Immune complexed (IC) hepatitis C virus (HCV) in chronically and acutely HCV-infected patients

Riva, Elisabetta; Maggi, Fabrizio; Abbruzzese, Franca; Bellomi, Francesca; Giannelli, Gianluigi; Picardi, Antonio; Scagnolari, Carolina; Folgori, Antonella; Spada, Enea; Piccolella, Enza; Dianzani, F.; Antonelli, Guido

doi:10.1007/s00430-008-0099-9

Cited by 6 publications

(6 citation statements)

References 21 publications

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“…In our study only positive sense HCV RNA was detected, and other studies have shown that HCV RNA can form immune-complexes with immunoglobulins and bind to the surface of PBMCs [107,108]. This suggests that residual HCV RNA associated with PBMCs does not necessarily replicate in PBMCs, but could merely be bound to the surface of some immune cells.…”

Section: Discussioncontrasting

confidence: 46%

Diabetes and Cirrhosis Are Risk Factors for Hepatocellular Carcinoma After Successful Treatment of Chronic Hepatitis C

et al. 2016

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Section: Discussioncontrasting

confidence: 46%

Diabetes and Cirrhosis Are Risk Factors for Hepatocellular Carcinoma After Successful Treatment of Chronic Hepatitis C

et al. 2016

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“…Although some reports describe the detection of negative‐strand HCV RNA in PBMCs indicating that low‐level HCV replication in PBMCs may be possible, recent studies analysing the association of HCV with PBMCs show that HCV is bound to the surface of PBMCs, in particular B cells . In HCV‐infected patients circulating virus can be complexed with immunoglobulins . Thus, immune‐complexed HCV may associate with immunoglobulin receptors present on PBMCs.…”

Section: Discussionmentioning

confidence: 99%

“…28,29 In HCV-infected patients circulating virus can be complexed with immunoglobulins. 30 Thus, immune-complexed HCV may associate with immunoglobulin receptors present on PBMCs.…”

Section: Discussionmentioning

confidence: 99%

Long-term follow-up of successful hepatitis C virus therapy: waning immune responses and disappearance of liver disease are consistent with cure

Hedenstierna

Weiland

Brass

et al. 2015

Aliment Pharmacol Ther

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Summary Background A sustained viral response (SVR) after interferon‐based therapy of chronic hepatitis C virus (HCV) infection is regarded to represent a cure. Previous studies have used different markers to clarify whether an SVR truly represents a cure, but no study has combined a clinical work‐up with highly sensitive HCV RNA detection, and the determination of immune responses. Aim To determine clinical, histological, virological and immunological markers 5–20 years after SVR. Methods In 54 patients, liver biochemistry, histology and elastography were evaluated. Liver biopsies, plasma and peripheral blood mononuclear cells (PBMCs) were tested for minute amounts of HCV RNA. HCV‐specific T‐cell responses were monitored by ELISpot and pentamer staining, and humoral responses by measuring HCV nonstructural (NS)3‐specific antibodies and virus neutralisation. Results Liver disease regressed significantly in all patients, and 51 were HCV RNA‐negative in all tissues tested. There was an inverse association between liver disease, HCV‐specific T‐cell responses and HCV antibody levels with time from SVR, supporting that the virus had been cleared. The three patients, who all lacked signs of liver disease, had HCV RNA in PBMCs 5–9 years after SVR. All three had HCV‐specific T cells and NS3 antibodies, but no cross‐neutralising antibodies. Conclusions Our combined data confirm that a SVR corresponds to a long‐term clinical cure. The waning immune responses support the disappearance of the antigenic stimulus. Transient HCV RNA traces may be detected in some patients up to 9 years after SVR, but no marker associates this with an increased risk for liver disease.

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“…Thus, the finding of HCV RNA in PBMCs or their subsets in HCV carriers does not necessarily imply viral replication or an occult site of infection, but rather that PMBCs may be a passive carrier of HCV that is replicated in other sites. There is a logical explanation for this observation, in that most HCV in chronic carriers circulates as immune complexes30 and that PBMCs, particularly B cells, are rich in immunoglobulin receptors. Alternatively, unbound HCV could attach to known HCV receptors present on PBMCs, such as CD81, sheep anti‐BubR1, and claudin‐1, without truly supporting HCV replication in vitro 31.…”

Section: Discussionmentioning

confidence: 99%

Investigation of Residual Hepatitis C Virus in Presumed Recovered Subjects

et al. 2013

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Recent studies have found hepatitis C virus (HCV) RNA in peripheral blood mononuclear cells (PBMCs) of the majority of presumed recovered subjects. We investigated this unexpected finding using samples from patients whose HCV RNA and anti-HCV status had been serially confirmed. HCV RNA was detected in PBMCs from 66/67 chronic HCV carriers. Subpopulation analysis revealed that the viral load (log copies/106 cells) in B cells (4.14 ± 0.71) was higher than in total PBMCs (3.62 ± 0.71, p<0.05), T cells (1.67 ± 0.88, p<0.05), and non-B/T cells (2.48 ± 1.15, p<0.05). HCV negative-strand RNA was not detected in PBMCs from any of 25 chronically infected patients. No residual viral RNA was detected in total PBMCs or plasma of 59 presumed recovered subjects (11 spontaneous, 48 treatment-induced) using nested real-time PCR with a detection limit of 2 copies/μg RNA (from ~1×106 cells). PBMCs from two healthy HCV-negative blood donors became HCV RNA positive, with B-cell predominance, when mixed in vitro with HCV RNA positive plasma, thus passively mimicking cells from chronic HCV carriers. No residual HCV was detected in liver or other tissues from two spontaneously recovered chimpanzees. Conclusion: 1) HCV RNA was detected in PBMCs of most chronic HCV carriers and was predominant in the B cell subpopulation; 2) HCV detected in PBMCs was in a non-replicative form; 3) HCV passively adsorbed to PBMCs of healthy controls in vitro becoming indistinguishable from PBMCs of chronic HCV carriers; 4) Residual HCV was not detected in the plasma or PBMCs of any spontaneous or treatment recovered subjects or in chimpanzee liver suggesting that the classic pattern of recovery from HCV infection is generally equivalent to viral eradication.

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Immune complexed (IC) hepatitis C virus (HCV) in chronically and acutely HCV-infected patients

Cited by 6 publications

References 21 publications

Diabetes and Cirrhosis Are Risk Factors for Hepatocellular Carcinoma After Successful Treatment of Chronic Hepatitis C

Diabetes and Cirrhosis Are Risk Factors for Hepatocellular Carcinoma After Successful Treatment of Chronic Hepatitis C

Long-term follow-up of successful hepatitis C virus therapy: waning immune responses and disappearance of liver disease are consistent with cure

Investigation of Residual Hepatitis C Virus in Presumed Recovered Subjects

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