SUMMARY: EuroRotaNet, a laboratory network, was established in order to determine the diversity of co-circulating rotavirus strains in Europe over three or more rotavirus seasons from 2006/2007 and currently includes 16 countries. This report highlights the tremendous diversity of rotavirus strains co-circulating in the European population during three years of surveillance since 2006/2007 and points to the possible origins of these strains including genetic reassortment and interspecies transmission. Furthermore, the ability of the network to identify strains circulating with an incidence of ⩾1% allowed the identification of possible emerging strains such as G8 and G12 since the beginning of the study; analysis of recent data indicates their increased incidence. The introduction of universal rotavirus vaccination in at least two of the participating countries, and partial vaccine coverage in some others may provide data on diversity driven by vaccine introduction and possible strain replacement in Europe.

Background: In the German federal state Mecklenburg-Western Pomerania, routine rotavirus (RV) vaccination in infants has been recommended since 2009. The effectiveness of RV vaccination was investigated after an unexpectedly high number of RV infections in fully vaccinated children occurred. Methods: Intensified RV surveillance was performed in Mecklenburg-Western Pomerania between 2010 and 2011. The screening method was applied to assess vaccine effectiveness (VE) in children up to 24 months after vaccination. To identify risk factors for breakthrough infections, a case-control study and genotyping were conducted in vaccinated and unvaccinated RV-infected children. Results: VE for the prevention of RV infection requiring medical attention or hospitalization was 68% (95% confidence interval [CI]: 61–71) and 80% (95% CI: 77–83), respectively. VE for preventing hospitalization but not medical attention remained stable over 2 years. Vaccinated were less often hospitalized (23%) than unvaccinated RV-infected children (61%; P < 0.001). Breastfeeding (odds ratio, 3.99; 95% CI: 1.92–8.27) and attending daycare (odds ratio, 3.42; 95% CI: 1.64–7.12) were independently associated with breakthrough infections. Genotype G1P[8] was detected more frequently in RotaTeq-vaccinated (44% versus 11%; P < 0.03) and G2P[4] in Rotarix-vaccinated children (42% versus 6%; P < 0.02). Conclusions: RV vaccination protects young children effectively from RV disease and can reduce disease severity. Breastfeeding might impair VE, but further research is needed to identify the critical time window for this interference and to develop appropriate recommendations.

The principle of a capture ELISA is binding of specific capture antibodies (polyclonal or monoclonal) to the surface of a suitable 96 well plate. These immobilized antibodies are capable of specifically binding a virus present in a clinical sample. Subsequently, the captured virus is detected using a specific detection antibody. The drawback of this method is that a capture ELISA can only function for a single virus captured by the primary antibody. Human Apolipoprotein H (ApoH) or β2-glycoprotein 1 is able to poly-specifically bind viral pathogens. Replacing specific capture antibodies by ApoH should allow poly-specific capture of different viruses that subsequently could be revealed using specific detection antibodies. Thus, using a single capture ELISA format different viruses could be analysed depending on the detection antibody that is applied. In order to demonstrate that this is a valid approach we show detection of group A rotaviruses from stool samples as a proof of principle for a new method of capture ELISA that should also be applicable to other viruses.

Both a double–stranded RNA–dependent protein kinase (PKR)–phosphorylation homology domain (PePHD) within the E2 protein and a PKR–binding domain within the nonstructural 5A (NS5A) protein of hepatitis C virus (HCV) genotype 1 isolates inhibit the function of the interferon alfa (IFN–α)–induced antiviral effector protein PKRin vitro. We investigated whether the mutational pattern of the E2 region (codons 618–681, including PePHD) of 81 HCV genotype 1–infected patients (HCV–1b [n = 54], HCV–1a [n = 27]) influences the response to IFN–α. Initial viral decline (ΔHCV RNA) was determined at week 1 hereby covering the effector reactions of IFN–α–mediated first phase and the immune–mediated second phase. ΔHCV RNA less than 50% (group 1); ΔHCV RNA greater than 50% but less than 90% (group 2); and ΔHCV RNA ≥90% (group 3) were differentiated. The PePHD region was highly conserved; the few mutations (5 patients) did not correlate with ΔHCV RNA or sustained virologic response to IFN–α. Within the flanking regions before and after PePHD (codons 618–681) 72 of 81 patients (89%) had 2.6 ± 0.17 mutations (median, 3; range, 1–8) that did not correlate with treatment response. Sequence analysis of the NS5A protein (codons 2,209–2,274, including interferon sensitivity determining region [ISDR]) in 39 of 81 patients showed a higher mean number of mutations in the ISDR (codons 2,209–2,248) in groups 2 (1.28 ± 0.43 [n = 18]) and 3 (1.89 ± 0.54 [n = 9]) than in group 1 (0.67 ± 0.19 [n = 12];P= .049 group 1 vs. 3) and a mutant type ISDR (e.g., ≥4 mutations) was significantly more frequent in sustained virologic responders than in nonresponders or relapsers (2 of 4 [50%] vs. 2 of 35 [6%];P= .045). Thus, NS5A appears to be functionally relevant in IFN–α–induced effector reactions.