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Influenza virus characterisation, September 2013 (ECDC, October 12 2013, edited)
[Source: European Centre for Disease Prevention and Control (ECDC), full PDF document: (LINK). Edited.]
SURVEILLANCE REPORT
Influenza virus characterisation, September 2013
In the course of the 2012?13 season, A(H1N1)pdm09, A(H3N2) and B/Victoria- and B/Yamagata-lineage influenza viruses have co-circulated in ECDC-affiliated countries over what was an extended influenza season. The relative prevalences of each virus type/subtype/lineage has varied between countries.
Viruses from specimens collected between 1 January 2013 and 31 May 2013, spanning the peak of the 2012?13 season, were received from 28 countries in the EU/EEA region at the MRC National Institute for Medical Research, WHO Collaborating Centre for Reference and Research on Influenza. A summary of specimens received is shown in Table 1.
The overall proportions of influenza type A (58%) and type B (42%) viruses received have become increasingly similar, reflecting the decreasing proportion of influenza A towards the end of the season at the same time as the numbers of influenza virus detections were also falling.
For type A, H1N1pdm09 viruses were received in greater numbers than H3N2 viruses (ratio 1.5:1). Among influenza B receipts, viruses of the B/Yamagata and B/Victoria lineages were received at a ratio of 5:1.
(...)
Influenza A(H1N1)pdm09 virus analyses
The results of HI assays carried out on influenza A(H1N1)pdm09 viruses since the July report [1] are shown in Table 2. All 27 test viruses showed good reactivity with antiserum raised against the vaccine virus, A/California/7/2009, with all titres being within twofold of its recognition of the homologous virus. As described previously [2], antiserum raised against A/Christchurch/16/2010, a virus from a genetic group not seemingly in circulation at present (group 4), reacted less well than the other antisera with the test viruses: the titre was reduced eightfold or greater compared with the titre of the antiserum with the homologous virus for 25 of the 27 test viruses.
Figure 1 shows a phylogenetic tree for the HA genes of representative H1N1 viruses. Over the course of the last four years the HA genes have been observed to fall into eight designated genetic groups, with a ninth ?outlier? group largely restricted to countries of west Africa. However, viruses collected after 31 January 2013 fell into genetic groups 6 and 7, with group 6 viruses clustering in three subgroups, 6A−C (Figure 1). Both groups carry the substitutions S185T and S203T in HA1 and E47K and S124N in HA2 compared to A/California/7/2009.
The two groups and three subgroups are further defined by the following amino acid substitutions in HA1/HA2.
Group 6 viruses:
Group 7 viruses:
The majority of H1N1 viruses from EU/EEA countries collected during the 2012?13 season cluster within genetic groups 6 and 7, with viruses belonging to subgroup 6C predominating, notably so for those with collection dates since 1 March 2013. HA gene sequencing was performed on 16 of the 27 test viruses, and their genetic grouping is shown in Table 2; 14 were in genetic subgroup 6C, one in subgroup 6B, and one in group 7.
(...)
Influenza A(H3N2) virus analyses
Influenza A(H3N2) viruses continue to be difficult to characterise antigenically by HI assay due to variable agglutination of red blood cells from guinea pigs, turkeys and humans as described before [3]. The change in agglutination of red blood cells is associated with a reduced avidity of H3N2 viruses for the sialic acid receptor on the surface of the cell (Lin et al. 2012) [4]. Antigenic analyses of viruses conducted since the July report [1] are shown in Table 3. HI assays were carried out using guinea pig red blood cells in the presence of 20 nM oseltamivir, added to circumvent the NA-mediated binding of H3N2 viruses to the red blood cells (Lin et al. 2010) [5].
All 27 test viruses were propagated in MDCK-SIAT1 cells and reacted poorly in HI assays (≥ eightfold titre decrease), with post-infection ferret antiserum raised against the previous egg-propagated vaccine virus, A/Victoria/361/2011, compared to the titre of the antiserum with the homologous virus. The test viruses also reacted poorly with antisera raised against other reference viruses and previous vaccine viruses propagated in eggs (A/Perth/16/2009, A/Iowa/19/2010 and A/Hawaii/22/2012).
