Hepatitis G infection: role in cryptogenic chronic liver disease and primary liver cell cancer in the UK

Hollingsworth, Rosalind; Minton, E. J.; Fraser-Moodie, C.; Metivier, Elizabeth M.; Rizzi, Paolo; Irving, William L.; Jenkins, David; Ryder, Stephen D.

doi:10.1046/j.1365-2893.1998.00102.x

Cited by 14 publications

(7 citation statements)

References 15 publications

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“…Hepatitis G virus (GBV‐C, HGV), identified in 199672 and TT virus (TTV), identified in 199773 have also been examined for a relationship with PLC. Although HGB was significantly associated with PLC in some studies,56, 74 others have reported little if any association 40, 44, 55, 75–78. TTV has been examined in a number of studies, but no significant association with PLC has yet been reported 79–84…”

Section: Discussionmentioning

confidence: 98%

International trends and patterns of primary liver cancer

et al. 2001

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Primary liver cancer (PLC) is common in many areas of the developing world, but uncommon in most of the developed world. Some evidence suggests, however, that the global pattern of PLC may be changing. To clarify this issue, we examined incidence rates for PLC over the 15-year time period, 1978 -92, in selected cancer registries around the world. With some exceptions, developed countries have experienced PLC increases in incidence whereas developing countries have experienced declines. Although the reasons for the trends are not entirely clear, the increased seroprevalence of HCV in the developed world and the elimination of HBV-cofactors in the developing world are likely to have contributed to the patterns. Further progress against PLC may be seen in the developing world once the HBV-vaccinated segment of the population reaches adulthood. Primary liver cancer (PLC) is the fifth most common cancer in the world 1 and the fourth most common cause of cancer mortality. 2 PLC is composed of several subtypes, including hepatocellular carcinoma, cholangiocarcinoma, hepatoblastoma, and angiosarcoma. In most countries, hepatocellular carcinoma comprises 85-90% of PLC and so the terms are often used interchangeably.PLC rates have an extremely wide geographic variation, such that 80% of the cases arise in developing countries, particularly those of southeast Asia and sub-Saharan Africa. Even within a confined geographic area, certain ethnic groups have higher PLC rates than others. In these high-rate populations, chronic infection with hepatitis B virus (HBV), and contamination of foodstuffs with aflatoxin B1 (AFB1) are recognized major risk factors. In contrast, neither HBV nor AFB1 is considered to be a major factor in low-rate areas of the developed world. Alcohol ingestion and, increasingly, hepatitis C virus (HCV) infection are more likely to be related to PLC in these areas. Reports of incidence rates declining in some high-risk populations 3 while increasing in some low-risk populations 4 -6 suggest that the global patterns of liver cancer may be changing. To determine whether the reported changes are isolated phenomena or whether new global patterns of liver cancer are emerging, we examined incidence trends over the 15-year period 1978 -92. MATERIAL AND METHODS Incidence dataTo examine the current global pattern of PLC incidence, genderspecific rates in 53 registries were abstracted for 67 populations by Parkin et al. 7 An effort was made to include registries from each continent and registries that reported data for more than 1 ethnic group, but no more than 1 registry from any single country was included. To examine the trends over time, gender and age-specific and -standardized incidence rates in 23 populations from 21 registries were retrieved by The abstracted rates cover 3 5-year intervals : 1978 -82, 1983-87 and 1988 -92 and are age-adjusted to the world standard population. Use of a fourth time period (1973-77) was considered but rejected due to its use of the International Classification of Diseases, ...

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Section: Discussionmentioning

confidence: 98%

International trends and patterns of primary liver cancer

et al. 2001

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“…Since its discovery, the primary site(s) of replication and cellular receptors for HPgV has (have) not been identifi ed and a correlation with non-A/non-E hepatitis remains a controversial issue even though HPgV RNA has been detected more frequently in patients with acute and chronic non-A/non-E hepatitis than in healthy subjects. Early studies indicated that the virus was hepatotropic (Grassi et al, 2000;Hollingsworth et al, 1998;Guilera et al, 1998), although numerous studies carried out since the late 1990s, have shown that HPgV is not hepatotropic or only barely detectable in the liver of infected individuals (Pessoa et al, 1998;Chivero et al, 2014). Th e virus can persist for at least one month in culture in peripheral blood mononuclear cells (PBMCs) from infected individuals (Th ézé et al, 2015;Chivero and Stapleton, 2015).…”

Section: Clinical Relevance Of Hpgv Infectionmentioning

confidence: 99%

The human pegivirus: A new name for an “ancient” virus. Can transfusion medicine come up with something new?

