The natural course of chronic hepatitis C: A comparison between patients with genotypes 1 and 2 hepatitis C viruses

Kobayashi, Masakazu; Tanaka, Eihachirô; Sodeyama, T; Urushihara, Akihiko; Matsumoto, Akihiro; Kiyosawa, K

doi:10.1002/hep.510230406

Cited by 158 publications

(78 citation statements)

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“…Multivariate analysis in those studies confirmed increasing patient age at the time of diagnosis to be an independent factor for progression from chronic hepatitis to cirrhosis 22 and the incidence of HCC. 23 However, aging was associated with histologic severity and induced carcinogenesis, and the authors did not provide clear data regarding a relation between aging and HCC development by multivariate Cox regression analyses. The results of the current study demonstrated that age at diagnosis was an independent factor for HCC development by multivariate Cox regression analyses in a cohort study.…”

Section: Discussionmentioning

confidence: 98%

Impact of aging on the development of hepatocellular carcinoma in patients with posttransfusion chronic hepatitis C

Hamada

Yatsuhashi

Yano

et al. 2002

Cancer

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BACKGROUNDHepatitis C virus (HCV) infection is a heterogeneous disease, the natural history of which remains controversial. There is solid evidence that chronic HCV infection is responsible for the occurrence of hepatocellular carcinoma (HCC). The aim of the current cohort study was to determine the rate of the development of HCC from the time of primary HCV infection and to assess the risk factors for the development of HCC in chronic posttransfusion hepatitis C patients.METHODSFour hundred sixty‐nine patients with clinically compensated HCV, who had undergone a single blood transfusion comprised the current study cohort. Patients with other risk factors for chronic liver disease were excluded. All patients were referred to the liver center at the National Nagasaki Medical Center between December 1980 and December 1998 and were followed prospectively until the end of the analysis (June 2000).RESULTSFollow‐up data were obtained for 445 patients. The mean duration from HCV infection to the end of the observation was 28 years. Fifty‐two patients (11.1%) progressed to HCC. The mean duration from the time of blood transfusion to the diagnosis of HCC was 31 years. Multivariate Cox regression analyses revealed age, fibrosis, duration from HCV infection to study entry, and alcohol consumption to be the independent factors affecting the development of HCC. The risk of developing HCC in patients age ≥ 56 years was increased 7.8‐fold compared with that in patients age < 56 years. The mean age of patients at the time of HCC diagnosis was 65 years (range, 58–79 years).CONCLUSIONSAt the time of diagnosis, 92% of the 52 HCC patients were age > 60 years and 38 of the HCC patients (73%) were in their 60s. There was a significantly negative correlation between the duration from HCV infection to the development of HCC and the age of the patient at the time of infection (correlation coefficient = 0.702; P < 0.0001; Y = 61.1–0.82X), indicating that the age of patients, rather than the duration of HCV infection, is more significant for HCC development in patients with posttransfusion HCV. Moreover, these data may contribute to the design of an optimal follow‐up schedule for patients with posttransfusion HCV. Cancer 2002;95:331–9. © 2002 American Cancer Society.DOI 10.1002/cncr.10662

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Section: Discussionmentioning

confidence: 98%

Impact of aging on the development of hepatocellular carcinoma in patients with posttransfusion chronic hepatitis C

Hamada

Yatsuhashi

Yano

et al. 2002

Cancer

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“…Several reports suggest, in fact, a difference in pathogenicity and responsiveness to IFN treatment according to the genotype. In this setting, patients with genotype 1b have a more severe and progressive liver disease [12][13][14][15] and are more likely to have a decreased likelihood of success with IFN therapy. [16][17][18][19] On the contrary, genotype 2a is more likely to be found among apparently healthy blood donors than in patients with CLD, 32 or in patients with mild CLD or in those who respond better to IFN therapy.…”

Section: Discussionmentioning

confidence: 99%

“…[16][17][18][19] On the contrary, genotype 2a is more likely to be found among apparently healthy blood donors than in patients with CLD, 32 or in patients with mild CLD or in those who respond better to IFN therapy. [12][13][14][15][16][17][18][19] HCV might be a causative cofactor in the pathogenesis of B cell NHL: it is found in a significative percentage of some histotypes of NHL, 8,11,33,34 it is known to be able to infect B lymphocytes circulating in the peripheral blood (PB) 35 or infiltrating the bone marrow (BM) 36 and the liver, 37 and in vitro studies have shown its ability to infect a human BM-derived B cell line and the PB MNC from healthy subjects. [38][39][40] If this is the case, it would appear appropriate to assess the prevalence of different HCV genotypes among the patients bearing a B cell NHL, with the aim of finding a possible correlation between a particular genotype and the lympho-proliferative disorder.…”

Section: Discussionmentioning

confidence: 99%

“…7 On the basis of its prevalence among 537 patients with different lymphoproliferative disorders, 180 with MGUS (monoclonal gammopathy of unknown significance), and 470 with B cell NHL, we previously identified the B cell NHL (in particular the immunocytoma) associated with the production of cryoglobulins (in particular type II), as the probable pathogenetic target of HCV. [8][9][10][11] Since several investigators have reported on the significance of specific HCV genotypes as determinants of liver disease severity and responsiveness to interferon-␣ (IFN), [12][13][14][15][16][17][18][19] one might speculate on the involvement of particular viral genotypes in the pathogenesis, clinical features and response to therapy of HCV-related B cell NHL. With this in mind we have now assessed the prevalence of viral genotypes in our group of patients with HCV-related B cell NHL.…”