Somewhat better reactivity was seen with antiserum raised against egg-propagated A/Texas/50/2012 (the H3N2 vaccine virus recommendation for the northern hemisphere 2013?14 and southern hemisphere 2014) [6].
Although this virus induced an antiserum with a high homologous titre (2560), 21/27 (78%) of test viruses reacted within fourfold of the titre with the homologous virus.
The test viruses reacted well with antisera raised against reference viruses exclusively propagated in MDCK cells, and/or the derivative MDCK-SIAT-1 cells when compared to the titres with the homologous viruses. These antisera were raised against cell-propagated virus isolates of A/Victoria/361/2011, A/Alabama/5/2010, A/Stockholm/18/2011, A/Berlin/93/2011 and A/Athens/112/2012.
Phylogenetic analysis of the HA gene sequences of representative viruses is shown in Figure 2. Viruses from EU/EEA countries collected since 1 January 2013 have HA genes that fall predominantly into genetic group 3C, as is the case for the 19 test viruses sequenced during the preparation of this report. Viruses carrying HA genes falling into groups 3A and 3B (described in previous reports), 5 (e.g. A/Plzen/22/2013) and 6 (e.g. A/Lisboa/SU91/2012) have also been isolated earlier in the EU/EEA 2012−13 influenza season.
The amino acid substitutions in HA1/HA2 associated with these groupings of recently collected viruses are:
Group 3 viruses:
The 3C subgroup can be subdivided into three subsets:
Group 5 viruses:
Group 6 viruses:
Note: In Figure 2, the G186V substitutions in HA1 occur during adaptation of H3N2 viruses to passage in hens' eggs and are not group-specific.
There is no evidence for antigenic change associated with any of the genetic groups or emerging subgroups and subsets, including the emerging 3C.3 subset that carries substitutions in HA1 at amino acid residues 128 and 142.
(...)
Influenza B virus analyses
B/Victoria-lineage virus
Table 4 shows the results of antigenic analyses for viruses of the B/Victoria-lineage performed since the July report [1]. The three test viruses were isolated and propagated in MDCK cells or a derivative thereof (SIAT-1) and gave ≥ eightfold reductions in HI titres, compared to the titres with the homologous viruses, with post-infection ferret antiserum raised against the egg-propagated virus B/Brisbane/60/2008, a component of trivalent vaccines for the 2010?11 season and a recommended component of quadrivalent vaccines [6] for the 2013?14 northern hemisphere and southern hemisphere 2014 influenza seasons. The test viruses also showed similarly reduced reactivities with antisera raised against other reference viruses propagated in hens' eggs: B/England/393/2008, B/Malta/636714/2011 and B/Johannesburg/3964/2012. These observations probably relate to the loss of an N-linked carbohydrate site at position 197 of HA1, which is commonly associated with growth of B/Victoria-lineage viruses in hens? eggs, resulting in the exposure of a dominant antigenic site. The HAs of the test viruses sequenced retained the glycosylation site (NET). All test viruses gave titres close to the homologous titres, with antisera raised against cell-grown reference viruses B/Paris/1762/2008, B/Hong Kong/514/2009 and B/Odessa/3886/2010, which are genetically closely related to egg-propagataed B/Brisbane/60/2008. These three reference viruses are considered as surrogate cell-propagated antigens representing the egg-derived B/Brisbane/60/2008 prototype strain. Reactivity was somewhat reduced, with antiserum raised against cell-grown B/Formosa/V2367/2012.
Phylogenetic analysis of the HA genes of representative B/Victoria-lineage viruses is shown in Figure 3. All the viruses received with collection dates in 2013 from EU/EEA laboratories carried HA genes that fell into genetic clade 1A. The amino acid substitution associated with the separation of clade 1 into clades 1A and 1B, L58P, has no apparent effect on antigenicity. The HAs of recent viruses show few amino acid substitutions compared with B/Brisbane/60/2008.
