Virus characteristics

Most influenza 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 influenza A(H1N1)pdm09 viruses. Details of the distribution of viruses detected in sentinel-source specimens can be found in the Primary care data section.

Since week 1/2018, 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, the majority of non-sentinel influenza A viruses subtyped were A(H3N2). 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 between countries may lead to variation in (sub)type proportions between countries within the Region.

Viruses detected in non-sentinel source specimens 

For week 10/2018, 12 564 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, 44% were type A and 56% type B viruses. The majority of viruses from non-sentinel specimens were not subtyped or assigned to a lineage.

While relatively few of the viruses detected in non-sentinel specimens since week 40/2017 have been ascribed to a subtype or lineage, 55% of all subtyped A viruses were A(H3N2) and 99% of influenza type B viruses ascribed to a lineage were B/Yamagata lineage.

Genetic characterization

For specimens collected since week 40/2017, genetic characterization of 2 120 viruses has been reported.

Among 707 influenza A(H3N2) viruses attributed to a clade, 400 (57%) fell in the vaccine virus component clade (3C.2a), 288 (41%) in subclade 3C.2a1 with viruses defined by N171K, often with N121K, amino acid substitutions in the haemagglutinin, and 19 (3%) in clade 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, thereby requiring continued monitoring of antigenic characteristics.

Of the 291 A(H1N1)pdm09 viruses attributed to a clade, all fell in the A/Michigan/45/2015 vaccine component clade (6B.1).

48 (48%) of the 99 B/Victoria-lineage clade 1A viruses belonged to a subgroup represented by B/Norway/2409/2017, which carries the HA1 double amino acid deletion, Δ162-163, characteristic of a new antigenically distinct subgroup of viruses that has been detected in several countries. All of the 1023 B/Yamagata lineage viruses belonged to clade 3 represented by B/Phuket/3073/2013. For more information on virus characterizations for EU/EEA countries, see the WHO CC London December 2017 report.

Viruses attributed to genetic groups, cumulative for weeks 40–6/2018

Phylogenetic group

Number of viruses

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


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(H3) representative A/Switzerland/9715293/2013 subgroup (clade 3C.3a)


A(H3N2) not attributable to any clade


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


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


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


B(Vic) lineage not attributed to clade


B/Yamagata lineage not attributed to any clade


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

b Vaccine component for northern hemisphere 2017–2018 season

c  Vaccine component for southern hemisphere 2018 season

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 vaccine component.

f Vaccine component of quadrivalent vaccines for use in northern hemisphere 2017–2018 season


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. Two 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, in all age groups, influenza vaccine effectiveness was 25 to 52% against any influenza, 55 to 68% against influenza A(H1N1)pdm09, 7 to 42% against influenza A(H3N2) and 36 to 54% against influenza B, which is consistent with previous estimates from Canada, Finland, Germany, Spain, Stockholm County and the United States of America. It is encouraging that trivalent vaccine with lineage mismatched influenza B virus has an estimated 36 to 54% effectiveness against the dominant B/Yamagata influenza virus circulating.

Antiviral susceptibility testing

Neuraminidase inhibitor susceptibility has been assessed for 1 436 viruses; 667 type B, 449 A(H3N2), and 320 A(H1N1)pdm09) with collection dates since week 40/2017. 1 A(H3N2) virus carried amino acid substitution R292K in neuraminidase and showed evidence of reduced inhibition by both oseltamivir and zanamivir. 1 A(H1N1)pdm09 showed evidence of reduced inhibition by oseltamivir. 3 type B viruses showed evidence of reduced inhibition by zanamivir and 1, carrying amino acid substitution D198N in neuraminidase, to both oseltamivir and zanamivir.