Can We Predict Sustained Virologic Response to Interferon α Therapy in Patients With Chronic Hepatitis Delta Virus Infection?

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Hepatitis C virus spread from HIV-positive to HIV-negative men who have sex with men.

The aim of this study was to evaluate the potential transmission of HCV strains between HIV-positive men who have sex with men (MSM) and HIV-negative MSM. Since 2000, an ongoing epidemic of HCV infections is observed among HIV-positive MSM in high-income countries. However, HCV infections in HIV-negative MSM are investigated to a lesser extent due to the lack of follow-up in this population and only limited information is available on the risk of HCV transmission between HIV-positive MSM and HIV-negative MSM. We enrolled 49 MSM of which 43 were HIV-positive and 6 HIV-negative, including 4 being enrolled or waiting for enrolment in a preexposure prophylaxis (PrEP) program. All patients were diagnosed with acute HCV infection at the Infectious Disease Unit at the Hospices Civils de Lyon from 2014 to 2016. Risk factors for HCV infection were similar in both groups and included IV or nasal drug use, and rough sex practices. Typing and phylogenetic cluster analysis of HCV variants were performed by NS5B sequencing. Several clusters of infections were identified (genotype 1a: 3 clusters and 1 pair; genotype 4d: 1 cluster and 2 pairs), suggesting that several transmission events occurred within the study population. Every HCV strain identified in HIV-negative MSM was included in a cluster with HIV-positive MSM. Chronological analysis of contagiousness suggested the transmission of HCV from HIV-positive to HIV-negative patients. We conclude that recommendations for HCV surveillance should not be confined to HIV-positive MSM but should be extended to HIV-negative MSM with similar risk factors

Evolution of the incidence of hepatitis B virus infection and immunization rates in a large French cohort born between 1960 and 1994

International audienceIn France, several successive changes in anti-hepatitis B virus (HBV) vaccination policies occurred since 1982. We estimated the incidence and prevalence of HBV infection according to years of birth 1960 to 1994 in a large sentinel cohort to evaluate the epidemiology of HBV during vaccination policy changes. A retrospective cohort study included data from all HIV, HBV and hepatitis C virus (HCV) screening facilities in Grand Lyon. From 2005 to 2010, all 57113 individuals with complete HBV serologic status were enrolled. Survival analyses modeled separately various ages in each birth cohort. The proportion of immunized individuals increased in birth cohorts 1978 to 1984 (up to 58.3% (95% confidence interval (CI), 43.3-68.2 at age 15). In post-1985 birth cohorts, this proportion decreased to 19.5% (95% CI, 15.5-24) in birth cohort 1987 at age 15. Probability of past or current HBV infection increased constantly in birth cohorts 1960 to 1967, up to 12% (95% CI, 10.4-14) at age 30, then decreased gradually in birth cohorts 1968 to 1991, down to 0.9% (95% CI, 0.7-1.2) at age 17.5. In post-1991 cohorts, the probability of HBV infection increased again, up to 2.5% (95% CI, 1.7-3.6) at age 17.5. HBV incidence fluctuated between 5 and 8 per 1000 person-years in pre-1986 birth cohorts, decreased to 2.1 (95% CI, 1.5-2.7) in birth cohorts 1986 to 1991 but rebounded to 5 (95% CI, 3.5-7.1) in post-1991 birth cohorts. HBV incidence was remarkably high in young adults with noticeable variations concomitantly to vaccination policy changes. A dramatic decline in immunization rate was temporally associated with a sharp rebound of infection after withdrawal of systematic adolescent vaccination in 1998

Sofosbuvir plus daclatasvir with or without ribavirin for chronic hepatitis C infection: Impact of drug concentration on viral load decay

International audienceBACKGROUND: Sofosbuvir (SOF) plus daclatasvir (DCV) with or without ribavirin is one of the currently recommended treatment option for chronic hepatitis C. AIMS: Our objectives were to identify factors associated with SOF/DCV plasma concentrations [C] variations and to evaluate their impact on viral kinetics. METHODS: 130 consecutive HCV patients initiating SOF/DCV therapy with or without ribavirin were enrolled. Clinical, biological, virological and pharmacological data were collected at baseline, at week 4, 8, 12, and 24 of therapy and 12 weeks after the end of therapy. RESULTS: Mean age was 57 years, 68% of patients were males, 69% were infected by HCV genotype 1 and cirrhosis was observed in 76% of patients. Multivariate analysis showed that higher SOF [C] and DCV [C] during treatment were associated with eGFR impairment and absence of cirrhosis. We found a significant correlation between the magnitude of HCV viral load decrease from day 0 to week 4 and a higher SOF [C] at week 4 (p=0.032) and a higher DCV [C] at week 8 (p=0.013). CONCLUSIONS: Pharmacological monitoring showed significant associations between elevated SOF or DCV [C] and absence of cirrhosis, decreased eGFR and viral load decrease during the first month of treatmen

Hepatitis A outbreak in HIV-infected MSM and in PrEP-using MSM despite a high level of immunity, Lyon, France, January to June 2017

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Preliminary Evidence for Hepatitis Delta Virus Exposure in Patients Who Are Apparently Not Infected With Hepatitis B Virus

International audienceHepatitis delta virus (HDV) is a defective human virus that lacks the ability to produce its own envelope proteins and is thus dependent on the presence of a helper virus, which causes its surface proteins to produce infectious particles. Hepatitis B virus (HBV) was so far thought to be the only helper virus described to be associated to HDV. However, recent studies showed that divergent HDV-like viruses can be detected in fishes, birds, amphibians, and invertebrates without evidence of any HBV-like agent supporting infection (reviewed in Maya and Ploss(1)). Another recent study demonstrated that HDV can be transmitted and propagated in experimental infections ex vivo and in vivo by different enveloped viruses unrelated to HBV, including hepatitis C virus (HCV), flaviviruses like dengue and West Nile virus, and vesiculovirus.(2) Altogether, these results suggested that hepatitis D infection may, in theory, occur in patients carrying either virus.(2) These observations prompted us to search for HDV infection among patients who are HCV infected and in geographical regions with high HDV endemicity.The exact prevalence of HDV infection in Venezuela is unknown, but outbreaks of fulminant HDV infections have been reported in indigenous populations from the Amazon basin and Western Venezuela.(3) The high prevalence of HDV infection among these indigenous populations might have favored dissemination of HDV infection among other inhabitants in the country. Here, we investigated the possible HDV exposure in a cohort of Venezuelan patients infected with HCV

Characteristics of HIV-positive and HIV-negative MSM with HCV infection.

<p>Characteristics of HIV-positive and HIV-negative MSM with HCV infection.</p

Individual periods of contagiousness within clusters of HCV-infected MSM.

<p>The period of contagiousness, as defined in the material and methods section, is represented by a horizontal black line. HIV-positive and HIV-negative MSM infected by HCV are indicated by red and green circles, respectively.</p

Characteristics of MSM within clusters of HCV infection.

<p>Characteristics of MSM within clusters of HCV infection.</p