(...)
B/Yamagata-lineage viruses
Tables 5 and 6 show the results of HI analyses of B/Yamagata lineage viruses tested since the July report [1]. The genetic clade into which sequenced HA genes of test viruses fall is indicated.
Approximately 90% (43/47) of the test viruses showed good reactivity (within fourfold of the homologous titre) with antiserum raised against the egg-propagated vaccine virus recommended for the northern hemisphere 2013−2014 and southern hemisphere 2014 influenza seasons [6], B/Massachusetts/02/2012 (clade 2). Antiserum raised against egg-propagated B/Wisconsin/1/2010, the clade 3 virus used in the vaccine for 2012-2013, showed reactivity within fourfold of the titre against the homologous virus for only ~30% (14/47) of these viruses. Many, but not all, viruses carrying clade 2 HA genes, represented by B/Massachusetts/02/2012, could be differentiated antigenically from those carrying clade 3 HA genes, represented by B/Wisconsin/1/2010, by certain post-infection ferret antisera. However, not all antisera were able to antigenically differentiate viruses falling in the alternate clades.
Twenty of the test viruses had been genetically characterised at the time of preparation of this report, with 15 falling into genetic group 2 and five into genetic group 3.
Figure 4 shows a phylogenetic analysis of the HA genes of representative B/Yamagata-lineage viruses. The analysis shows that the HA genes of recent viruses continue to fall into two genetic clades: clade 3 (represented by the vaccine virus B/Wisconsin/1/2010 and reference viruses B/Stockholm/12/2011 and B/Novosibirsk/1/2012) and clade 2 (represented by the reference viruses B/Brisbane/3/2007, B/Estonia/55669/2011, B/Hong Kong/3577/2012 and the 2013−14 vaccine virus B/Massachusetts/02/2012). The two clades are differentiated by substitutions at HA1 residues 48, 108, 150, 165, 181 and 229. The HA genes of viruses of clade 2 encode K48, A108, S150, N165, A181 and G229; the HA genes of viruses in clade 3 encode R48, P108, I150, Y165, T181 and D229. The proportion of viruses received with HA genes that fall into clade 2 has continued to increase over the number of HA genes falling into clade 3.
(...)
Influenza A(H7N9) virus
On 1 April 2013, the WHO Global Alert and Response [7] reported that the China Health and Family Planning Commission notified the World Health Organization (WHO) of three cases of human infection with influenza A(H7N9). The cases were confirmed by laboratory testing on 29 March by the Chinese CDC. A description of the characteristics of H7N9 viruses can be found on the WHO website [8]. WHO is updating information on the outbreak regularly [8] and ECDC is posting epidemiological updates [9]. A Rapid Risk Assessment [10] for these A(H7N9) viruses has been carried out and posted by ECDC [11] on 3 April 2013, and an updated risk assessment has been posted by WHO [12]. As of 11 August 2013, WHO reported [13] 135 laboratory-confirmed cases and 44 associated fatalities (case fatality ratio [CFR] of 33%).
A description of results generated by the WHO Collaborating Centre for Reference and Research on Influenza at the MRC National Institute for Medical Research in London, and evaluated at the WHO Vaccine Composition Meetings held at WHO Geneva on 18?20 February 2013 and 23?25 September 2013, can be found at: http://www.nimr.mrc.ac.uk/documents/about/Interim_Report_February 2013.pdf [14] and http://www.nimr.mrc.ac.uk/documents/about/NIMR-report-Sep2013final.pdf [15]
Note on the figures
The phylogenetic trees were constructed using RAxML and drawn using FigTree. The bars indicate the proportion of nucleotide changes between sequences. Reference strains are viruses to which post-infection ferret antisera have been raised. The colours indicate the month of sample collection. Isolates from WHO NICs in ECDC countries are highlighted within boxes. Sequences for some of the viruses from non-EU/EEA countries were recovered from GISAID. We acknowledge all laboratories who submitted sequences directly to the London WHO Collaborating Centre.
