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We assessed the presence of hepatitis B virus (HBV) DNA in liver or serum samples from 134 patients with hepatitis B surface antigen (HBsAg)-negative chronic liver disease, including 20 with hepatocellular carcinoma. HBV DNA sequences were detected in 52 of the 88 liver samples (59 per cent), including 17 of the 20 samples from patients with hepatocellular carcinoma. Presumably "replicative forms" of HBV DNA were detected in only 5 of the 88 liver samples, 3 of which were from patients with no serologic marker for HBV. In most of the liver samples the DNA patterns were consistent with the presence of HBV or a closely related virus. Of the 105 serum samples tested, HBV DNA sequences were identified in 10 (9.5 per cent), 6 of which had no HBV serologic marker. Moreover, HBsAg-associated determinants were detected in 5 of 17 patients who were positive for HBV DNA and in none of 14 patients who were negative. This study demonstrates the high frequency of HBsAg-negative HBV DNA-positive viral infection of the liver and suggests that multiplication of HBV may occur in the absence of any conventional serologic marker for HBV.

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We have investigated hepatitis C virus (HCV) viremia before and after orthotopic liver transplantation (OLT). 38 patients were examined; 16 were anti-HCV positive and 22 anti-HCV negative pre-OLT in a RIBA-2 test (Ortho Diagnostic Systems Inc., Westwood, MA). HCV-RNA was detected using a modified nested polymerase chain reaction in 14/38 and 10/38 patients before and after OLT, respectively. 7 of these 14 subjects who were HCV-RNA positive before OLT were also positive for serum hepatitis B surface antigen. After

The accumulation of lipid droplets (LD) is frequently observed in hepatitis C virus (HCV) infection and represents an important risk factor for the development of liver steatosis and cirrhosis. The mechanisms of LD biogenesis and growth remain open questions. Here, transcriptome analysis reveals a significant upregulation of septin 9 in HCV-induced cirrhosis compared with the normal liver. HCV infection increases septin 9 expression and induces its assembly into filaments. Septin 9 regulates LD growth and perinuclear accumulation in a manner dependent on dynamic microtubules. The effects of septin 9 on LDs are also dependent on binding to PtdIns5P, which, in turn, controls the formation of septin 9 filaments and its interaction with microtubules. This previously undescribed cooperation between PtdIns5P and septin 9 regulates oleate-induced accumulation of LDs. Overall, our data offer a novel route for LD growth through the involvement of a septin 9/PtdIns5P signalling pathway.

After describing two cases of Hashimoto's thyroiditis associated with chronic hepatitis C, we set up a prospective study to assess the prevalence of thyroid autoantibodies (thyroglobulin and thyroid microsomal autoantibodies) in 72 chronic hepatitis C patients (43 men and 29 women; mean age = 51 +/- 2.1 yr) before interferon therapy admitted between January and December 1991 to our liver unit. Thyroid autoantibodies were systematically assayed in 60 chronic HBsAg-positive patients (34 men and 26 women; mean age = 50 +/- 2.2 yr), who served as controls. Antibody to hepatitis C virus was detected with a second-generation enzyme immunoassay and then confirmed with a recombinant immunoblot assay and a supplemental enzyme immunoassay using two beads. In chronic hepatitis C patients, no men had thyroid autoantibodies. Nine of 29 women (31%) had thyroid autoantibodies. Among them, six (20.7%) had high titers of thyroid autoantibodies, and two had hypothyroidism. In all nine of these women, hepatitis C virus viremia was detected on nested polymerase chain reaction (with primers located in the 5' untranslated region). One year later, titers of thyroid autoantibodies had increased in one patient. Three other patients progressed to hypothyroidism. We judged four of 29 patients (13.8%) to have Hashimoto's thyroiditis on the basis of their high titers of thyroid autoantibodies and biological features of hypothyroidism. In the control group, only one man had thyroid microsome autoantibodies, at a very low titer (1:100). The association between chronic hepatitis C and presence of thyroid autoantibodies is clearly confirmed (p = 0.021) by this study.

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