Occult hepatitis C virus infection： A new form of hepatitis C

INTRODUCTION The etiology of liver disease is unknown in approximately 10% of patients with abnormal results on liver function tests. Some authors have reported that occult hepatitis B virus could be the cause of a proportion of these cryptogenic chronic …     

Transmission of hepatitis C virus: Self-limiting hepatitis or chronic hepatitis?

It has been suggested that hepatitis C virus(HCV)is selectively transmitted to a new host as an infectious clone from multiple HCV variants(quasispecies)in the donor.Most individuals with HCV infection develop chronic hepatitis,but approximately 15%-40%of them clear the virus spontaneously and the hepatitis is resolved in a self-limiting manner in the acute phase of infection.This difference in the outcome of acute hepatitis C is attributable to both viral characteristics and genetic regulation of infection.In particular,the evolutionary dynamics of the infecting virus and host genetic polymorphisms pertaining mainly to the immune system,including polymorphisms in the region of the Interleukin 28B gene encoding interferon-λ-3,are associated with susceptibility to HCV infection.     

Acute hepatitis C complicated by pancreatitis: another extrahepatic manifestation of hepatitis C virus?

In hepatitis C virus (HCV) infection a number of extrahepatic manifestations have been described, generally caused by immune phenomena. Here we report a case of acute pancreatitis, detected during an acute hepatitis C infection, in an elderly female patient.     

Does the clinical outcome of hepatitis C infection vary with the infecting hepatitis C virus type?

Whether differences in the natural history of hepatitis C virus (HCV) can be explained by differences in the infecting HCV type is unknown. The aim of this study was to investigate whether the HCV type might influence the clinical outcome of infection. Study serum samples were assembled from 749 individuals enrolled into the UK HCV National Register from which data on clinical outcomes were extracted. HCV-RNA-positive specimens were genotyped and HCV-RNA-negative specimens serotyped. Logistic regression analysis was used to investigate the independent effect of HCV type on viral clearance by comparing patients who were HCV RNA negative (n = 86) with those who were HCV RNA positive (n = 508). The same method was used to investigate whether HCV type was associated with histological stage of liver disease. The prevalence of HCV type 1 among those who cleared infection was 69% and among those who remained HCV RNA positive was 51%: Type 1 infections were more likely to be HCV RNA negative than non-1 types (OR 0.47, 95% CI 0.29-0.78, P = 0.003). Type 1 infections were also more likely to be associated with histological stage scores above the median when compared with non-1 types (OR 2.03, 95% CI 1.07-3.83, P = 0.03). In conclusion, HCV type 1 infection was more often HCV RNA negative, suggesting that spontaneous clearance may occur more commonly with this type. Among the RNA-positive infections, type 1 infection may be more aggressive than types 2/3.     

Low‐level hepatitis C viremia and humoral immune response to NS4 in chronic hepatitis B virus‐hepatitis C virus coinfection

Background: There is a limited amount of published data on the interference of hepatitis B virus (HBV) on hepatitis C virus (HCV). The aim of this study was to investigate the effect of concurrent HBV infection on serum titers of HCV RNA and HCV antibody profiles in chronic HCV infection. Methods: The clinical and virological profiles (serum titers of HCV RNA, HCV genotypes and antibody profiles) of 25 patients with chronic HBV‐HCV coinfection were compared with those of 25 age‐ and sex‐matched patients with HCV infection alone. Results: Among the 25 patients with HBV‐HCV coinfection, only 3 were found hepatitis Be antigen (HBeAg) and HBV DNA positive by hybridization assays, and the other 11 were found HBV DNA positive by polymerase chain reaction. Genotype 1b was dominant in both HBV‐HCV coinfection and HCV infection alone (64% versus 84%, P?>?0.1). Patients with HBV‐HCV coinfection had significantly lower alanine aminotransferase (ALAT) levels and inflammatory scores but higher fibrosis scores than those with HCV infection alone. Serum titers of HCV RNA were significantly lower in HBV‐HCV coinfection than in HCV infection alone. The frequency and relative intensity of antibody response to core, E2/NS1, NS3, and NS5 showed no significant difference between the two groups, but antibody response to NS4 was diminished significantly in HBV‐HCV coinfection. Conclusions: In HBV‐HCV coinfection, serum levels of HBV DNA are usually low or undetectable. Concurrent HBV infection, however, could interfere with HCV replication and suppress antibody response to NS4. The biological significance of selective inhibition of humoral immune response to NS4 in HBV‐HCV coinfection should be further studied.     

