respectively. Of 21 anti-HCV antibody positive patients, 8 (38%) had received blood transfusions previously. HCV is present in 15-20% of patients with chronic liver disease in Bombay.     

丙型肝炎患者血清和外周血单个核细胞中HCV RNA检测及意义

目的 了解丙肝患者血清和外周血单个核细胞（ＰＢＭＣ）中ＨＣＶＲＮＡ存在情况及有其临床意义，方法 应用套式ＰＣＲ检测４６例急性丙型肝炎（丙型肝炎以下简称丙肝）和４２例慢性丙型肝炎患者血清和ＰＢＭＣ中ＨＣＶＲＮＡ。结果 慢性丙型肝炎患者ＰＢＭＣ中ＨＣＶＲＮＡ检出率显著高于急性丙型患者（Ｐ〈０．００１），急，慢性丙型肝患者血清和慢性丙肝患者ＰＢＭＣ中ＨＣＶ ＲＮＡ检出率显著高于ＡＬＴ正常的抗－ＨＣＶ阳性     

IgM antibody response in acute hepatitis C viral infection.

IgM antibody against hepatitis C virus (IgM anti-HCV) was measured in serial samples from 15 transfusion recipients in whom posttransfusion chronic non-A, non-B hepatitis (NANBH) developed and three plasmapheresis donors during acute HCV infection using recombinant proteins derived from three immunodominant regions: core, NS-3, and NS-4 (c100). IgM anti-HCV core was detected in 13 of 15 posttransfusion patients. Nine of these patients had transient, acute-phase IgM anti-HCV core detected coincidentally or earlier than active IgG anti-HCV core response. The average duration of IgM anti-HCV core reactivity was 8.1 +/- 3.7 weeks. One patient lacking an IgM anti-HCV core response had detectable IgM anti-HCV NS-3 during the acute phase. Passive transfer of IgM anti-HCV was not observed in these posttransfusion cases, in contrast to the high frequency observed for IgG anti-HCV. Late IgM anti-HCV was detectable against core, c100, and NS-3 in three, two, and one posttransfusion patients, respectively. These data indicate that IgM anti-HCV core is a useful acute-phase marker in HCV infection.     

Hepatitis C Virus (HCV) RNA among Anti-HCV-Positive Blood Donors and Their Recipients

Seven of 24 blood donors positive in Ortho's first-generation antibody to hepatitis C virus (anti-HCV) test (EIA-1) were also positive in Ortho's second-generation test (EIA-2). All 7 had at least two anti-HCV positive recipients, whereas only 1 of the 17 EIA-2-negative donors had an anti-HCV-positive recipient. This recipient was a multitransfused patient with von Willebrand's disease. Five of the 7 EIA-2-positive donors had detectable HCV RNA. We traced and tested 38 of the still living blood recipients from the 7 EIA-2-positive donors. Twenty-eight of these were EIA-2 positive and 22 were HCV-PCR positive. One patient with Waldenstroem's hypergammaglobulinemia was EIA-2 negative but HCV-PCR positive. All the EIA-2-positive sera showed reactivity in Ortho's recombinant immunoblot assay (RIBA-2), but 5 of the 28 recipients and 1 of the donors reacted with only one band (RIBA-2 indeterminate). Among 32 recipients who probably had received EIA-2-positive blood, 29 (91%) had markers of an HCV infection. Twenty-two (75%) of the HCV-infected recipients had detectable HCV RNA more than 6 months after transfusion and hence were chronic HCV carriers.     

Evidence that use of a second-generation hepatitis C antibody assay prevents additional cases of transfusion-transmitted hepatitis

SUMMARY. The aim of this study was to determine if using hepatitis C antibody (anti-HCV) enzyme immunoassay version 2.0 (EIA2) in addition to version 1.0 (EIA1) increased the safety of the blood supply. Blood non-reactive by anti-HCV EIA1 was transfused in 1990-92. Stored samples from 40098 units, donated prior to 13 March 1992 were later tested by EIA2. For donor units reactive for anti-HCV by EIA2. a recombinant immunoblot assay (RIBA2) was also carried out. In 63 cases, recipients of transfusions which were EIAZ negative or EIA2 reactive were tested for anti-HCV and elevated alanine aminotransferase (ALT) levels 9-1 2 months after transfusion: pretransfusion anti-HCV status of recipients was unknown. Among these multitransfused patients receiving units that were negative by both EIA1 and EIA2, 1/26 (4%) had anti-HCV. Among transfusion recipients of units negative by EIA1, but who received at least one unit reactive by EIA2,4/37 recipients (11%) were anti-HCV reactive (P = 0.59). For the recipients of EIA2 reactive blood, when the donor unit was RIBA2 non-reactive. 0/23 recipients were reactive by anti-HCV. Among the recipients of a RIBA2 indeterminate unit, 1/10 recipients had anti-HCV, but for patients who received at least one RIBA2 reactive unit, 3/4 recipients had anti-HCV (P = 0.0 3). Hence. second-generation anti-HCV testing detected additional units capable of transmitting hepatitis C that were not detected by first-generation testing. However, RIBA2 is a more specific method than EM2 for determining units capable of transmitting HCV.     

