ABSTRACT
Enterovirus D68 (EV-D68) infections are associated with severe respiratory disease and acute flaccid myelitis (AFM). The European Non-Polio Enterovirus Network (ENPEN) aimed to investigate the epidemiological and genetic characteristics of EV-D68 and its clinical impact during the fall-winter season of 2021/22. From 19 European countries, 58 institutes reported 10,481 (6.8%) EV-positive samples of which 1,004 (9.6%) were identified as EV-D68 (852 respiratory samples). Clinical data was reported for 969 cases. 78.9% of infections were reported in children (0-5 years); 37.9% of cases were hospitalised. Acute respiratory distress was commonly noted (93.1%) followed by fever (49.4%). Neurological problems were observed in 6.4% of cases with six reported with AFM. Phylodynamic/Nextstrain and phylogenetic analyses based on 694 sequences showed the emergence of two novel B3-derived lineages, with no regional clustering. In conclusion, we describe a large-scale EV-D68 European upsurge with severe clinical impact and the emergence of B3-derived lineages.
ABSTRACT
BACKGROUND: Antiviral resistance in Norwegian influenza viruses is rare. Only one A(H1N1)pdm09 virus from May 2015 had been found resistant to oseltamivir since the introduction of these viruses in 2009. OBJECTIVES: Surveillance of antiviral resistance is part of the Norwegian surveillance system, to rapidly detect the development of antiviral-resistant viruses and spread in the community. We describe the spread of oseltamivir-resistant A(H1N1)pdm09 viruses in Norway in the 2016-17 season, found as part of the routine surveillance. METHODS: Influenza H1N1 viruses were analysed for antiviral resistance by pyrosequencing, neuraminidase susceptibility assay and by Sanger sequencing of the HA and NA genes. RESULTS: During the 2015-16 influenza season, 3% of all A(H1N1)pdm09 viruses screened for resistance in Norway were resistant to oseltamivir, possessing the H275Y substitution in the neuraminidase protein. In comparison, the overall frequency in Europe was 0.87%. Out of these, 37% (n = 10) were reported from Norway. Most cases in Norway were not related to antiviral treatment, and the cases were from several different locations of southern Norway. Genetic analysis revealed that resistant virus emerged independently on several occasions and that there was some spread of oseltamivir-resistant influenza A(H1N1)6B.1 viruses in the community, characterised by a N370S substitution in the haemagglutinin and T48I in the neuraminidase. CONCLUSIONS: Our findings emphasise the importance of antiviral resistance surveillance in the community, not only in immunocompromised patients or other patients undergoing antiviral treatment.
Subject(s)
Antiviral Agents/pharmacology , Drug Resistance, Viral/genetics , Influenza A Virus, H1N1 Subtype/drug effects , Influenza, Human/epidemiology , Oseltamivir/pharmacology , Adult , Aged , Child, Preschool , Female , Humans , Incidence , Influenza A Virus, H1N1 Subtype/genetics , Male , Middle Aged , Norway , Point Mutation , Sequence Analysis, DNA , Viral ProteinsABSTRACT
BACKGROUND & AIMS: On-going risk behaviour can lead to hepatitis C virus (HCV) reinfection following successful treatment. We aimed to assess the incidence of persistent HCV reinfection in a population of people who inject drugs (PWID) who had achieved sustained virological response (SVR) seven years earlier. METHODS: In 2004-2006 we conducted a multicentre treatment trial comprising HCV genotype 2 or 3 patients in Sweden, Norway and Denmark (NORTH-C). Six months of abstinence from injecting drug use (IDU) was required before treatment. All Norwegian patients who had obtained SVR (n=161) were eligible for participation in this long-term follow-up study assessing virological and behavioural characteristics. RESULTS: Follow-up data were available in 138 of 161 (86%) individuals. Persistent reinfection was identified in 10 of 94 (11%) individuals with a history of IDU prior to treatment (incidence rate 1.7/100 person-years (PY); 95% CI 0.8-3.1) and in 10 of 37 (27%) individuals who had relapsed to IDU after treatment (incidence rate 4.9/100 PY; 95% CI 2.3-8.9). Although relapse to IDU perfectly predicted reinfection, no baseline factor was associated with reinfection. Relapse to IDU was associated with age <30 years (vs. ⩾40 years) at treatment (adjusted odds ratio [aOR] 7.03; 95% CI 1.78-27.8) and low education level (aOR 3.64; 95% CI 1.44-9.18). CONCLUSIONS: Over time, persistent HCV reinfection was common among individuals who had relapsed to IDU after treatment. Reinfection should be systematically addressed and prevented when providing HCV care for PWID.
