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SVR persons:Persistence of HCV After Successful Treatment of Chronic Hepatitis C: Is HCV Infection for Life?
Persistence of HCV After Successful Treatment of Chronic Hepatitis C: Is HCV Infection for Life?
It is presumed that resolution of hepatitis C reflects virus eradication, as evidenced by normalization of liver function tests and disappearance of hepatitis C virus (HCV) RNA from serum, as determined by conventional laboratory assays.
In this study, researchers in Poland examined the expression of the HCV genome in the sera, peripheral blood mononuclear cells (PBMC), and, on some occasions, monocyte-derived dendritic cells (DC) long after resolution of hepatitis C by using a highly sensitive reverse transcription (RT)-polymerase chain reaction-nucleic acid hybridization (RT-PCR-NAH) assay.
The samples obtained from 16 randomly selected patients (5 with spontaneous resolution and 11 with treatment-induced resolution), monitored for up to 5 years, were studied by qualitative and semi-quantitative RT-PCR-NAH and by real-time RT-PCR to detect the HCV RNA positive strand.
The replicative HCV RNA negative strand was examined in PBMC after culture with a T cell proliferation stimulating mitogen.
Results
The findings show that HCV RNA was carried in the convalescent-phase sera and/or PBMC in all 16 individuals investigated.
Also, DC from six of seven patients were reactive for the HCV genome. Importantly, traces of the HCV RNA negative strand, suggesting progressing virus replication, were detected in the majority of mitogen-stimulated PBMC, including four samples collected 5 years after recovery.
Sequencing of the HCV 5' untranslated region fragment revealed genotype 1b in four of nine individuals examined and genotypes 1a and 2a in three and two patients, respectively.
In conclusion, these results imply that HCV RNA can persist at very low levels in the serum and peripheral lymphoid cells and that an intermediate replicative form of the HCV genome can persist in PBMC for many years after apparently complete spontaneous or antiviral therapy-induced resolution of chronic hepatitis C.
Warsaw Medical Academy, Poland.
It is presumed that resolution of hepatitis C reflects virus eradication, as evidenced by normalization of liver function tests and disappearance of hepatitis C virus (HCV) RNA from serum, as determined by conventional laboratory assays.
In this study, researchers in Poland examined the expression of the HCV genome in the sera, peripheral blood mononuclear cells (PBMC), and, on some occasions, monocyte-derived dendritic cells (DC) long after resolution of hepatitis C by using a highly sensitive reverse transcription (RT)-polymerase chain reaction-nucleic acid hybridization (RT-PCR-NAH) assay.
The samples obtained from 16 randomly selected patients (5 with spontaneous resolution and 11 with treatment-induced resolution), monitored for up to 5 years, were studied by qualitative and semi-quantitative RT-PCR-NAH and by real-time RT-PCR to detect the HCV RNA positive strand.
The replicative HCV RNA negative strand was examined in PBMC after culture with a T cell proliferation stimulating mitogen.
Results
The findings show that HCV RNA was carried in the convalescent-phase sera and/or PBMC in all 16 individuals investigated.
Also, DC from six of seven patients were reactive for the HCV genome. Importantly, traces of the HCV RNA negative strand, suggesting progressing virus replication, were detected in the majority of mitogen-stimulated PBMC, including four samples collected 5 years after recovery.
Sequencing of the HCV 5' untranslated region fragment revealed genotype 1b in four of nine individuals examined and genotypes 1a and 2a in three and two patients, respectively.
In conclusion, these results imply that HCV RNA can persist at very low levels in the serum and peripheral lymphoid cells and that an intermediate replicative form of the HCV genome can persist in PBMC for many years after apparently complete spontaneous or antiviral therapy-induced resolution of chronic hepatitis C.
Warsaw Medical Academy, Poland.
I did get the article and I thank you so much for sending it to me. I will study it carefully and, if you have no objection, I will forward it to my surgeon, although it is quite possible he's already seen it. If I or he has any additional insight I will post it here and email it to you but it may take me a while to digest it. Again Willing, thank you very much. It is rather curious that a thread that started like this one evolved to this level. It has me in a state of wonderment. Mike
Thanks for saying that but I sure ain't the best. I just try to be as decent as I can but it get hard sometimes just to be civil. Mike
Kraus MR, Al-Taie O, Schafer A, Pfersdorff M, Lesch KP, Scheurlen M.
Medizinische Klinik und Poliklinik II, Department of Gastroenterology and Hepatology, University of Wurzburg, Wurzburg, Germany. kraus_m***@****-wuerzburg.de
BACKGROUND & AIMS: Interferon-induced depression is a major complication in antiviral therapy of chronic hepatitis C. Little is known about underlying mechanisms and reliable predictive factors associated with cytokine-induced depressive symptoms. METHODS: In a cohort of 139 hepatitis C-infected outpatients treated with interferon alfa-2b, we investigated the impact of functional gene variants of the cerebral serotonin (5-HT) signalling pathway previously implicated in depression risk. Depression was monitored using the Hospital Anxiety and Depression Scale (HADS). All patients were genotyped for functional variations in the 5-HT(1A) receptor (HTR1A), 5-HT transporter (SLC6A4, 5-HTT), and tryptophan hydoxylase-2 (TPH2). RESULTS: Homozygosity for the HTR1A-1019G variant significantly increased both incidence and severity of interferon-induced depression. Maximum increases in HADS depression scores during antiviral therapy correlated with HTR1A variation (P = .011). Clinically relevant depression was significantly associated with the HTR1A-1019G genotype (P = .017; OR, 2.95). 5-HTT and TPH2 variations did not contribute significantly to the prediction of interferon-induced depression by HTR1A (sensitivity, 35.9%; specificity, 84.0%). CONCLUSIONS: Our findings suggest an impact of allelic variation in 5-HT(1A) receptor expression on the development of interferon alfa-induced depression during antiviral treatment of chronic hepatitis C. Prediction models of interferon-induced depressive symptoms based on HTR1A variation offer a perspective for an antidepressant selective serotonin reuptake inhibitor prophylaxis in patients genetically at risk for interferon-induced depression.
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