Recommended #composition of #influenza virus #vaccines for use in the 2026 – 2027 northern hemisphere influenza season (#WHO, Feb. 27 '26)

 

February 2026 

WHO convenes technical consultations {1} in February and September each year to recommend viruses for inclusion in influenza vaccines {2} for the northern hemisphere (NH) and southern hemisphere (SH) influenza seasons, respectively. 

This recommendation relates to the influenza vaccines for use in the NH 2026-2027 influenza season. 

A recommendation will be made in September 2026 relating to vaccines that will be used for the SH 2027 influenza season. 

WHO guidance for choosing between the NH and SH formulations for countries in tropical and subtropical regions is available on the WHO Global Influenza Programme website {3}.  

National or regional authorities approve the composition and formulation of influenza vaccines used in each country. 

National public health authorities are responsible for making recommendations regarding the use of the vaccine. 

WHO has published recommendations on the prevention of influenza {4}.  

Seasonal influenza activity 

From September 2025 through January 2026, influenza activity was reported in all transmission zones. 

Overall influenza virus detections were higher compared to the same reporting period in 2024-2025 but peaked in December 2025 for this recent period compared to February 2025 for the previous period. 

During this reporting period, influenza A viruses predominated, although the proportion of virus detections varied among transmission zones. 

In Africa, influenza activity increased during the start of the reporting period, with a predominance of influenza A viruses in all transmission zones. 

In Eastern, Northern, and Western Africa, among subtyped influenza A viruses, A(H1N1)pdm09 viruses accounted for the majority of detections early in the reporting period while A(H3N2) viruses predominated later in the reporting period. 

Influenza detections peaked in November in Western Africa and December in Eastern and Northern Africa. 

In Middle Africa, influenza detections remained low throughout the reporting period with a slight predominance of A(H1N1)pdm09 viruses early in the reporting period. 

In Southern Africa, influenza detections remained low throughout the reporting period, with a predominance of influenza A viruses. 

In Northern and Middle Africa, there was low and sustained influenza B activity throughout the reporting period. 

In Asia, influenza activity increased during the start of the reporting period in South East and Western Asia, from October in Central and Eastern Asia, and from November in Southern Asia, with a predominance of influenza A viruses in all transmission zones. 

Most influenza detections were reported from Eastern Asia, where activity peaked in early December. 

In Southern Asia, influenza activity also peaked in December; in Central Asia influenza activity peaked in November, and in Western and South East Asia, influenza activity peaked in October. 

Among subtyped influenza A viruses, A(H3N2) viruses accounted for the majority of detections in all transmission zones; detections of A(H1N1)pdm09 and influenza B viruses remained low in most transmission zones throughout the reporting period, except in Eastern Asia where there was a substantial rise in influenza B viruses in recent weeks. 

In Europe, influenza activity increased from mid-September in Northern Europe, from October in South West Europe and from mid-November in Eastern Europe, with a predominance of influenza A viruses in all transmission zones. 

Influenza detections peaked in December in Northern and South West Europe but remained elevated through January. 

Influenza detections continued to increase through January in Eastern Europe. 

Among subtyped influenza A viruses, A(H3N2) viruses predominated. 

In South West Europe, detections of A(H1N1)pdm09 viruses slightly increased in mid-November. 

In Eastern and Northern Europe, detections of A(H1N1)pdm09 and influenza B viruses remained low throughout the reporting period.  

In the Americas, influenza activity increased from the start of the reporting period in Temperate and Tropical South America and from November in North America and Central America Caribbean. 

Influenza A viruses accounted for most detections, and influenza B virus detections remained low throughout the reporting period in all transmission zones, except in North America where there was a substantial rise in influenza B viruses in recent weeks. 

In North America, activity peaked in late December. 

Among subtyped influenza A viruses, there was a predominance of A(H3N2) viruses. 

In Central America Caribbean, influenza activity remained elevated through mid-January with A(H3N2) virus detections predominant from December. 

In Tropical South America, influenza activity peaked in early November and slowly declined until the end of the reporting period. 

Among subtyped influenza A viruses, A(H3N2) predominated through November then co-circulated at similar proportions to A(H1N1)pdm09 until the end of the reporting period. 

In Temperate South America, influenza activity peaked in mid-November and among subtyped influenza A viruses, A(H3N2) viruses predominated throughout the reporting period.  