References
____
This report was prepared by Rod Daniels, Vicki Gregory and John McCauley on behalf of the European Reference Laboratory Network for Human Influenza (ERLI-Net), under contract to the European Centre for Disease Prevention and Control (ECDC).
? European Centre for Disease Prevention and Control, Stockholm, 2013.
Reproduction is authorised, provided the source is acknowledged.
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SURVEILLANCE REPORT
Influenza virus characterisation, September 2013
In the course of the 2012?13 season, A(H1N1)pdm09, A(H3N2) and B/Victoria- and B/Yamagata-lineage influenza viruses have co-circulated in ECDC-affiliated countries over what was an extended influenza season. The relative prevalences of each virus type/subtype/lineage has varied between countries.
- Type A (~60%) and type B (~40%) viruses have been detected in similar proportions but with type A peaking and declining slightly before type B.
- A(H1N1)pdm09 viruses have been detected at approximately twice the level of A(H3N2) viruses.
- The vast majority of A(H1N1)pdm09 viruses have remained antigenically similar to the vaccine virus, A/California/07/2009, but continued to show genetic drift with an increasing prevalence of genetic group 6 viruses, predominant in the 6C subgroup.
- The vast majority of A(H3N2) viruses have been antigenically and genetically similar to cell-propagated A/Victoria/361/2011, a genetic subgroup 3C virus and the prototype vaccine virus for the 2012?13 influenza season; subgroup 3C viruses have circulated exclusively in recent months, and the recommended vaccine virus for the 2013?14 season, A/Texas/50/2012, is in this genetic group.
- Viruses of the B/Yamagata-lineage have predominated over those of the B/Victoria-lineage.
- B/Victoria-lineage viruses have remained antigenically similar to cell-propagated reference viruses of the B/Brisbane/60/2008 genetic clade.
- B/Yamagata-lineage viruses formed two antigenically distinguishable genetic clades: clade 3 represented by B/Wisconsin/1/2010 (the recommended vaccine component for the 2012?13 influenza season) and, in increasing numbers, clade 2 (75% of B/Yamagata detections recently) represented by B/Massachusetts/2/2012 (the recommended vaccine component for the 2013?14 influenza season).
Viruses from specimens collected between 1 January 2013 and 31 May 2013, spanning the peak of the 2012?13 season, were received from 28 countries in the EU/EEA region at the MRC National Institute for Medical Research, WHO Collaborating Centre for Reference and Research on Influenza. A summary of specimens received is shown in Table 1.
The overall proportions of influenza type A (58%) and type B (42%) viruses received have become increasingly similar, reflecting the decreasing proportion of influenza A towards the end of the season at the same time as the numbers of influenza virus detections were also falling.
For type A, H1N1pdm09 viruses were received in greater numbers than H3N2 viruses (ratio 1.5:1). Among influenza B receipts, viruses of the B/Yamagata and B/Victoria lineages were received at a ratio of 5:1.
(...)
Influenza A(H1N1)pdm09 virus analyses
The results of HI assays carried out on influenza A(H1N1)pdm09 viruses since the July report [1] are shown in Table 2. All 27 test viruses showed good reactivity with antiserum raised against the vaccine virus, A/California/7/2009, with all titres being within twofold of its recognition of the homologous virus. As described previously [2], antiserum raised against A/Christchurch/16/2010, a virus from a genetic group not seemingly in circulation at present (group 4), reacted less well than the other antisera with the test viruses: the titre was reduced eightfold or greater compared with the titre of the antiserum with the homologous virus for 25 of the 27 test viruses.
Figure 1 shows a phylogenetic tree for the HA genes of representative H1N1 viruses. Over the course of the last four years the HA genes have been observed to fall into eight designated genetic groups, with a ninth ?outlier? group largely restricted to countries of west Africa. However, viruses collected after 31 January 2013 fell into genetic groups 6 and 7, with group 6 viruses clustering in three subgroups, 6A−C (Figure 1). Both groups carry the substitutions S185T and S203T in HA1 and E47K and S124N in HA2 compared to A/California/7/2009.
