HIV increases hepatitis C viraemia irrespective of the hepatitis C virus genotype

Cribier, B.; Schmitt, Carine; Rey, David; Uhl, George R.; Lang, J. M.; Vetter, D; Kirn, A.; Stoll‐Keller, Françoise

doi:10.1016/s0923-2516(97)88363-x

Cited by 45 publications

(23 citation statements)

References 11 publications

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“…Immunosuppressed patients have higher viral loads and more rapid disease progression than their immunocompetent counterparts. [41][42][43][44] An innate diversity of immune competence may account for variance in the change in viral load over time observed in the population presented here. Individuals who possess the alleles DRB1*0701 and/or DQB1*0201 have a relatively stable viral load over time, which is significantly different from those who have DRB1*15 and/or DQB1*0602 (Tables 3 and 4).…”

Section: Discussionmentioning

confidence: 99%

Hla Class Ii Genes Determine the Natural Variance of Hepatitis C Viral Load

et al. 2001

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The aim of this study was to investigate the relationship between human leukocyte antigen (HLA) class II genes and the natural fluctuations in hepatitis C viral load in a homogeneous patient population. The study group consisted of 57 viremic (hepatitis C virus [HCV] 1b) women for whom HLA class II DRB1 and DQB1 haplotyping, virologic, histologic, and biochemical markers of disease activity were available. All patients were infected with HCV 1b from the same source of hepatitis C-contaminated anti-D immunoglobulin during the period from May 1977 to November 1978. The mean slope of change of viral load was 0.34 (SD ؎ 0.73) log 10 viral copies/mL/year, which is significantly different from zero, P < 10 ؊9 . Analysis of the relationship between the slope of change of viral load and HLA class II haplotype indicated a significantly different slope of change of viral load between the alleles of (1) DRB1*15 and DRB1*0701, and (2) DQB1*0602 and DQB1*0201, P c ‫؍‬ .036 and P c ‫؍‬ .026 after Bonferroni correction for multiple comparisons, respectively. Significant differences for grade and stage of disease at liver biopsy were observed for DQB1*0501 and DQB1*0201 alleles; P ‫؍‬ .019, r s ‫؍‬ .64, and P ‫؍‬ .047, r s ‫؍‬ .57, respectively. In addition, significant differences in stage of disease were found to exist between DRB1*13 and DRB1*0701, P ‫؍‬ .031, r s ‫؍‬ ؊.71. The rate of disease progression in chronic hepatitis C is variable and influenced by both viral and host-related factors. Relevant virus-related factors might include size of inoculum, quasispecies diversity, and genotype. Transfusion-associated infection has a more rapid progression to active liver disease than needle stick-associated infection. 1,2 This is presumably related to the smaller viral burden at exposure for the latter case. Hepatitis C viral production is estimated to reach 10 10 to 10 13 virions/day with a short half-life of several hours. [3][4][5][6] The magnitude of the serum viral load has relevance for the success of antiviral therapy. Serum viremia at or below the threshold of 6.3 log 10 viral copies/mL is a good prognostic indicator of likely response to either interferon monotherapy or interferon and ribavirin combination therapy. 7-9 Similar to the human immunodeficiency virus (HIV), the high turnover rates and error-prone replication exhibited by the hepatitis C virus (HCV) provides a mechanism for the generation of immune escape and antiviral therapy-resistant mutants. [10][11][12][13] Host factors that influence disease progression in individuals infected with HCV include age at exposure, excessive alcohol consumption, and the presence of competing causes for liver disease such as the hepatitis B virus and hepatitis A virus superinfection. Individuals infected with HCV who are greater than 50 years of age have a more severe disease and higher mortality rate than younger individuals. 14,15 The genetic background of the host as assessed by human leukocyteassociated antigen (HLA) typing has shown some associations with clearance of ...