In Oceania, influenza activity decreased until mid-October, increased in December and decreased since mid-December. A(H1N1)pdm09 and B viruses were detected at similar levels until mid-September and A(H3N2) virus detections predominated since then. 

Influenza A 

Globally, influenza A virus detections greatly outnumbered those of influenza B. 

Among subtyped influenza A viruses, A(H3N2) viruses predominated throughout the reporting period in most transmission zones. 

In Eastern, Northern, Western Africa, Central America Caribbean and Oceania, influenza A(H1N1)pdm09 virus detections predominated during the first part of the reporting period, and A(H3N2) virus detections predominated in the latter part of the reporting period. 

Influenza A(H1N1)pdm09 virus detections increased slightly towards the latter part of the reporting period in Eastern and South West Europe, Central America Caribbean and Tropical South America. 

The overall number of influenza detections was low in Middle and Southern Africa. 

Influenza B 

Globally, influenza B virus detections remained low throughout the reporting period. 

Increases in influenza B virus detections in January were reported in North America and Eastern Asia. 

All influenza B viruses where lineage was confirmed belonged to the B/Victoria lineage. 

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Zoonotic influenza  

From 23 September 2025, sporadic zoonotic influenza infections were reported, in most cases, following exposure to infected birds, swine or contaminated environments. 

Single cases of A(H5N1) from Bangladesh, A(H5N2) from Mexico, and A(H5N5) from the United States of America were reported. 

Three A(H5N1) cases were reported from Cambodia. 

Fourteen cases of A(H9N2) and one case of A(H10N3) were reported from China. 

Single cases of A(H1N1)v and A(H1N2)v were reported from China, a case of A(H1N2)v from the United States of America, and a case of A(H3N2)v from Brazil. 

Genetic and antigenic characteristics of recent seasonal influenza viruses, human serology and antiviral susceptibility 

Influenza A(H1N1)pdm09 viruses  

Since September 2025, A(H1N1)pdm09 viruses circulated globally, but did not predominate in any region. 

The haemagglutinin (HA) genes of viruses that were genetically characterized belonged to the 5a.2a and 5a.2a.1 clades. 

Viruses from clade 5a.2a subclades C.1, C.1.9 and C.1.9.3 circulated in low numbers, with the largest proportion of detections in Africa {5}. 

Since September 2025, clade 5a.2a.1 subclades D.3.1 and D.3.1.1 viruses circulated globally. 

The D.3.1 subclade with substitutions T120A, I372V, I460T and V520A predominated in Western Pacific, Africa, South East Asia and several countries in the Americas. 

D.3.1.1 viruses characterized by R113K and more recently acquired substitutions A139D, E283K and K302E predominated in some countries in Europe, the Middle East and North America. 

The antigenic properties of A(H1N1)pdm09 viruses were assessed in haemagglutination inhibition (HI) assays with post-infection ferret antisera. 

HI results for viruses with collection dates since September 2025 showed that ferret antisera raised against cell culture-propagated A/Wisconsin/67/2022-like and eggpropagated A/Victoria/4897/2022-like viruses from the 5a.2a.1 clade recognized viruses in both 5a.2a and 5a.2a.1 clades well. 

However, post-infection ferret antisera raised against viruses from clade 5a.2a showed some reduction in recognition of the now predominating D.3.1 and D.3.1.1 subclade viruses. 

Post-infection ferret antisera raised against viruses from subclade D.3.1 (e.g., A/Missouri/11/2025) recognized recently circulating viruses from both 5a.2a and 5a.2a.1 clades well.  

Human serology studies used 15 serum panels from children, adults (18 to 64 years) and older adults (≥65 years) who had received egg-propagated inactivated (standard, high dose or adjuvanted), cell culture-propagated inactivated or recombinant trivalent or quadrivalent vaccines with NH 2025-2026 influenza vaccine formulations. 

-- NH 2025-2026 egg-based vaccines contained A/Victoria/4897/2022 (H1N1)pdm09like, 

-- A/Croatia/10136RV/2023 (H3N2)-like, 

-- B/Austria/1359417/2021-like (B/Victoria lineage) and, in quadrivalent vaccines, 

-- B/Phuket/3073/2013-like (B/Yamagata lineage) virus antigens. 

Cell culture-propagated and recombinant vaccines contained A/Wisconsin/67/2022 (H1N1)pdm09-like, A/District of Columbia/27/2023 (H3N2)-like and B/Austria/1359417/2021-like (B/Victoria lineage) virus antigens. 

