Table 2.

Virus and patient characteristics of 11 influenza type B viruses showing reduced (RI) or highly reduced inhibition (HRI) tested by WHO CCs.^a

Virus	n	IC50 fold-change compared to reference median IC50 values b				NA substitution c		Patient setting	Antiviral treatment	Immuno-compromised
		Oseltamivir	Zanamivir	Peramivir	Laninamivir	Virus isolate	Clinical specimen
B/Victoria- lineage; n = 2242 d	2	2.9–4.1	1.4–2.0	26–30	1.8–2.2	I221V (2)	Not available f (2)	Unknown (2)	Unknown (2)	Unknown (2)
	1	3.3	96	n/t e	n/t	T43A & P124T	Not available	Hospital	Unknown	No
	1	11	7.2	n/t	n/t	P76S	Not available	Hospital	Unknown	No
	1	2.3	1.5	8.4	0.8	H134Y/H mix	None g	Community	No	No
	1	3.6	5.0	n/t	n/t	D197N	Not available	Hospital	Unknown	No
	1	27	11	42	6.4	A200T	A200T	Unknown	Unknown	Unknown
	1	2.3	40	n/t	n/t	S246P	Not available	Hospital	Unknown	No
B/Yamagata- lineage; n = 1592	1	1.0	7.9	n/t	n/t	K125T	Not available	Hospital	No	Unknown
	1	210	129	2869	473	R150K	R150K	Community	No	Unknown
	1	5.8	4.4	11	2.5	D197N	D197N	Unknown	Unknown	Unknown

^aBetween brackets the number of viruses for which data was reported if the number reported in column ‘n’ is greater than 1.

^bRI and HRI fold-change values are displayed underlined and in bold typeface.

^cAmino acid position numbering is B lineage specific. The majority of samples are sequenced using next generation sequencing methodology. Precise methodology differs by WHOCC. A minority of samples are sequenced by Sanger methodology.

^dIncludes 47 B/Yamagata-lineage haemagglutinin (HA) – B/Victoria-lineage neuraminidase (NA) reassortants.

^en/t: not tested.

^fClinical specimen not available for testing.

^gNone: no amino acid substitutions compared to viruses with a normal inhibition (NI) phenotype.