The two groups and three subgroups are further defined by the following amino acid substitutions in HA1/HA2.
Group 6 viruses:
- D97N, with the subgroups defined by the substitutions:
- 6A: H138R and V249L, e.g. A/Hong Kong/5659/2012.
- 6B: K163Q, A256T, K283E and E172K, e.g. A/Norway/2417/2013.
- 6C: V234I, K283E and E172K e.g. A/Estonia/76677/2013.
Group 7 viruses:
- S143G and A197T, often with S84G, K163I and V193A, e.g. A/Norway/1675/2013.
The majority of H1N1 viruses from EU/EEA countries collected during the 2012?13 season cluster within genetic groups 6 and 7, with viruses belonging to subgroup 6C predominating, notably so for those with collection dates since 1 March 2013. HA gene sequencing was performed on 16 of the 27 test viruses, and their genetic grouping is shown in Table 2; 14 were in genetic subgroup 6C, one in subgroup 6B, and one in group 7.
(...)
Influenza A(H3N2) virus analyses
Influenza A(H3N2) viruses continue to be difficult to characterise antigenically by HI assay due to variable agglutination of red blood cells from guinea pigs, turkeys and humans as described before [3]. The change in agglutination of red blood cells is associated with a reduced avidity of H3N2 viruses for the sialic acid receptor on the surface of the cell (Lin et al. 2012) [4]. Antigenic analyses of viruses conducted since the July report [1] are shown in Table 3. HI assays were carried out using guinea pig red blood cells in the presence of 20 nM oseltamivir, added to circumvent the NA-mediated binding of H3N2 viruses to the red blood cells (Lin et al. 2010) [5].
All 27 test viruses were propagated in MDCK-SIAT1 cells and reacted poorly in HI assays (≥ eightfold titre decrease), with post-infection ferret antiserum raised against the previous egg-propagated vaccine virus, A/Victoria/361/2011, compared to the titre of the antiserum with the homologous virus. The test viruses also reacted poorly with antisera raised against other reference viruses and previous vaccine viruses propagated in eggs (A/Perth/16/2009, A/Iowa/19/2010 and A/Hawaii/22/2012).
Somewhat better reactivity was seen with antiserum raised against egg-propagated A/Texas/50/2012 (the H3N2 vaccine virus recommendation for the northern hemisphere 2013?14 and southern hemisphere 2014) [6].
Although this virus induced an antiserum with a high homologous titre (2560), 21/27 (78%) of test viruses reacted within fourfold of the titre with the homologous virus.
The test viruses reacted well with antisera raised against reference viruses exclusively propagated in MDCK cells, and/or the derivative MDCK-SIAT-1 cells when compared to the titres with the homologous viruses. These antisera were raised against cell-propagated virus isolates of A/Victoria/361/2011, A/Alabama/5/2010, A/Stockholm/18/2011, A/Berlin/93/2011 and A/Athens/112/2012.
Phylogenetic analysis of the HA gene sequences of representative viruses is shown in Figure 2. Viruses from EU/EEA countries collected since 1 January 2013 have HA genes that fall predominantly into genetic group 3C, as is the case for the 19 test viruses sequenced during the preparation of this report. Viruses carrying HA genes falling into groups 3A and 3B (described in previous reports), 5 (e.g. A/Plzen/22/2013) and 6 (e.g. A/Lisboa/SU91/2012) have also been isolated earlier in the EU/EEA 2012−13 influenza season.
The amino acid substitutions in HA1/HA2 associated with these groupings of recently collected viruses are:
Group 3 viruses:
- N145S and V223I, with the subgroups defined by the substitutions:
- 3A: N144D (resulting in the loss of a potential glycosylation site) and D158N, e.g. A/Stockholm/18/2011;
- 3B: A198S, N312S and D158N, e.g. A/Athens/112/2012;
- 3C: S45N (resulting in gain of a potential glycosylation site), T48I, A198S and N312S, e.g. the prototype vaccine virus A/Victoria/361/2011.