Recent A(H1N1)pdm09 viruses with HA genes from clades 5a.2a (subclade C.1.9.3) and 5a.2a.1 (subclades D.3.1 and D.3.1.1) were analysed in HI assays using these human serum panels. 

When compared to the responses to cell culture-propagated A/Wisconsin/67/2022 (H1N1)pdm09-like vaccine reference viruses, post-vaccination geometric mean titres (GMTs) were significantly reduced for some recently circulating viruses from D.3.1 and D.3.1.1 subclades. 

Of 1 161 A(H1N1)pdm09 virus clinical samples and isolates examined by genetic and/or phenotypic analyses, 15 viruses showed evidence of reduced susceptibility to neuraminidase inhibitors (NAIs): seven had an H275Y neuraminidase (NA) substitution and eight had I223V and S247N substitutions. 

Of 1 331 A(H1N1)pdm09 viruses examined by genetic and/or phenotypic analyses, no viruses showed evidence of reduced susceptibility to the endonuclease inhibitor baloxavir marboxil. 

Influenza A(H3N2) viruses  

Phylogenetic analysis of the HA gene sequences of A(H3N2) viruses collected since September 2025 showed that the vast majority of viruses belonged to one of the J.2 subclades {6}, expressing HA N122D and K276E substitutions. 

HA genes have diversified with many subclades; J.2.2 (characterized by S124N), J.2.3 (characterized by N158K, K189R and S378N), J.2.4 (characterized by T135K [a potential loss of an N-glycosylation site] and K189R), and K (formerly designated as J.2.4.1; characterized by K2N, S144N [a potential addition of an N-glycosylation site], N158D, I160K, Q173R, T328A and S378N). 

During this reporting period, subclade K viruses were detected in all regions and predominated in many countries. 

There was still circulation of other J.2 subclades, notably J.2 or J.2.3 in South America, J.2.2 or J.2.4 in Africa and Asia.  

Post-infection ferret antisera raised against cell culture-propagated A/District of Columbia/27/2023-like and egg-propagated A/Croatia/10136RV/2023-like (clade 2a.3a.1, subclade J.2) viruses, representing the A(H3N2) component for the NH 2025-2026 influenza vaccines, showed poor recognition with recently circulating subclade J.2.3 (e.g., A/Netherlands/10685/2024), J.2.4 (e.g., A/Sydney/1359/2024) and K (e.g., A/Darwin/1415/2025) viruses. 

Ferret antisera raised against reference viruses from J.2.3 subclades showed good recognition of viruses expressing HA from J.2.3, but poor recognition of other subclades.  

Post-infection ferret antisera raised against cell culture-propagated A/Sydney/1359/2024-like and eggpropagated A/Singapore/GP20238/2024-like J.2.4 viruses, representing SH 2026 influenza vaccines, recognized most J.2.4 viruses and many subclade K viruses well. 

However, subclade K viruses and J.2.4 viruses with HA substitutions F79V, S144N (addition of a potential N-glycosylation site), N158D, I160K, T328A were better recognized by post-infection ferret antisera raised against cell culture-propagated A/Darwin/1415/2025-like and egg-propagated A/Darwin/1454/2025-like (subclade K) viruses. 

Human serology studies were conducted using the serum panels as described above by HI and virus neutralization (VN) assays with recent circulating A(H3N2) viruses with HA genes from subclades J.2, J.2.2, J.2.3, J.2.4, J.2.5 and K. 

When compared to titres against cell-propagated A/District of Columbia/27/2023-like vaccine reference viruses, post-vaccination HI GMTs or VN GMTs against many of the recent viruses in all subclades tested were significantly reduced in many serum panels.  

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Of 4 458 influenza A(H3N2) viruses examined by genetic and/or phenotypic analyses, two viruses showed evidence of reduced susceptibility to NAIs; both had an NA E119V substitution. 

Of 4 828 A(H3N2) viruses examined by genetic and/or phenotypic analyses, nine viruses showed evidence of reduced susceptibility to the endonuclease inhibitor baloxavir marboxil: three had a PA I38T substitution, three had a PA I38I/T substitution, two had a PA I38I/M substitution and one had a PA E199E/G substitution.  

Influenza B viruses  

Since September 2025, influenza B viruses were detected in all WHO regions, and all those characterized belonged to the B/Victoria lineage. 