Seroprevalence of antibody against hepatitis C virus (anti-HCV) in various groups of individuals in Korea

We studied the prevalence of anti-HCV in 585 sera from various individuals, using enzyme immunoassay (ElA, Abbott Lab.). Anti-HCV was detected in 16 (10.7%) out of the 150 patients with HBsAg positive liver diseases diagnosed by liver biopsy and they consisted of none out of 10 acute viral hepatitis, 3 out of 15 chronic persistent hepatitis, 4 out of 50 chronic active hepatitis, 2 out of 32 liver cirrhosis, and 7 out of 43 hepatocellular carcinoma. Anti-HCV was detected in 43 (45.3%) out of 95 patients with HBsAg negative liver diseases diagnosed by liver biopsy and they consisted of 5 out of 8 acute viral hepatitis, 2 out of 10 chronic persistent hepatitis, 17 out of 30 chronic active hepatitis, 4 out of 15 liver cirrhosis, and 15 out of 32 hepatocellular carcinoma. Anti-HCV was detected in 22 (38.6%) out of 57 hemodialysis patients, in 3 (6.7%) out of 45 kidney transplants, in 2 (11.1%) out of 18 fatty liver diagnosed by liver biopsy, in 2 (1.3%) out of 150 healthy blood donors, in none out of 40 healthy volunteers, in 6 (31.6%) out of 19 rheumatoid arthritis and in 6 (54.5%) out of 11 systemic lupus erythematosis cases. There were familial clusters of chronic liver diseases in 4.7% of patients with HBsAg negative/anti-HCV positive chronic liver diseases, while in 19.4% of patients with HBsAg positive/anti-HCV negative liver diseases. Incidence of anti-HCV within patients with HBsAg positive liver diseases was higher in HBsAg negative patients than in HBsAg positive patients (17.6% and 10.3%, respectively). In hemodialysis patients, the number of hemodialysis procedures was significantly higher in anti-HCV positive patients than in anti-HCV negative patients (P<0.009), but the amount of blood transfusion showed no difference between anti-HCV positive and negative patients. We concluded that HCV might be an important cause of various types of HBsAg negative liver diseases in Korea, and intrafamilial transmission of HCV might be less common than of hepatitis B virus (HBV), and long duration of hemodialysis might be related to the increment of incidence of anti-HCV in hemodialysis units, and the high frequency of false positive anti-HCV in autoimmune disorders without evidence of any liver diseases might limit the use of the current anti-HCV tests.     

Management of viral hepatitis in hematologic malignancies

Viral hepatitis is the third major cause of liver dysfunction in allogeneic transplant recipients and has become a significant concern in patients with hematological malignancies receiving chemotherapy. Thus, identification of patients at risk for viral hepatitis is very important when evaluating and treating hematological malignancies. Serologic screening for all patients should include anti-HCV, hepatitis B surface antigen (HBsAg), hepatitis B surface antibody (anti-HBs), and hepatitis B core antibody (anti-HBc) testing. Current therapies for hepatitis B (HBV) virus infection are aimed at viral suppression, while treatment for hepatitis C (HCV) virus can eradicate infection in many treated patients. To prevent HBV viral reactivation, prophylaxis with nucleoside analogues should be initiated for all HBsAg-positive patients. HCV infection appears to have little impact on short-term survival after bone marrow transplantation (BMT), but eventually can impact long-term survival due to progression of liver disease. In this review we will highlight the mechanisms of virus reactivation, clinical manifestations, and management strategies to minimize acute and chronic morbidity in this population.     

The accuracy of SM-HCV rapid test for the detection of antibody to hepatitis C virus

OBJECTIVE: Conventional tests for antibody to hepatitis C virus (HCV) require considerable time before results are available. The aim of this study is to examine the accuracy of a new quick test (SM-HCV Rapid Test) for the detection of antibody to hepatitis C virus with reference to the well-established third generation enzyme immunoblot assay (EIA-3; Abbott Laboratories, Chicago, IL). METHODS: A total of 290 subjects (100 patients with chronic hepatitis C infections, 95 patients with other chronic liver diseases, 95 healthy subjects) were recruited. Thirty microliters of serum was tested for anti-HCV by SM-HCV Rapid Test according to the manufacturer's instruction. Liver function tests and serum HCV RNA by polymerase chain reaction (PCR) were measured. RESULTS: In the 100 patients positive for anti-HCV by EIA-3, 98 of these patients were also positive for anti-HCV by SM-HCV Rapid Test. In the 95 patients with other chronic liver diseases, 94 samples were negative for anti-HCV by both EIA-3 and SM-HCV Rapid Test. The remaining one patient was positive for anti-HCV by the EIA-3 but negative by the SM-HCV Rapid Test. In the 95 controls, which were negative for anti-HCV by EIA-3, all were also negative for anti-HCV by SM-HCV Rapid Test and HCV RNA by PCR. Using EIA-3 as the gold standard screening test for anti-HCV, the sensitivity and the specificity of SM-HCV Rapid Test were 98% and 100%, respectively. The positive predictive value and negative predictive value of SM-HCV Rapid Test were 100% and 97.9%, respectively. CONCLUSIONS: SM-HCV Rapid Test is a reliable test with high sensitivity and specificity. The anti-HCV result can be available within a very short period of time. It is a useful screening test for anti-HCV.     

Chronic hepatitis C without anti-hepatitis C antibodies by second-generation assay

To study the clinicopathologic features of hepatitis C viremic patients negative for hepatitis C antibodies (anti-HCV) by current second-generation assay, we categorized 139 consecutive histologically verified patients with chronic non-A, non-B hepatitis into three groups: 121 (87%) were positive for second-generation anti-HCV (group A); 10 (7%) were negative for second-generation anti-HCV but positive for HCV RNA (group B); and 8 (6%) were negative for both antibodies and viremia (group C). Six (60%) of group B patients could be further detected by a new third-generation assay, but none of group C patients was third-generation anti-HCV-positive. The demographic features, mean peak serum alanine aminotransferase levels, HCV genotype distribution, and histologic changes were comparable among the three groups. The study indicates that most patients with chronic hepatitis C in Taiwan could be identified by current second-generation assay, and viremic but antibody seronegative patients were clinicopathologically similar to the seropositives. Most patients of the latter group could be diagnosed by a third-generation assay, indicating the usefulness of this assay.