To study perinatal transmission of hepatitis C virus (HCV), 15 anti-HCV-positive carrier mothers without human immunodeficiency virus coinfection were recruited. At delivery, maternal blood was taken and anti-HCV titer was determined and HCV RNA measured in each serum sample by reverse transcription polymerase chain reaction (PCR). A competitive PCR was used in selected samples to quantitate HCV concentration. The 15 neonates were followed regularly for 1 year and their sera were also assayed for anti-HCV and for HCV RNA by reverse transcription PCR. All the mothers were positive for HCV RNA. Only one normal spontaneously delivered neonate of a mother with extremely high titer of anti-HCV (1:20,000) and HCV concentration (10(10) copies/mL) had both anti-HCV and HCV RNA in serum for up to 6 months of age. In contrast, none of the remaining 14 neonates born to mothers with low- to high-titer anti-HCV (1:4-1:1000) and moderate amounts of HCV RNA (10(5)-10(6) copies/mL) contracted HCV infection. The results imply that high-titer maternal viremia and normal spontaneous delivery may allow more HCV to infect the neonate intrapartum, therefore establishing perinatal transmission.

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Background Data regarding the real-world effectiveness and safety of sofosbuvir/velpatasvir (SOF/VEL) for East Asian patients with chronic hepatitis C virus (HCV) infection and compensated liver disease are limited. We evaluated the performance of SOF/VEL for 12 weeks for HCV-infected patients with compensated liver disease in a large real-world cohort in Taiwan. Methods Between July 2019 and March 2020, 1,880 HCV-infected patients with compensated liver disease who received SOF/VEL 400/100 mg once daily for 12 weeks were included at 15 academic centers in Taiwan. The sustained virologic response at off-treatment week 12 (SVR 12) was assessed for evaluable (EP) and per-protocol populations (PP). The tolerance was also reported. Results The SVR 12 rates by EP and PP analyses were 95.6% (1,798 of 1,880 patients; 95% con dence interval (CI): 94.6%-96.5%) and 99.3% (1,798 of 1,811 patients; 95% CI: 98.8%-99.6%), respectively. Among 82 patients who failed to achieve SVR 12 , 13 (15.9%) were attributed to virologic failures. The SVR 12 rates were comparable regardless of baseline characteristics. A total of 1,859 (98.9%) patients completed 12-week SOF/VEL treatment. Four (0.2%) patients discontinued treatment due to adverse events (AEs). All patients with serious AEs or deaths were judged not related to SOF/VEL. The AEs occurring in ≥ 10% included headache (16.8%), fatigue (16.2%), nausea (11.8%), and insomnia (11.1%). Nine (0.5%) and 2 (0.1%) patients had grade 3 total bilirubin and alanine aminotransferase elevations. Conclusions SOF/VEL for 12 weeks is e cacious and well-tolerated chronic HCV-infected patients with compensated liver disease in Taiwan.

The development of serological assays for hepatitis C virus (HCV) has made specific diagnosis possible. However, markers useful in indicating acute-phase HCV infection have not been identified. By an immunoblotting method, we characterized the IgM and IgG antibody response against HCV capsid antigen in patients with HCV infection. Among 88% of patients with acute posttransfusion hepatitis C recruited in a prospective study, there was a transient IgM antibody response. The IgM antibody appeared shortly after onset of hepatitis (average 3.7 weeks), persisted for several months (average 18 weeks), and then disappeared. In contrast, the IgG antibody persisted long-term once it appeared. Among patients with chronic hepatitis C with milder disease activities (serum aminotransferase increase above normal levels of <4-fold), the IgM antibody was negative in the majority (72%). In those with acute exacerbations (aminotransferase increase of >10-fold), about 55% were negative for the IgM antibody. The reactivity of the IgM antibody in the rest was weaker or became negative upon further dilution of serum. The results suggest that IgM anti-capsid antibody may serve as a marker indicating acute or active HCV infection.Hepatitis C virus (HCV) is the major cause of non-A, non-B hepatitis worldwide (1, 2). Currently, sensitive serological or immunoblot assays are available to identify most HCV carriers (3, 4) and are used in blood screening to reduce effectively the incidence of posttransfusion hepatitis (5). The present assay of anti-HCV antibodies, although useful, cannot differentiate whether the infection is acute or chronic. The distinction between acute and chronic HCV infection is important in management of these patients. As HCV infection frequently becomes chronic and results in significant sequelae (6, 7), therapeutic intervention (such as interferon treatment) should be implemented as soon as the infection occurs (8). Accordingly, a serological marker indicating acute HCV infection is desperately needed.Such a marker would also be useful for clarifying epidemiological discrepancies of HCV infection. For example, in the clinically acute non-A, non-B hepatitis, the anti-C100-3 seropositive rate in intravenous drug abusers is significantly higher than that in posttransfusion or sporadic cases (9, 10). Given the high likelihood of multiple exposures to HCV in intravenous drug abusers, many may have already contracted hepatitis C. Therefore, it is possible that a portion of such acute hepatitis C victims actually have chronic infection but with acute exacerbations.One feasible approach for finding an acute HCV infection marker is, by analogy with hepatitis A and B, to look for virus-specific IgM antibody. Indeed, one study to correlate IgM antibody for a viral nonstructural protein (the C100-3 antigen) with acute HCV infection has been performed, but the results are not convincing (11). In the present communication, we show that by immunoblotting assay, the IgM antibody for HCV capsid antigen (anti-HCc IgM) was tr...