There have been no confirmed detections of circulating B/Yamagata lineage viruses after March 2020.  

All HA genes of B/Victoria lineage viruses characterized during this reporting period belonged to clade 3a.2 with HA substitutions A127T, P144L, and K203R. 

Viruses with clade 3a.2 HA genes have diversified further, forming several subclades (C.1-C.5)7. 

Viruses designated as C.5, C.5.1, C.5.6, C.5.6.1 and C.5.7, all of which had the HA substitution D197E, circulated at varying proportions in different regions. 

Viruses designated as C.3 have HA substitutions E128K, A154E and S208P. 

Subclade C.3.1 viruses shared additional mutations D197N (addition of a potential N-glycosylation site) and P208S. 

Recent C.3 viruses which had additional changes D197N (addition of a potential N-glycosylation site), S255P and I267V and C.3.1 viruses have been detected in increasing proportions in Eastern Asia and North America in recent weeks. 

Antigenic analysis showed that post-infection ferret antisera raised against B/Austria/1359417/2021-like viruses (3a.2), representing the vaccine viruses for the SH 2026 and NH 2025-2026 influenza seasons, recognized viruses within the C.5.1, C.5.6, C.5.6.1 and C.5.7 subclades well. 

C.3 and C.3.1 subclade viruses with the HA substitution D197N were recognized poorly. 

Post-infection ferret antisera raised against cell culture-propagated viruses from subclade C.3.1 (e.g., B/Pennsylvania/14/2025) recognized recently circulating viruses from C.3, C.3.1 and other 3a.2 subclades well. 

All available egg isolates for subclade C.3 and C.3.1 viruses acquired substitutions that remove the potential N-glycosylation site at HA 197 to 199. 

Post-infection ferret antisera raised against egg-propagated viruses from subclade C.3.1 (e.g., B/Tokyo/EIS13-175/2025, B/Tokyo/EIS13-011/2025, B/Perth/115/2025) showed reduced recognition of recently circulating viruses from C.3 and C.3.1 subclades compared to that of the cell equivalent.  

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In human serology studies, recently circulating B/Victoria lineage viruses with HA genes from clade 3a.2 subclades C.3, C.3.1, C.5.1, C.5.6, C.5.6.1 and C.5.7 were tested using the serum panels described above. 

When compared to titres against egg- or cell culture-propagated B/Austria/1359417/2021-like vaccine reference virus, titres against most viruses with HA genes from C.5.1, C.5.6, C.5.6.1 and C.5.7 subclades were not significantly reduced; however, titres against viruses with HA genes from C.3 and C.3.1 were significantly reduced in most serum panels. Serology studies were not performed for B/Yamagata lineage viruses.  

Of 549 influenza B/Victoria lineage viruses examined by genetic and/or phenotypic analyses, two showed evidence of reduced or highly reduced susceptibility to NAIs, both with an NA M464T substitution. 

Of 760 B/Victoria lineage viruses examined by genetic and/or phenotypic analyses, no viruses showed evidence of reduced susceptibility to the endonuclease inhibitor baloxavir marboxil.  

Recommended composition of influenza virus vaccines for use in the 2026-2027 northern hemisphere influenza season  

Since September 2025, A(H1N1)pdm09 viruses circulated globally. The majority of viruses had HA genes belonging to the 5a.2a.1 clade which has further diversified into the D.3.1 and D.3.1.1 subclades. 

Postinfection ferret antisera raised against the northern hemisphere (NH) 2025-2026 A(H1N1)pdm09 vaccine viruses (cell culture-propagated A/Wisconsin/67/2022 and egg-propagated A/Victoria/4897/2022) and the southern hemisphere (SH) 2026 A(H1N1)pdm09 vaccine viruses A/Missouri/11/2025 recognized D.3.1 and D.3.1.1 viruses well. 

In human serology studies, post-vaccination geometric mean titres (GMTs) were significantly reduced for some recently circulating A(H1N1)pdm09 viruses when compared to the responses to cell culture-propagated A/Wisconsin/67/2022 A(H1N1)pdm09-like vaccine reference viruses. 

Since September 2025, A(H3N2) viruses circulated and predominated globally. 

The vast majority of A(H3N2) viruses collected had HA genes from subclades of J.2 and have continued to diversify with subclade K (previously designated as J.2.4.1) viruses predominating in most regions. 

