The issues of incomplete clinical and epidemiologic data accompanying
clinical specimens or virus isolates being referred to the
WHO CCs remains a limitation in determining the significance of
RI/HRI virus detection. NICs often cannot obtain this information
on all samples, particularly when they are received from non-sentinel
surveillance systems. Follow-up of individual samples requires
significant, often one-to-one interaction with sub-national laboratories
or physicians which is not possible for some NICs. In addition,
NAI susceptibility analysis of samples for surveillance purposes may
not be performed in a timely manner, making the collection of clinical
and epidemiologic data for characterisation of the risk factors for
NAI-RI/HRI virus infection difficult. Knowledge of whether the sample
originated from patients in the community or hospitals can more
easily be obtained. The WHO-AVWG is currently developing the
WHO database (FluNet) to collect this basic information, together
with H275Y screening data for influenza A(H1N1)pdm09 viruses,
from all NICs who perform such testing. This basic information,
which can also be supplied with the samples referred to the WHO
CCs, does at least facilitate screening for increased incidence of
viruses with HRI from untreated patients in the community, such
as detected in Japan in 2013–2014 and Australia in 2011.
This is the second global update on influenza NAI susceptibility
based on analysing data generated byWHOCCs on samples received
from the GISRS laboratories. Overall, the proportion of viruses showing
RI/HRI was similar between the two years, approximately 1% in
2012–2013 and 2% in 2013–2014. The slight increase in 2013–2014
is due to several clusters of untreated cases of A(H1N1)pdm09 viruses
carrying NA H275Y substitution in China, Japan and the United
States. Only 1% of A(H1N1)pdm09 viruses exhibited RI/HRI in
2012–2013, compared with 3% in 2013–2014. Rates of RI/HRI detection
in A(H3N2) (0.4% vs 0.3%), B/Victoria- (1% vs 2%) and B/
Yamagata- (0.3% both years) lineage viruses have remained very
similar for the two seasons analysed to date. Prevalence of RI/HRI
viruses has consistently been higher for B/Victoria-lineage over B/
Yamagata-lineage viruses. This could be a reflection of the overall
number of viruses analysed (more B/Yamagata-lineage in both seasons)
but could also be an indication of a slightly higher tendency for
B/Victoria-lineage NA to tolerate RI/HRI conferring substitutions.
This could merit further investigation, taking into account reassortant
events between the two lineages, notably the recent emergence
of B/Yamagata-lineage HA – B/Victoria-lineage NA reassortants.