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Hepatitis C virus (HCV) variability affects viral-host interactions. We analysed HCV 5′untranslated region (5′UTR) in sera and peripheral blood mononuclear cells (PBMC) from chronic hepatitis C patients undergoing antiviral treatment. We studied 139 patients treated with pegylated interferon and ribavirin. The primary endpoint was a sustained virological response (SVR) defined as negative HCV RNA level 24 weeks after the end of therapy. 5′UTR was analysed by single-strand conformational polymorphism (SSCP) and sequencing. The pretreatment SSCP pattern in serum and PBMC differed in 26 (18.7%) patients. During therapy, the SSCP pattern remained stable in 65 (60.8%) patients, number of bands declined in 16 (15.0%), and in 18 (16.8%) patients, changes were qualified as 'shift' indicating change in band positions. In univariate analysis, there was a significant ( P ≤ 0.05) positive association between SVR and pretreatment serum and PBMC dissimilarities, initial viral load <106 IU/mL, IL-28B CC genotype of the rs12979860 single nucleotide polymorphism and change in the SSCP band pattern (either 'shift' or decline) In multivariable analysis, only low initial viral load, IL-28B genotype, and changes in the SSCP band pattern were independent factors associated with SVR. In conclusion, stability of 5′UTR correlated with infection persistence, while changes correlated with SVR. [ABSTRACT FROM AUTHOR]

It has been reported that hepatitis C virus ( HCV) RNA may be present in serum and/or lymphoid cells in the absence of specific circulating antibodies. The current study analysed seronegative HCV infection in patients with lymphoproliferative disorders. We studied 77 anti- HCV-negative patients (45 male and 32 female, mean age 54.8 ± 14.2 years) with various lymphoproliferative disorders. HCV- RNA was detected by RT- PCR in plasma, peripheral blood mononuclear cells ( PBMC) and bone marrow. Furthermore, the presence of viral nonstructural protein 3 ( NS3) was determined in PBMC and bone marrow by immunostaining. HCV- RNA was detectable in at least one compartment in 27 (35.1%) patients. Viral RNA was found in bone marrow in 22 patients (28.6%), in PBMC in 13 (16.9%) and in plasma in 10 (13%) patients. In nine patients, evidence of infection was confined to the bone marrow compartment. Viral load in HCV- RNA-positive plasma ranged from 15 to 1.17 × 103 IU/mL. NS3 was detected in all but two HCV- RNA-positive bone marrow samples and in all but one HCV- RNA-positive PBMC samples. All 27 HCV- RNA-positive patients remained anti- HCV-negative when tested again after 6-12 months, but only four remained HCV- RNA positive. In conclusion, among patients with lymphoproliferative disorders, HCV can be present in plasma, PBMC and bone marrow despite the lack of circulating specific antibodies. Further studies are required to analyse the phenomenon of seronegative infection and to determine whether such patients are infectious. [ABSTRACT FROM AUTHOR]