SEN virus infection influences the pathological findings in liver but does not affect the incidence of hepatocellular carcinoma in patients with chronic hepatitis C and liver cirrhosis

Moriyama, Mitsuhiko; Mikuni, Morio; Matsumura, Hiroshi; Nakamura, Hitomi; Oshiro, Shyu; Aoki, Hiroshi; Shimizu, Toshihiro; Yanagimoto, Hiroaki; Shioda, Atsuo; Kushima, Miki; Tanaka, Naohide; Arakawa, Yasuyuki

doi:10.1111/j.1478-3231.2005.01076.x

Cited by 5 publications

(4 citation statements)

References 31 publications

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“…In addition, M.M. has been reported in a number of journals on the relationship between the degree of IR of hepatocytes and the pathogenesis of HCC development 3,13,[21][22][23][24][25][26][27][28] The sections were mounted on a laser-capture microscope (LMD6500 system, Leica Microsystems), and LCM was performed within 72 h of the staining. The micro-dissected sections were collected in tube caps (Thermo Scientific Japan, Yokohama, Japan) with 10 μL of solution no.…”

Section: Histological Evaluationmentioning

confidence: 99%

The proliferation of atypical hepatocytes and CDT1 expression in noncancerous tissue are associated with the postoperative recurrence of hepatocellular carcinoma

Moriyama

Midorikawa

Matsumura

et al. 2022

Sci Rep

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Recently, we reported that extent of proliferation of atypical hepatocytes (atypical hepatocytes) was most important histological risk factor for development of hepatocellular carcinoma (HCC) from chronic hepatitis C or liver cirrhosis. Here, we aimed to clarify whether the atypical hepatocytes in noncancerous sections is also involved in postoperative recurrence. Furthermore, we investigated significant genes involved in the atypical hepatocytes. Association between the extent of atypical hepatocytes in noncancerous tissue and postoperative recurrence was validated in 356 patients with HCC. Next, we identified putative signature genes involved in extent of atypical hepatocytes. First, atypical hepatocytes or hepatocytes other than the atypical hepatocyte in noncancerous sections of 4 HCC patients were selectively collected by laser capture microdissection (LCM). Second, the gene expression profiles of the selected hepatocyte populations were compared using Ion AmpliSeq Transcriptome Human Gene Expression Kit (Thermo Fisher SCIENTIFIC, Waltham, MA, USA) analysis. Finally, we validated the mRNA expression of the extracted genes in noncancerous frozen liver tissue from 62 patients with HCC by RT-qPCR to identify the signature genes involved in both the extent of atypical hepatocytes and postoperative recurrence. Furthermore, the extent of atypical hepatocytes and CDT1 expression in noncancerous sections from 8 patients with HCC were also validated by selectively collecting samples using LCM. The extent of atypical hepatocytes was associated with postoperative recurrence. Of the genes that showed significant differences in expression levels between two populations, the expression of the chromatin licensing and DNA replication factor 1 (CDT1) gene was most strongly associated with the extent of atypical hepatocytes and was also associated with postoperative recurrence. Furthermore, CDT1-positive cells that exhibited stronger expression resembled those morphologically considered to be atypical hepatocytes. CDT1 and Ki-67 were colocalized in the nuclei of both hepatocytes and cancer cells. The hepatocytes in noncancerous livers were not uniform in each hepatocyte population, suggesting that the accumulation of genetic abnormalities was variable. We found that the strong degree of atypical hepatocytes and high CDT1 mRNA expression represent a high carcinogenic state of the liver. Thus, we consider the evaluation of degree of these could support the personalized medicine.

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Section: Histological Evaluationmentioning

confidence: 99%

The proliferation of atypical hepatocytes and CDT1 expression in noncancerous tissue are associated with the postoperative recurrence of hepatocellular carcinoma

Moriyama

Midorikawa

Matsumura

et al. 2022

Sci Rep

Self Cite

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“…Although SEN virus is found in the serum of a large percentage (13–67%) of patients with HCC, no study has shown the incidence of the tumour in these patients to be significantly higher than that in the corresponding control groups . For example, a study in Thailand that included a control group and patients chronically infected with HCV or HBV showed that SEN virus infection alone was not associated with HCC development .…”

Section: Sen Virusmentioning

confidence: 99%

Hepatitis viruses (other than hepatitis B and C viruses) as causes of hepatocellular carcinoma: an update

