Virus characteristics

Most nfluenza viruses detected in sentinel surveillance systems this season were type B with those assigned to a lineage being mainly B/Yamagata viruses, while most of the type A viruses subtyped were A(H1N1)pdm09. Details of the distribution of viruses detected in sentinel-source specimens can be found in the Primary care data section.

For the season overall, the majority of influenza virus detections in non-sentinel systems have been type B with B/Yamagata lineage viruses predominating, as seen in sentinel systems. However, in contrast to sentinel systems, in non-sentinel sources similar numbers of A(H3N2) and A(H1N1)pdm09 viruses were reported. This may be related to the higher proportion of non-sentinel specimens being derived from hospital-based settings or outbreaks in long-term care facilities for the elderly, with A(H3N2) viruses often causing more severe disease in the elderly, while A(H1N1)pdm09 viruses do so in middle-aged patients. Further details are given in the section below.

Differences in the relative contributions of sentinel and non-sentinel specimen sources to influenza surveillance may lead to variation in (sub)type proportions between countries within the Region.

Viruses detected in non-sentinel source specimens 

For weeks 21–25/2018, 352 specimens from non-sentinel sources (such as hospitals, schools, primary care facilities not involved in sentinel surveillance, nursing homes and other institutions) tested positive for influenza viruses. Of these, 72% were type A and 28% type B viruses (Table). The majority of typed viruses from non-sentinel specimens were not subtyped or assigned to a lineage, but 59% of the subtyped type A viruses were A(H3N2).

Genetic characterization

For specimens collected since week 40/2017, genetic characterization 2 146 viruses has been reported (Table).

Among 1 118 influenza A(H3N2) viruses attributed to a clade, 650 (58%) fell in the vaccine virus component clade (3C.2a), 448 (40%) in subclade 3C.2a1 with viruses defined by N171K, often with N121K, amino acid substitutions in the haemagglutinin, and 20 (2%) in clades 3.C3 and 3C.3a. Viruses in the first 2 groups are antigenically similar, but both clade and subclade are evolving rapidly with the emergence of several virus clusters defined by additional amino acid substitutions in the haemagglutinin (see the latest WHO CC London Influenza virus characterisation reports), thereby requiring continued monitoring of antigenic characteristics.

All 814 A(H1N1)pdm09 viruses attributed to a clade, 812 fell in the A/Michigan/45/2015 vaccine component clade (6B.1) and 2 fell in clade 6B represented by A/South Africa/3626/2013.

74 (48%) of the 154 B/Victoria-lineage clade 1A viruses belonged to a subgroup represented by B/Norway/2409/2017, which carries HA1 double amino acid deletion, Δ162-163, characteristic of a new antigenically distinct subgroup of viruses that has been detected in several countries. For B/Yamagata lineage viruses, 1 782 belonged to clade 3 (represented by B/Phuket/3073/2013) and 1 belonged to clade 2 (represented by B/Massachusetts/02/2012). For more information on virus characterizations for EU/EEA countries, see the latest WHO CC London Influenza virus characterisation reports).

Countries that reported viruses falling into clades not represented in current reporting categories or that were not attributed to a clade are contacted for further clarification.

Viruses attributed to genetic groups, cumulative for weeks 40–25/2018

Phylogenetic group

Number of viruses

A(H1N1)pdm09 A/Michigan/45/2015 (clade 6B.1)a


A(H1N1)pdm09 group 6B representative A/South Africa/3626/2013


A(H1N1)pdm09 attributed to recognised group in the guidance but not listed here


A(H1N1)pdm09 not attributable to any clade


A(H3N2) A/Hong Kong/4801/2014 (clade 3C.2a)b


A(H3N2) A/Singapore/INFIMH-16-0019/2016 (clade 3C.2a1)c


A(H3N2) representative A/Switzerland/9715293/2013 subgroup (clade 3C.3a)


A(H3N2) clade 3C.3 representative A/Samara/73/2013 subgroup


A(H3N2) attributed to recognised group in current guidance but not listed here


B/Brisbane/60/2008 (Victoria lineage clade 1A)b, d


B/Norway/2409/2017 (Victoria lineage clade 1A Δ162-163)e


B(Victoria) lineage not attributed to clade


B/Phuket/3073/2013 (Yamagata lineage clade 3)c, f

1 782

B/Massachusetts/01/2012 (Yamagata lineage clade 2)


B(Yamagata) lineage not attributed to clade


a Vaccine component of vaccines for northern (2017–2018 and 2018-2019 seasons) and southern (2018 season) hemispheres

b Vaccine component for northern hemisphere 2017–2018 season

c Vaccine component for southern hemisphere 2018 and northern hemisphere 2018-2019 seasons

d Vaccine component of quadrivalent vaccines for use in southern hemisphere 2018 season

e Deletion of K162 and N163 in the HA1 subunit of the hemagglutinin and antigenically different from the 2017-2018 vaccine component: B/Norway/2409/2017 is B/Colorado/06/2017-like (trivalent vaccine component for the northern hemisphere 2018-2019 season).

f Vaccine component of quadrivalent vaccines for use in northern hemisphere 2017–2018 and 2018-2019 seasons

* reporting countries are contacted for clarification


The recommended composition of trivalent influenza vaccines for the 2017–2018 season in the northern hemisphere includes an A/Michigan/45/2015 (H1N1)pdm09-like virus; an A/Hong Kong/4801/2014 (H3N2)-like virus; and a B/Brisbane/60/2008-like virus (B/Victoria lineage). For quadrivalent vaccines, a B/Phuket/3073/2013-like virus (B/Yamagata lineage) was recommended.

On 21 February 2018 WHO published influenza vaccine recommendations for the 2018–2019 season in the northern hemisphere. 2 changes were recommended compared to the current trivalent and quadrivalent vaccines recommended for the 2017–2018 season in the northern hemisphere. Similar to the recommended composition for the 2018 southern hemisphere vaccine, the A(H3N2) component was changed to an A/Singapore/INFIMH-16-0019/2016 (H3N2)-like virus. In trivalent vaccines the B component was switched to a B/Colorado/06/2017-like virus, representing the emergent strain of B/Victoria-lineage viruses with deletion of K162 and N163 in the HA1 subunit. The A(H1N1)pdm09 component in trivalent and quadrivalent vaccines and the B/Yamagata component in quadrivalent vaccines remained the same.

Vaccine effectiveness

Interim results from 5 European studies indicate that influenza vaccine effectiveness in all age groups was 25 to 52% against any influenza, 55 to 68% against influenza A(H1N1)pdm09, -47 to 7% against influenza A(H3N2) and 36 to 54% against influenza B. This is consistent with earlier estimates from Canada, Finland, Germany, Spain, Stockholm County and the United States of America.

Antiviral susceptibility testing

Neuraminidase inhibitor susceptibility has been assessed for 3 703 viruses with collection dates since week 40/2017: 1 539 type B, 990 A(H3N2), and 1 174 A(H1N1)pdm09). 2 type B viruses carried the neuraminidase (NA) amino acid substitution D197N and showed evidence of reduced inhibition (RI) by oseltamivir and zanamivir, and 2 type B viruses showed RI by oseltamivir only. 19 A(H1N1)pdm09 viruses carried the NA amino acid substitution H275Y and showed evidence of highly reduced inhibition by oseltamivir and 2 showed RI by zanamivir only. 2 A(H3N2) viruses carried NA amino acid substitution R292K and showed evidence of RI by oseltamivir and zanamivir.