The 3C subgroup can be subdivided into three subsets:
- 3C.1 Q33R, S145N and N278K, e.g. A/Berlin/93/2011, A/Texas/50/2012 and A/Hawaii/22/2012;
- 3C.2 As 3C.1 plus N145S, e.g. A/Ireland/M28390/2013;
- 3C.3 As 3C.2 plus T128A (resulting in the loss of a potential glycosylation site) and R142G, e.g. A/Samara/73/2013
Group 5 viruses:
- D53N, Y94H, I230V and E280A (e.g. A/Alabama/05/2010), often in combination with K2E and N8D (resulting in the loss of a potential glycosylation site, e.g. A/Plzen/22/2013);
Group 6 viruses:
- As group 5 plus S199A (e.g. A/Iowa/19/2010).
Note: In Figure 2, the G186V substitutions in HA1 occur during adaptation of H3N2 viruses to passage in hens' eggs and are not group-specific.
There is no evidence for antigenic change associated with any of the genetic groups or emerging subgroups and subsets, including the emerging 3C.3 subset that carries substitutions in HA1 at amino acid residues 128 and 142.
(...)
Influenza B virus analyses
B/Victoria-lineage virus
Table 4 shows the results of antigenic analyses for viruses of the B/Victoria-lineage performed since the July report [1]. The three test viruses were isolated and propagated in MDCK cells or a derivative thereof (SIAT-1) and gave ≥ eightfold reductions in HI titres, compared to the titres with the homologous viruses, with post-infection ferret antiserum raised against the egg-propagated virus B/Brisbane/60/2008, a component of trivalent vaccines for the 2010?11 season and a recommended component of quadrivalent vaccines [6] for the 2013?14 northern hemisphere and southern hemisphere 2014 influenza seasons. The test viruses also showed similarly reduced reactivities with antisera raised against other reference viruses propagated in hens' eggs: B/England/393/2008, B/Malta/636714/2011 and B/Johannesburg/3964/2012. These observations probably relate to the loss of an N-linked carbohydrate site at position 197 of HA1, which is commonly associated with growth of B/Victoria-lineage viruses in hens? eggs, resulting in the exposure of a dominant antigenic site. The HAs of the test viruses sequenced retained the glycosylation site (NET). All test viruses gave titres close to the homologous titres, with antisera raised against cell-grown reference viruses B/Paris/1762/2008, B/Hong Kong/514/2009 and B/Odessa/3886/2010, which are genetically closely related to egg-propagataed B/Brisbane/60/2008. These three reference viruses are considered as surrogate cell-propagated antigens representing the egg-derived B/Brisbane/60/2008 prototype strain. Reactivity was somewhat reduced, with antiserum raised against cell-grown B/Formosa/V2367/2012.
Phylogenetic analysis of the HA genes of representative B/Victoria-lineage viruses is shown in Figure 3. All the viruses received with collection dates in 2013 from EU/EEA laboratories carried HA genes that fell into genetic clade 1A. The amino acid substitution associated with the separation of clade 1 into clades 1A and 1B, L58P, has no apparent effect on antigenicity. The HAs of recent viruses show few amino acid substitutions compared with B/Brisbane/60/2008.
(...)
B/Yamagata-lineage viruses
Tables 5 and 6 show the results of HI analyses of B/Yamagata lineage viruses tested since the July report [1]. The genetic clade into which sequenced HA genes of test viruses fall is indicated.