Kew

2012

Journal of Viral Hepatitis

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Chronic hepatitis B and C virus infections are universally accepted as causes of hepatocellular carcinoma in humans. Hepatitis A and E viruses cause only acute self-limiting infections of the liver. Of the remaining hepatitis viruses - Delta hepatitis, hepatitis G (GB-C), TT and SEN - all have at some time been incriminated as causes of hepatocellular carcinoma. Delta hepatitis virus requires helper functions from hepatitis B virus to become invasive. Chronic Delta/hepatitis B viral co-infection runs a more severe course than that resulting from chronic hepatitis B virus infection alone, with progression to cirrhosis being more likely and more rapid. A substantial majority of the early studies did not find an increased incidence of hepatocellular carcinoma in co-infected individuals. But more recently, an increased incidence of the tumour has been recorded more often than no increase. Further studies are needed to draw a firm conclusion with regard to the hepatocarcinogenic effect of dual Delta/hepatitis B virus co-infection. With one exception, no published study (of 13) has incriminated chronic infection with hepatitis G virus as a cause of hepatocellular carcinoma. The dissenting study, published in 1999, was the only one performed in the United States. Fewer studies of the hepatocarcinogenic effect of TT virus have been performed. Apart from one study, published in 1999, no convincing evidence is available that supports a causal role for TT virus in hepatocarcinogenesis. The exception was in Japanese patients with high hepatitis C viral loads but independent of chronic hepatitis C virus infection. No evidence has been produced to indicate that SEN virus causes hepatocellular carcinoma.

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“…In addition, Yoshida et al (2002) reported no significant differences between SENVpositive and SENV negative patients regarding serum albumin, total bilirubin and transaminase levels. Also, many studies reported absence of significant difference in the blood biochemical parameters between the SENV DNA-positive and -negative chronic hepatitis patients (Tangkijvanich et al, 2003;Moriyama et al, 2005).…”

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confidence: 99%

“…On the contrary, another study documented that SENV co-infection may influence the histopathological features of the livers of patients with CHC but does not affect the outcome of patients with type C chronic liver disease. The histological features of the livers of SENV DNA-positive patients included more severe parenchymal inflammatory cell infiltration and more immune response (Moriyama et al, 2005).…”

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confidence: 99%

Does SEN virus (SENV) infection affect the progression of chronic hepatitis C or B among Egyptian patients?

Elsherbiny¹,

Hassan²,

Ahmed³

et al. 2015

Afr. J. Microbiol. Res.

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The effect of SENV infection on chronic viral hepatitis is not very clear till now. Information regarding SENV infections in the Egyptian population where hepatitis viruses are prevalent is limited to a certain extent. We aimed to determine the frequency of SENV and its genotypes H and D in Egyptian patients with chronic hepatitis B (CHB) or C (CHC) and to study its possible role in the progression of liver disease. A total of 112 patients with chronic hepatitis (18 CHB and 94 CHC) were subjected to clinical assessment, laboratory and histological examinations. DNA from sera was extracted and SENV DNA was amplified by polymerase chain reaction. SENV DNA was detected in 28.6% of patients with chronic hepatitis (32/112). The percentage was 33.3 and 27.7% in CHB and CHC patients respectively. SENV-H was detected more frequently than SENV-D genotype. For CHC patients without cirrhosis (n=44), SENV was negative in 90.9% (40/44) compared to 9.1% (4/44) SENV positive giving a statistically significant difference (<0.001). A significantly higher percentage of patients showed twofold or more increase in the aspartate transaminase (AST) and alkaline phosphatase (ALP) among SENV negative CHC patients compared to SENV positive patients (P=0.04 , 0.03 respectively). In cirrhotic patients (n=58), both the levels of ALP and serum total bilirubin were significantly higher in SENV negative compared to SENV positive patients (P values were 0.01). For CHB patients, no statistically significant difference was detected regarding any of the studied parameters. We conclude that SENV does not worsen the progression of chronic viral hepatitis. This may reflect a possible protective effect of SENV in CHC patients which needs to be emphasized by further larger studies.

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SEN virus infection influences the pathological findings in liver but does not affect the incidence of hepatocellular carcinoma in patients with chronic hepatitis C and liver cirrhosis

Abstract: SEN-V co-infection may influence the histopathological features of the livers of patients with type C CH and LC but does not affect the outcome of patients with type C chronic liver disease.

Cited by 5 publications

References 31 publications

The proliferation of atypical hepatocytes and CDT1 expression in noncancerous tissue are associated with the postoperative recurrence of hepatocellular carcinoma

The proliferation of atypical hepatocytes and CDT1 expression in noncancerous tissue are associated with the postoperative recurrence of hepatocellular carcinoma

Hepatitis viruses (other than hepatitis B and C viruses) as causes of hepatocellular carcinoma: an update

Does SEN virus (SENV) infection affect the progression of chronic hepatitis C or B among Egyptian patients?

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