Marano¹,

Franchini²,

Farina³

et al. 2017

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Human pegivirus (HPgV, formerly called GB virus C/hepatitis G virus) is a poorly understood RNA virus of the Flaviviridae family. The HPgV infection is common worldwide and the virus is likely transmitted by blood products. At this time, no causal association between HPgV and human diseases has been identified. While waiting for new findings to better understand the Pegivirus genus, the aim of our narrative review is to discuss the currently available information on HPgV focusing on its prevalence in blood donors and its potential threat to transfusion safety.

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“…In the context of recently published studies [3,[15][16][17][18][19] an etiologic role of GBV-C/HGV cannot be excluded in a minority of non-A-E hepatitis cases. Thus, the testing for HGV may be a useful extension of the diagnostic procedure for non-A-E hepatitis.A possible benefit of interferon alpha treatment that suppresses GBV-C/HGV replication effectively [20,21] should be discussed for patients with cryptogenic hepatitis and GBV-C/HGV viremia.The controversial data of other authors may be due to different study designs [13,22,23], geographical differences [8], or to insignificant associations due to the small number of individuals examined [24].…”

Section: Discussionmentioning

confidence: 99%

“…Consequently, GBV-C/HGV appears to be well adapted to the human host and its importance as a viral pathogen has been questioned. Recently published data suggest that GBV-C/HGV may play a role in the pathogenesis of acute non-A-E hepatitis [7], but not in chronic cryptogenic liver disease or hepatocellular carcinoma [8,9].Additionally, GBV-C/HGV is associated with non-Hodgkin's lymphoma [10], but its association with other extrahepatic malignancies is unclear [11]. The aim of this study was i) to determine the prevalence of anti-GBV-C/HGV antibodies and GBV-C/HGV RNA in traumatologic outpatients as a control group for further epidemiological studies, ii) to examine GBV-C/HGV prevalences in chronic non-A-E hepatitis patients and iii) in a group of patients suffering from extrahepatic malignancies.…”

Section: Introductionmentioning

confidence: 99%

GB Virus C/Hepatitis G Virus Infections in Traumatologic Outpatients, Chronic Non-A-E Hepatitis and Extrahepatic Malignancies

Schaade¹,

Platzer²,

Kleines³

et al. 2000

Infection

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GB virus C/hepatitis G virus (GBV-C/HGV) is a recently discovered flavivirus of still unknown pathogenic relevance. We examined traumatologic outpatients to determine GBV-C/HGV viremia for further epidemiological studies, as blood donors hitherto used as controls represent healthy individuals without risk factors. Anti-GBV-C/HGV antibodies were detectable in 13.2% (95% confidence interval [CI] 9.3-18.2) and GBV-C/HGV RNA was detectable in 4.5% (95% CI 2.4-8.2) of the outpatients. In chronic non-A-E hepatitis patients GBV-C/HGV viremia was detectable at a significantly higher level of 16.1% (95% CI 6.1-34.5), while the prevalence of anti-GBV-C/HGV antibodies was 12.9% (95% CI 4.2-30.8). The rate of GBV-C/HGV viremia in patients with malignant diseases (different types of tumors, blood recipients were excluded) was 12.5% (95% CI 8.4-18.1), a significant elevation compared to traumatologic outpatients. The seroprevalence in the tumor group was 22.1% (95% CI 16.7-28.6), also significantly elevated. Thus, there are two messages. Firstly, testing for GBV-C/HGV may be a useful extension of the diagnostic procedure of viral hepatitis. Secondly, common risk factors or etiologic relations of GBV-C/HGV and extrahepatic malignancies should be discussed.

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Hepatitis G infection: role in cryptogenic chronic liver disease and primary liver cell cancer in the UK

Cited by 14 publications

References 15 publications

International trends and patterns of primary liver cancer

International trends and patterns of primary liver cancer

The human pegivirus: A new name for an “ancient” virus. Can transfusion medicine come up with something new?

GB Virus C/Hepatitis G Virus Infections in Traumatologic Outpatients, Chronic Non-A-E Hepatitis and Extrahepatic Malignancies

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