Approximately 90% (43/47) of the test viruses showed good reactivity (within fourfold of the homologous titre) with antiserum raised against the egg-propagated vaccine virus recommended for the northern hemisphere 2013−2014 and southern hemisphere 2014 influenza seasons [6], B/Massachusetts/02/2012 (clade 2). Antiserum raised against egg-propagated B/Wisconsin/1/2010, the clade 3 virus used in the vaccine for 2012-2013, showed reactivity within fourfold of the titre against the homologous virus for only ~30% (14/47) of these viruses. Many, but not all, viruses carrying clade 2 HA genes, represented by B/Massachusetts/02/2012, could be differentiated antigenically from those carrying clade 3 HA genes, represented by B/Wisconsin/1/2010, by certain post-infection ferret antisera. However, not all antisera were able to antigenically differentiate viruses falling in the alternate clades.
Twenty of the test viruses had been genetically characterised at the time of preparation of this report, with 15 falling into genetic group 2 and five into genetic group 3.
Figure 4 shows a phylogenetic analysis of the HA genes of representative B/Yamagata-lineage viruses. The analysis shows that the HA genes of recent viruses continue to fall into two genetic clades: clade 3 (represented by the vaccine virus B/Wisconsin/1/2010 and reference viruses B/Stockholm/12/2011 and B/Novosibirsk/1/2012) and clade 2 (represented by the reference viruses B/Brisbane/3/2007, B/Estonia/55669/2011, B/Hong Kong/3577/2012 and the 2013−14 vaccine virus B/Massachusetts/02/2012). The two clades are differentiated by substitutions at HA1 residues 48, 108, 150, 165, 181 and 229. The HA genes of viruses of clade 2 encode K48, A108, S150, N165, A181 and G229; the HA genes of viruses in clade 3 encode R48, P108, I150, Y165, T181 and D229. The proportion of viruses received with HA genes that fall into clade 2 has continued to increase over the number of HA genes falling into clade 3.
(...)
Influenza A(H7N9) virus
On 1 April 2013, the WHO Global Alert and Response [7] reported that the China Health and Family Planning Commission notified the World Health Organization (WHO) of three cases of human infection with influenza A(H7N9). The cases were confirmed by laboratory testing on 29 March by the Chinese CDC. A description of the characteristics of H7N9 viruses can be found on the WHO website [8]. WHO is updating information on the outbreak regularly [8] and ECDC is posting epidemiological updates [9]. A Rapid Risk Assessment [10] for these A(H7N9) viruses has been carried out and posted by ECDC [11] on 3 April 2013, and an updated risk assessment has been posted by WHO [12]. As of 11 August 2013, WHO reported [13] 135 laboratory-confirmed cases and 44 associated fatalities (case fatality ratio [CFR] of 33%).
A description of results generated by the WHO Collaborating Centre for Reference and Research on Influenza at the MRC National Institute for Medical Research in London, and evaluated at the WHO Vaccine Composition Meetings held at WHO Geneva on 18?20 February 2013 and 23?25 September 2013, can be found at: http://www.nimr.mrc.ac.uk/documents/about/Interim_Report_February 2013.pdf [14] and http://www.nimr.mrc.ac.uk/documents/about/NIMR-report-Sep2013final.pdf [15]
Note on the figures
The phylogenetic trees were constructed using RAxML and drawn using FigTree. The bars indicate the proportion of nucleotide changes between sequences. Reference strains are viruses to which post-infection ferret antisera have been raised. The colours indicate the month of sample collection. Isolates from WHO NICs in ECDC countries are highlighted within boxes. Sequences for some of the viruses from non-EU/EEA countries were recovered from GISAID. We acknowledge all laboratories who submitted sequences directly to the London WHO Collaborating Centre.
References
- European Centre for Disease Prevention and Control. Influenza virus characterisation ? Summary Europe, July 2013. Stockholm: ECDC; 2013. Available from: http://www.ecdc.europa.eu/en/publications/Publications/influenza-virus-characterisation-July-2013.pdf
- European Centre for Disease Prevention and Control. Influenza virus characterisation ? Summary Europe, April 2013. Stockholm: ECDC; 2013. Available from: http://www.ecdc.europa.eu/en/publications/Publications/influenza-virus-characterisation-April-2013.pdf
- European Centre for Disease Prevention and Control. Influenza virus characterisation ? Summary Europe, April 2011. Stockholm: ECDC; 2011. Available from: http://ecdc.europa.eu/en/publications/Publications/1304_Influenza_virus_characterisation_2011_April.p df.
