| Resumo: | The continuous monitoring of the antigenic and genetic properties of circulating influenza viruses is essential in order to detect any changes that may justify the selection of different vaccine candidates or changes in antiviral recommendations. During the 2012/2013 season, the influenza activity in Portugal was characterized by the co-circulation of influenza B/Yamagata and A(H1)pdm09 viruses with sporadic detections of influenza A(H3) and B/Victoria viruses. This study reports the antigenic and genetic characterisation of influenza viruses isolated in Portugal during the 2012/2013 influenza season. During the 2012/2013 influenza season, nasopharyngeal swabs were obtained through the National Influenza Surveillance Programme (ILI cases from primary health care-based surveillance, n=1266) and from the Portuguese Laboratory Network for the Influenza Diagnosis (hospital-based surveillance, n=165). The National Influenza Reference Laboratory has characterised antigenically by hemagglutination-inhibition assays 388 influenza strains after isolation on MDCK-Siat1 cell culture (233 B/Yamagata, 138 AH1pdm09, 10 B/Victoria and 7 AH3 viruses). Ninety influenza viruses were selected from the beginning, middle and end of the season for HA1 genetic characterisation (43 B/Yamagata, 33 AH1pdm09, 8 AH3 and 6 B/Victoria). In this season, the 145 isolated influenza A viruses showed a good reactivity with antisera raised against vaccine viral strains (A/California/7/2009 and A/Victoria/361/2011). Genetically, most pandemic viruses (28 of 33) were from clade 6 (A/St. Petersburg/27/2011) and 5 from clade 7 (A/St. Petersburg/100/2011). Seven seasonal AH3 viruses clustered in the group 3C (A/Victoria/361/2011) but one virus in the group 5 (A/Alabama/05/2010). Isolated viruses from B/Victoria lineage antigenically and genetically were similar to B/Brisbane/60/2008 (genetic clade 1A). The majority of influenza B/Yamagata viruses (which predominated in this season), showed higher reactivity with B/Massachusetts/02/2012 antiserum than with antiserum raised against the vaccine strain B/Wisconsin/1/2010. Sequence analysis showed that isolated B/Yamagata viruses were distributed between the clade 2 (B/Estonia/55669/2011) and clade 3 (B/Wisconsin/1/2010). Most B/Yamagata viruses from clade 3 presented 6 amino acid substitutions (only one of these substitutions was located in an antigenic site of the HA: S202N) while all B/Yamagata from clade 2 revealed 7 amino acid substitutions (including 3 in antigenic sites: I150S, Y165N and S202N). Influenza A viruses, although genetically grouped in different genetic clades, all remained antigenically similar to the vaccine strains. This season influenza B/Yamagata viruses have co-predominated with influenza A(H1)pdm09, however, they showed a greater antigenic and genetic variability. Most of these viruses have diverged antigenically from the vaccine strain and genetically belong now to the clade 2 (B/Estonia/55669/2011 and B/Massachusetts/02/2012). Comparing with the vaccine strain, viruses from clade 2 presented, at least, 3 amino acid substitutions located at antigenic sites of B hemagglutinin. The few B/Victoria viruses detected in circulation remain similar to the former vaccine strain B/Brisbane/60/2008. This antigenic and genetic scenario was very similar to the one observed at the European level. All the different genetic clades of influenza viruses detected in circulation were uniformly distributed throughout the 2012/2013 season.
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