Treatment of hepatitis C in HIV/hepatitis C co-infected patients: what is the evidence?

Before the advent of highly active antiretroviral therapy (HAART), the vast majority of HIV-infected patients died from AIDS-related diseases. But, amongst those with access to HAART, AIDS is no longer the leading cause of death. Instead, liver disease is fast becoming the commonest cause of death in HIV-infected patients, particularly in those who have a co-infection with hepatitis C (HCV). The four recent comparative trials of peginterferon and ribavirin in HIV/HCV coinfected patients have provided valuable new information about the most appropriate treatment of this difficult group of patients. As with HIV-negative patients, it is clear that peginterferon alpha has advantages over non-pegylated treatment, with superior efficacy, in the form of higher sustained virological responders and comparable safety. Discontinuation rates were higher than reported in HCV mono-infected patients but comparable for most treatment arms. Furthermore, in about half the patients, treatments were not stopped during the first months of treatment because of side effects, but due to non-early virological response.     

Acute hepatitis C： Prospects and challenges

More than 170 million people worldwide have chronic hepatitis C. Acute hepatitis C is rarely diagnosed because it is commonly asymptomatic. Most infected patients are unaware of their condition until the symptoms of chronic infection manifest. Treatment of acute hepatitis C is something of a paradox because spontaneous resolution is possible and many patients do not have symptoms. However, several factors provide a rationale for treating patients who have acute hepatitis C. Compared with acute hepatitis C, chronic hepatitis C is associated with a worse prognosis, the need for more intensive treatment, longer treatment duration, and a decrease in successful treatment outcomes. Conversely, early intervention is associated with improved viral eradication, using a regimen that is better tolerated, less expensive, more convenient, and of shorter duration than the currently approved combination therapies for chronic hepatitis C.     

Predictive value of different hepatitis C serological assays in the treatment of chronic hepatitis C with interferon α

In order to predict the complete response rate of natural interferon-α (nIFN-α) treatment in patients with chronic active hepatitis C, we examined the predictive value (PV) of different hepatitis C serological assays. We performed first generation (ver.1) and second generation (ver.2) hepatitis C virus (HCV) branched DNA-probe assays (bDNA-probe), HCV core protein assay (core protein), HCV Amplicor Monitor assay (amplicor monitor), and HCV competitive polymerase chain reaction (competitive PCR) assay, using serum samples collected immediately before initiation of treatment. For each marker, we studied, in patients stratified by serological group (Gr), which predictive value (PV) of the HCV titers showed association with the therapeutic effect. In 59 Gr 1 patients, complete response to nIFN-α treatment was predicted from the following PVs for each marker: 0.5 Meq/ml or less (odds ratio 11.7; P = 0.0010) with ver.1, 1.0 Meq/ml or less (odds ratio 5.3; P = 0.0119) with ver.2 of the bDNA-probe, 50 pg/ml or less (odds ratio 10.3; P = 0.0062) with core protein, 200 × 10³ copy/ml or less (odds ratio 7.8; P = 0.0031) with amplicor monitor, and 10⁴ copy/ml or less (odds ratio 6.2; p = 0.8395) with competitive PCR. In 27 Gr 2 patients, the PV for each marker indicating complete response was as follows: There was no relationship between PV and therapeutic effect with ver.1 of the bDNA-probe, while the PVs for the other markers were 0.2 Meq/ml or less (odds ratio 2.2; P = 0.3788) with ver.2, 20 pg/ml or less (odds ratio 5.6; P = 0.0597) with core protein, 400 × 10³ copy/ml or less (odds ratio 4.0; P = 0.2965) with amplicor monitor, and 10^5.5 copy/ml or less (odds ratio 29.2; P = 0.0096) with competitive PCR. Our findings showed that complete response to the treatment may be predicted using the appropriate PV for each marker. (Received Apr. 13, 1998; accepted Aug. 28, 1998)     

Does previous hepatitis A infection affect the clinicopathological status of chronic hepatitis C?