Post-infection ferret antisera raised against NH 2025-2026 influenza season vaccine viruses (cell culture-propagated A/District of Columbia/27/2023 and egg-propagated A/Croatia/10136RV/2023) recognized some J.2 viruses well but showed poor recognition of viruses from subclades J.2.3, J.2.4 and K. 

Post-infection ferret antisera raised against subclade K viruses (cell culture-propagated A/Darwin/1415/2025 and egg-propagated A/Darwin/1454/2025) showed improved recognition of K viruses compared to post-infection antisera raised against NH 2025-2026 and SH 2026 A(H3N2) vaccine viruses. 

When compared to titres against cell culture-propagated A/District of Columbia/27/2023-like vaccine reference viruses, human post-vaccination haemagglutinin inhibition (HI) GMTs or virus neutralisation (VN) GMTs against many of the recent viruses in J.2.3, J.2.4 and K subclades were significantly reduced. 

Since September 2025, influenza B virus detections remained low globally, although some countries had increased detections in recent weeks. All circulating influenza B viruses characterized belonged to the B/Victoria lineage, and had HA genes belonging to clade 3a.2 with substitutions A127T, P144L and K203R. 

Post-infection ferret antisera raised against B/Austria/1359417/2021-like viruses (3a.2), representing the vaccine viruses for the SH 2026 and NH 2025-2026 influenza seasons, recognized viruses within the C.5.1, C.5.6, C.5.6.1 and C.5.7 subclades well. C.3 and C.3.1 subclade viruses with HA substitution D197N were recognized poorly. 

Post-infection ferret antisera raised against cell culture-propagated viruses from subclade C.3.1 (e.g., B/Pennsylvania/14/2025) recognized recently circulating viruses from C.3, C.3.1 and other 3a.2 subclades well. All available egg isolates for subclade C.3 and C.3.1 viruses (e.g., B/Tokyo/EIS13-175/2025) acquired egg-adaptive mutations that remove the potential N-glycosylation site at HA 197 to 199, leading to post-infection ferret antisera raised against egg-propagated viruses from subclade C.3.1 (e.g., B/Tokyo/EIS13-175/2025) showing reduced recognition of recently circulating viruses from C.3 and C.3.1 subclades compared to that of the cell equivalent. 

Human serology assays showed that post-vaccination titres against most recent B/Victoria lineage viruses with HA genes from subclades C.5.1, C.5.6, C.5.6.1 and C.5.7 were not significantly reduced when compared to titres against egg- or cell culturepropagated B/Austria/1359417/2021-like vaccine reference viruses. Titres against viruses with HA genes from subclade C.3 and C.3.1 were significantly reduced in most serum panels.  

For vaccines for use in the 2026-2027 northern hemisphere influenza season, WHO recommends the following:  

Egg-based vaccines  

• an A/Missouri/11/2025 (H1N1)pdm09-like virus;  

• an A/Darwin/1454/2025 (H3N2)-like virus; and  

• a B/Tokyo/EIS13-175/2025 (B/Victoria lineage)-like virus.  

Cell culture-, recombinant protein- or nucleic acid-based vaccines  

• an A/Missouri/11/2025 (H1N1)pdm09-like virus;  

• an A/Darwin/1415/2025 (H3N2)-like virus; and  

• a B/Pennsylvania/14/2025 (B/Victoria lineage)-like virus.  

Lists of prototype viruses for egg-, cell culture-, recombinant protein- and nucleic acid-based vaccines together with candidate vaccine viruses (CVVs) suitable for the development and production of human influenza vaccines are available on the WHO website {8}. 

A list of reagents for vaccine standardization, including those for this recommendation, can also be found on the WHO website.  

CVVs and reagents for use in the laboratory standardization of inactivated vaccines may be obtained from:  

• Therapeutic Goods Administration, P.O. Box 100, Woden, ACT, 2606, Australia (email: influenza.reagents@health.gov.au; website: http://www.tga.gov.au).  

• Medicines and Healthcare products Regulatory Agency (MHRA), Blanche Lane, South Mimms, Potters Bar, Hertfordshire, EN6 3QG, the United Kingdom of Great Britain and Northern Ireland  • (email: enquiries@mhra.gov.uk; website: http://www.nibsc.org/science_and_research/virology/influenza_resource_.aspx). 

• Division of Biological Standards and Quality Control, Center for Biologics Evaluation and Research, Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, Maryland, 20993, the United States of America (email: cbershippingrequests@fda.hhs.gov).  