- Lin YP, Xiong X, Wharton SA, Martin SR, Coombs PJ, Vachieri SG, et al. Evolution of the receptor binding properties of the influenza A(H3N2) hemagglutinin. Proc Natl Acad Sci USA. 2012 Dec 26;109(52):21474-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23236176
- Lin YP, Gregory V, Collins P, Kloess J, Wharton S, Cattle N, et al. Neuraminidase receptor binding variants of human influenza A(H3N2) viruses resulting from substitution of aspartic acid 151 in the catalytic site: a role in virus attachment? J Virol. 2010 Jul;84(13):6769-81. Available from: http://jvi.asm.org/content/84/13/6769.full?view=long&pmid=20410266
- World Health Organization. WHO recommendations on the composition of influenza virus vaccines. [internet] [cited 2013 Sep 1]. Available from: http://www.who.int/influenza/vaccines/virus/recommendations/en/
- World Health Organization. Global Alert and Response (GAR) ? 2013 [internet]. 2013 [cited 2013 Sep 1]. Available from: http://www.who.int/csr/don/archive/year/2013/en/index.html
- World Health Organization. Avian influenza A(H7N9) virus. [internet]. 2013 [cited 2013 June 20]. Available from: http://www.who.int/influenza/human_animal_interface/influenza_h7n9/en/index.html
- European Centre for Disease Prevention and Control. Epidemiological updates. [internet]. 2013 [cited 2013 Sep 12]. Available from: http://ecdc.europa.eu/en/press/epidemiological_updates/Pages/epidemiological_updates.aspx
- European Centre for Disease Prevention and Control. Rapid risk assessment ? Severe respiratory disease associated with a novel influenza A virus, A(H7N9) ? China, 3 April 2013. Available from: http://ecdc.europa.eu/en/publications/Publications/AH7N9-China-rapid-risk-assessment.pdf
- European Centre for Disease Prevention and Control. [internet]. 2013 [cited 2013 Oct 2]. Available from: http://ecdc.europa.eu/en/Pages/home.aspx
- World Health Organization. WHO risk assessment: Human infections with avian influenza A(H7N9) virus, 7 June 2013. Geneva: WHO; 2013. Available from: http://www.who.int/influenza/human_animal_interface/influenza_h7n9/RiskAssessment_H7N9_07Jun13.pdf
- World Health Organization. Human infection with avian influenza A(H7N9) virus ? update. Global Alert and Response (GAR) [internet]. Jul 20 2013 [cited 2013 July 21]. Available from: http://www.who.int/csr/don/2013_08_11/en/index.html
- National Institute for Medical Research, WHO Influenza Centre London. Report prepared for the WHO annual consultation on the composition of influenza vaccine for the northern hemisphere 2013/14, 18th?20th February 2013. London: WHO Collaborating Centre for Reference and Research on Influenza, National Institute for Medical Research; 2013. Available from: http://www.nimr.mrc.ac.uk/documents/about/Interim_Report_February 2013.pdf
- National Institute for Medical Research, WHO Influenza Centre London. Report prepared for the WHO annual consultation on the composition of influenza vaccine for the southern hemisphere 2014, 23rd?25th September 2013. London: WHO Collaborating Centre for Reference and Research on Influenza, National Institute for Medical Research; 2013. Available from: http://www.nimr.mrc.ac.uk/documents/about/NIMR-report-Sep2013final.pdf
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This report was prepared by Rod Daniels, Vicki Gregory and John McCauley on behalf of the European Reference Laboratory Network for Human Influenza (ERLI-Net), under contract to the European Centre for Disease Prevention and Control (ECDC).
? European Centre for Disease Prevention and Control, Stockholm, 2013.
Reproduction is authorised, provided the source is acknowledged.
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