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Section: Discussionmentioning

confidence: 99%

Hla Class Ii Genes Determine the Natural Variance of Hepatitis C Viral Load

et al. 2001

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“…Accumulating molecular and clinical evidence indicated that the effects of HIV infection can be modified by coinfection with other viruses [101][102][103][104] . However, limited information is available about the prevalence and possible pathogenic role of TTV in HIV infected patients with or without AIDS in relation to specific risk factors, and about the viral titres of TTV.…”

Section: Ttv Coinfectionmentioning

confidence: 99%

Transfusion transmitted virus: A review on its molecular characteristics and role in medicine

Irshad¹,

Yk²,

Dhar³

2006

WJG

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The present review gives an updated overview of transfusion transmitted virus (TTV), a novel agent, in relation to its molecular characteristics, epidemiological features, modes of transmission, tissue tropism, pathogenesis, role in various diseases and its eradication from the body. TTV, a DNA virus, is a single stranded, non-enveloped, 3.8 kb long DNA virus with a small and covalently closed circular genome comprising 3852 bases. It was tentatively designated Circinoviridae virus.TTV genome sequence is heterogeneous and reveals the existence of six different genotypes and several subtypes. TTV has been reported to transmit not only via parenteral routes, but also via alternate routes. This virus has been detected in different non-human primates as well. At present, TTV is detected by polymerase chain reaction (PCR) with no other available diagnostic assays. It shows its presence globally and was detected in high percent populations of healthy persons as well as in various disease groups. Initially it was supposed to have strong association with liver disease; however, there is little evidence to show its liver tropism and contribution in causing liver diseases. It shows high prevalence in hemodialysis patients, pointing towards its significance in renal diseases. In addition, TTV is associated with several infectious and non-infectious diseases. Although its exact pathogenesis is not yet clear, TTV virus possibly resides and multiplies in bone marrow cells and peripheral blood mononuclear cells (PBMCs). Recently, attempts have been made to eradicate this virus with interferon treatment. More information is still needed to extricate various mysteries related to TTV.

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“…HCV-related liver disease may be more severe in HIV-infected people [Garcia-Samaniego et al, 1997] with a more rapid clinical progression to fibrosis and cirrhosis [Sherman et al, 1993;Soto et al, 1997;Benhamou et al, 1999]. Plasma HCV viral load is significantly higher in HIV-HCV co-infected patients [Sherman et al, 1993;Eyster et al, 1994;Cribier et al, 1997;Bonacini et al, 1999]. HAART may interfere with the course of HCV-related chronic hepatitis and HCV replication.…”

Section: Introductionmentioning

confidence: 99%

Intrahepatic HCV RNA loads in 37 HIV‐HCV co‐infected patients with controlled HIV infection

Trimoulet

Néau

Bail³

et al. 2002

Journal of Medical Virology

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Serum and intrahepatic hepatitis C virus (HCV) RNA were measured in 37 HIV-HCV co-infected patients with controlled human immunodeficiency virus (HIV) infection and correlated with clinical, biological, and histological parameters. Thirty-seven interferon-naive patients underwent liver biopsy. HCV-induced activity (A) and fibrosis (F) were evaluated with METAVIR score. The 37 patients included had HIV plasma loads < 10,000 copies/ml, CD4(+) count > 250/microl. All the patients but two were receiving antiretroviral treatment. Liver tissue and sera were used for measurement of HCV RNA by the Cobas Amplicor HCV Monitor. All patients had serum and liver HCV RNA, and both levels were correlated (r = 0.47; P = 0.003). Intrahepatic HCV load did not depend on age, sex, duration of HCV infection, CD4(+), HCV genotype, or fibrosis. AST levels correlated with intrahepatic HCV load (r = 0.52; P = 0.001). Patients with METAVIR A1/A2 had significantly lower levels of liver HCV-RNA than were found in patients with METAVIR A3 (P = 0.026). Highly active antiretroviral therapy (HAART) including protease inhibitors(PI)-treated patients had significantly lower intrahepatic HCV load (P = 0.04). A weak but significant correlation between serum and liver HCV RNA was found. The amount of hepatic HCV RNA was correlated with AST levels, histological activity, but not with HCV genotype or fibrosis. The immune improvement associated with PI regimens could help reduce HCV load, supporting a protective effect of PI-induced immune restoration.

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HIV increases hepatitis C viraemia irrespective of the hepatitis C virus genotype

Cited by 45 publications

References 11 publications

Hla Class Ii Genes Determine the Natural Variance of Hepatitis C Viral Load

Hla Class Ii Genes Determine the Natural Variance of Hepatitis C Viral Load

Transfusion transmitted virus: A review on its molecular characteristics and role in medicine

Intrahepatic HCV RNA loads in 37 HIV‐HCV co‐infected patients with controlled HIV infection

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