• Research Centre for Influenza and Respiratory Viruses, National Institute of Infectious Diseases, 4-7-1 Gakuen, Musashi-Murayama, Tokyo 208-0011, Japan (email: flu-vaccine@nih.go.jp).  

Requests for reference viruses should be addressed to:  

• WHO Collaborating Centre for Reference and Research on Influenza, VIDRL, Peter Doherty Institute, 792 Elizabeth Street, Melbourne, Victoria 3000, Australia (email: whoflu@influenzacentre.org; website: http://www.influenzacentre.org).  

• WHO Collaborating Centre for Reference and Research on Influenza, National Institute of Infectious Diseases, Japan Institute for Health Security 4-7-1 Gakuen, Musashi-Murayama, Tokyo 208-0011, Japan (email: whocc-flu@nih.go.jp).  

• Influenza Division, Centers for Disease Control and Prevention, 1600 Clifton Road, Mail Stop H17-5, Atlanta, GA 30329, the United States of America (email: InfluenzaVirusSurvei@cdc.gov; website: http://www.cdc.gov/flu/).  

- WHO Collaborating Centre for Reference and Research on Influenza, The Francis Crick Institute, 1 Midland Road, London NW1 1AT, the United Kingdom of Great Britain and Northern Ireland (Tel: +44 203 796 1520 or +44 203 796 2444, email: whocc@crick.ac.uk;  • website: http://www.crick.ac.uk/research/worldwideinfluenza-centre).  

• WHO Collaborating Centre for Reference and Research on Influenza, National Institute for Viral Disease Control and Prevention, China CDC, 155 Changbai Road, Changping District, 102206, Beijing, China. (tel: +86 10 5890 0851; email: fluchina@ivdc.chinacdc.cn; website: https://ivdc.chinacdc.cn/cnic/en/).  

WHO provides weekly updates {9} of global influenza activity. Other information about influenza surveillance, risk assessment, preparedness and response can be found on the WHO Global Influenza Programme website {10}.  

Acknowledgements  

The WHO recommendation on vaccine composition is based on the year-round work of the WHO Global Influenza Surveillance and Response System (GISRS). We thank the National Influenza Centres (NICs) of GISRS, and non-GISRS laboratories including the World Organization for Animal Health (WOAH) and the Food and Agriculture Organization of the United Nations (FAO) Network of Expertise on Animal Influenza (OFFLU), who contributed information, clinical specimens, viruses and associated data; WHO Collaborating Centres of GISRS for their in-depth characterization and comprehensive analysis of viruses; University of Cambridge for performing antigenic cartography and phylogenetic analysis; WHO Essential Regulatory Laboratories of GISRS for their complementary virus analyses and contributions from a regulatory perspective; and laboratories involved in the production of high growth/yield reassortants as candidate vaccine viruses. We also acknowledge the GISAID Global Data Science Initiative for the EpiFluTM database and other sequence databases which were used to share gene sequences and associated information; modelling groups for virus fitness forecasting; and the Global Influenza Vaccine Effectiveness (GIVE) Collaboration for sharing estimates of influenza vaccine effectiveness on a confidential basis.  

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{1} Recommendations for influenza vaccine composition: https://www.who.int/teams/global-influenza-programme/vaccines/who-recommendations 

{2} Description of the process of influenza vaccine virus selection and development: http://www.who.int/gb/pip/pdf_files/Fluvaccvirusselection.pdf 

{3} Vaccines in tropics and subtropics: https://www.who.int/teams/global-influenza-programme/vaccines/vaccine-in-tropics-and-subtropics 

{4} Vaccines against influenza WHO position paper – May 2022. Wkly Epidemiol Rec 2022; 97 (19): 185 - 208. Available at: https://iris.who.int/handle/10665/354264 

{5} Real-time tracking of influenza A(H1N1)pdm09 evolution: https://nextstrain.org/seasonal-flu/h1n1pdm/ha/2y?c=subclade 

{6} Real-time tracking of influenza A(H3N2) evolution: https://nextstrain.org/seasonal-flu/h3n2/ha/2y?c=subclade 

{7} Real-time tracking of influenza B/Victoria lineage evolution: https://nextstrain.org/seasonal-flu/vic/ha/2y?c=subclade 

{8} Candidate vaccine viruses: https://www.who.int/teams/global-influenza-programme/vaccines/who-recommendations/candidate-vaccine-viruses 