Section: Introductionmentioning

confidence: 99%

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The genotype of the hepatitis C virus in patients with HCV-related B cell non-Hodgkin’s lymphoma

et al. 1997

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Increasing evidence suggests that the hepatitis C virus (HCV) might be involved in the pathogenesis of B cell non-Hodgkin's lymphomas (NHL). Since several HCV genotypes are currently identifiable and might be involved in the pathogenesis of different diseases (with different severity and responsiveness to therapy), the aim of our study was to assess the prevalence of viral genotypes in a group of patients with HCV-related NHL. Among 470 consecutive patients, 42 HCV Ab-positive cases were identified. HCV RNA could be detected by reverse transcriptase-polymerase chain reaction and genotyping performed in 31 of these cases. As compared to our control group (211 healthy blood donors and patients with chronic liver disease), a striking high prevalence of genotype 2ac was detected among B cell NHL (48.4 vs 9.0%), with a relative risk of infection of 5.37 (P Ͻ 0.0001). No major differences were observed in the distribution of NHL histotypes and in the clinical features among patients with genotype 1b (the other most frequent genotype) or 2ac, a part from a trend towards a higher percentage of liver disease and a lower likelihood of response to interferon for patients with genotype 1b. The same high prevalence of genotype 2ac has been recently reported in patients with mixed cryoglobulinemia (MC), monoclonal gammopathies, B cell NHL complicating MC and autoimmune hepatitis. All these data taken together suggest that genotype 2ac might be involved in the pathogenesis of lymphoproliferative and autoimmune disorders.

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“…Studies suggest that specific genotypes, such as genotype 1, can be more cytopathic [31] or can induce more rapid progression of the disease than do other genotypes [32]. Genotype 1 has been shown to be the genotype most strongly associated with chronic HCV infection [33].…”

Section: Life Cycle and Pathogenicity Of Hcvmentioning

confidence: 99%

Pathogenesis of hepatitis C: HCV consensus 2007

Viso¹

2007

Braz J Infect Dis

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The chronic hepatitis C virus (HCV) infects approximately 130 million people worldwide [1]. It is estimated that approximately 15% of HCV-infected individuals eliminate the virus spontaneously, that 25% develop a mild form of the disease, and that 60% develop the chronic progressive form [2]. The elimination or persistence of HCV infection depends on the balance between the effectiveness, specificity and rapidity of the innate and adaptive immune responses, as well as on the HCV replication rate [3]. Persistence of HCV can also be caused by infection at privileged (extrahepatic) sites, viral inhibition of antigen presentation, selective immune suppression, negative regulation of HCV gene expression, viral mutations, immune exhaustion of T cells and the incomplete differentiation of memory T cells [4,5].Fibrosis is the principal complication of chronic hepatitis C, and it is estimated that 20% of patients develop cirrhosis over a period of 10, 20 or 30 years [2,6]. The progression of fibrosis increases morbidity and mortality in chronic hepatitis C [7], since it can lead to death due to complications caused by cirrhosis or hepatocarcinoma [2].Various studies have associated the progression of fibrosis in hepatitis C with diverse factors such as: the kinetics and pathogenicity of HCV; host-HCV interaction; intrinsic host factors such as demographic profile, body mass index and diabetes mellitus; host exposure to external factors; and the form of HCV acquisition. Life Cycle and Pathogenicity of HCVBelonging to the Flaviviridae family, HCV is a small enveloped virus [8]. Its genome consists of one RNA molecule that is composed of two terminal regions, 5'-and 3'-untranslated regions, and between these there is a single open reading frame that encodes a polyprotein with approximately 3000 amino acids. This polyprotein cleaves at the N-terminal side of three structural proteins, the nucleocapsid (core), envelope 1 (E1) and envelope 2 (E2), all of which are involved in the architectural organization of HCV. At the carboxylterminal side, the polyprotein cleaves to six nonstructural proteins, NS2, NS3, NS4 (NS4A and NS4B), NS5 (NS5A and NS5B) and NS6, which are responsible for the life cycle of the virus [9].After entering a susceptible host, HCV invades, infects and replicates within the blood stream, repeating the process in various tissues, as well as in peripheral B and T lymphocytes, as it proceeds to the liver by tropism, passing through various tissues such as those of the pancreas, thyroid, adrenal glands, spleen and bone marrow [10][11][12]. Since HCV can also directly infect the lymphatic tissue, its stimulation can lead to the development of B-cell lymphomas [13]. It is known that the liver is the principal site of HCV replication, and various studies have shown that this virus infects approximately 10% of hepatic cells [5]. Infection with HCV at extrahepatic sites can promote the appearance of HCV variants [14,15], thereby decreasing the chance that the immune system will recognize the virus.To enter the host ...

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The natural course of chronic hepatitis C: A comparison between patients with genotypes 1 and 2 hepatitis C viruses

Cited by 158 publications

References 1 publication

Impact of aging on the development of hepatocellular carcinoma in patients with posttransfusion chronic hepatitis C

Impact of aging on the development of hepatocellular carcinoma in patients with posttransfusion chronic hepatitis C

The genotype of the hepatitis C virus in patients with HCV-related B cell non-Hodgkin’s lymphoma

Pathogenesis of hepatitis C: HCV consensus 2007

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