BACKGROUND/AIMS: The aim of the study was to evaluate the effect of previous infection with hepatitis A virus on histopathological and biochemical changes in chronic hepatitis C. METHODOLOGY: Anti-hepatitis A virus antibodies, liver histopathology and alanine aminotransferase activity were determined in 82 patients with chronic hepatitis C. The liver biopsy specimen of each patient was examined according to Scheuer's classification to indicate the severity of the inflammatory cell infiltration in the portal/periportal and parenchymal area (grading) in a 0-4 scale and fibrous stage (staging) in a 0-4 scale. RESULTS: The overall prevalence of anti-hepatitis A virus antibodies was 63.1%. Anti-HAV-positive patients were significantly older than anti-HAV-negative ones (mean age 42.5 and 33.1 years respectively, p < 0.05). After stratifying the study sample into two age groups (< 40 years and > or = 40 years) the percentage of anti-HAV-positive individuals was similar irrespective of grading, staging score or presence of steatosis. No remarkable differences were observed between the anti-HAV-positive and -negative group in the mean ALT activity. CONCLUSIONS: The results of our study indicate that previous hepatitis A is not associated with progressive course of chronic hepatitis C.     

Is the hepatitis C virus epidemic over in Egypt? Incidence and risk factors of new hepatitis C virus infections

Objectives: To estimate hepatitis C virus (HCV) incidence rates and identify risk factors for current HCV transmission with emphasis on the role of living with infected household family members in rural Egypt. Methods: A 4‐year population‐based, cohort study of seronegative villagers was conducted to identify incident HCV seroconversion cases. A risk factor questionnaire and blood samples for anti‐HCV EIA‐3 and HCV RNA polymerase chain reaction testing were collected at two rounds of follow‐up. Incidence rates, relative risks and 95% confidence interval (CI) were calculated based on a Poisson distribution. A matched case–control analysis to explore specific behavioural predictors of infection was conducted and odds ratios were obtained by conditional logistic regression. Results: Twenty‐five participants (11 females) seroconverted in 10 578 person years of follow‐up (PY), (incidence rate of 2.4/1000 PY; 95% CI: 1.6–3.5). The median age at seroconversion was 26 years [interquartile range (IQR) 19–35] among males and 20 years (IQR 13–24) among females. The only significant risk factor identified for these cases was receiving injections [adjusted odds ratio (OR_adj)=3.3; 95% CI: 1.1–9.8]. Two of the 17 viraemic seroconvertors were infected with the same strain as at least one of their family members. Conclusion: This study identified the important role of injections in spreading HCV infection in this rural community. National healthcare awareness and infection control programmes should be strengthened to prevent further transmission. Screening of families of infected HCV subjects should be an essential part of case management for early detection and management.     

Role of hepatitis C virus in myocarditis and cardiomyopathies

Recent nationwide clinico-epidemiological surveys in Japan showed that the occurrence of cardiomyop-athies was most frequently seen in the age of sixties,and that cardiomyopathies are important causes of heart failure inthe elderly.Viral infection was conventionally considered to cause myocarditis,which resulted in the development ofdilated cardiomyopathy.Recent studies suggest that hepatitis C virus(HCV)is involved in the development of dilatedcardiomyopathy,hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy in addition to myo-carditis.Furthermore,left ventricular aneurysm represents the same morbid state not only after myocardial infarctionbut also after myocarditis.There were wide variations in the frequency of detection of HCV genomes in cardiomyopathyin different regions and in different populations.Major histocompatibility complex class Ⅱ genes may play a role in thesusceptibility to HCV infection,and may influence the development of different phenotypes of cardiomyopathy.If infact the myocardial damage is caused by HCV,it might be expected that interferon(IFN)administration would beuseful for its treatment.Hepatitis patients receiving IFN treatment for hepatitis were screened by thallium myocardialscintigraphy,and an abnormality was discovered in half of the patients.Treatment with IFN resulted in a disappear-ance of the image abnormality.It has thus been suggested that mild myocarditis and myocardial damage may be curedwith IFN.We have recently found that high concentrations of circulating cardiac troponin T are a specific marker ofcardiac involvement in HCV infection.By measuring cardiac troponin T in patients with HCV infection,the preva-lence of cardiac involvement in HCV infection will be clarified.We are proposing a collaborative work on a globalnetwork on myocarditis/cardiomyopathies due to HCV infection.(J Geriatr Cardiol 2004;1(2):83-89.)     

Relationship between the pathogenesis of sarcoidosis and hepatitis C

I read the article by Kim et al with great interest[1]. This is arare case of systemic sarcoidosis in a patient