{9} Current respiratory virus update: https://www.who.int/teams/global-influenza-programme/surveillance-and-monitoring/influenza-updates 

{10} Global Influenza Programme: https://www.who.int/teams/global-influenza-programme 

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Source: 

Link: https://www.who.int/publications/m/item/recommended-composition-of-influenza-virus-vaccines-for-use-in-the-2026-2027-northern-hemisphere-influenza-season

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The #ORF6 accessory #protein contributes to #SARS-CoV-2 #virulence and pathogenicity in the naturally susceptible #feline model of infection

 

ABSTRACT

In this study, the infection dynamics, replication, and pathogenicity of a recombinant virus containing a deletion of ORF6 (rWA1ΔORF6) on the backbone of the highly virulent SARS-CoV-2 WA1 virus (rWA1) were investigated and compared to the parental rWA1 virus. While both rWA1 and rWA1ΔORF6 viruses replicated efficiently in cultured cells, the rWA1ΔORF6 virus produced smaller plaques, suggesting reduced cell-to-cell spread. Luciferase reporter assays revealed immune-suppressing effects of ORF6 on interferon (IFN) and nuclear factor kappa B (NF-κB) signaling pathways. Pathogenesis assessment in cats revealed that animals inoculated with rWA1 were lethargic and presented with fever on days 2 and 4 post-infection (pi), whereas rWA1ΔORF6-inoculated animals developed subclinical infection. Additionally, animals inoculated with rWA1ΔORF6 presented reduced infectious virus shedding in nasal and oral secretions and broncho-alveolar lavage fluid when compared with the rWA1-inoculated cats. Similarly, the rWA1ΔORF6-inoculated cats presented reduced virus replication in the respiratory tract as evidenced by lower viral loads and reduced lung inflammation on days 3 and 5 pi when compared to rWA1-inoculated animals. Host gene transcriptomic analysis revealed distinct differentially expressed gene (DEG) profiles in the nasal turbinate of animals infected with rWA1 when compared to rWA1ΔORF6. Importantly, type I IFN signaling was significantly upregulated in rWA1ΔORF6-infected cats when compared to rWA1-inoculated animals, which could potentially contribute to the reduced replication of rWA1ΔORF6 in the upper and lower respiratory tracts of infected animals. Collectively, these results demonstrate that the SARS-CoV-2 ORF6 is an important virulence determinant of the virus, contributing to the modulation of host antiviral immune responses.

Source: Journal of Virology, https://journals.asm.org/journal/jvi

Link: https://journals.asm.org/doi/full/10.1128/jvi.00644-25?af=R

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#USA, #Wastewater Data for Avian #Influenza #H5 (#CDC, Feb. 27 '26)

 

{Excerpt}

Time Period: February 15, 2026 - February 21, 2026

-- H5 Detection: 4 site(s) (0.8%)

-- No Detection: 495 site(s) (99.2%)

-- No samples in last week: 110 site(s)

(...)

Source: US CDC, https://www.cdc.gov/

Link: https://www.cdc.gov/nwss/rv/wwd-h5.html

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#Bosnia and Herzegovina - High pathogenicity avian #influenza viruses (Inf. with) (#poultry) - Follow up report 1

 

Note 27/02/2026: the number of dead animals in this outbreak was lowered after the country provided additional information.

Source: 

Link: https://wahis.woah.org/#/in-review/7309

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#Sweden - High pathogenicity avian #influenza #H5N1 viruses (Inf. with) (#poultry) - Immediate notification

 

This is a farm with broiler parents, housed in 3 barns. Clinical signs of increased mortality and severely depressed general condition were observed. Euthanization is in progress. A protection zone (3 km) and a surveillance zone (10 km) have been put in place around the infected farm and all other restrictions and necessary measures according to Regulation (EU) 2016/429 and EU DR 2020/687 are applied.

Source: WOAH.

Link: https://wahis.woah.org/#/in-review/7313

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Evolutionary #lineage and #host origin influence #virulence and #mammalian adaptation of #H7N9 avian #influenza viruses

 

Abstract

The H7N9 avian influenza virus (AIV) has posed a major global public health concern since its first detection in China in 2013. Transmitted among wild birds and poultry, this virus has crossed the species barrier to infect humans, causing severe respiratory disease and high mortality. Although the widespread use of H7 vaccines has markedly reduced human infections, the ongoing circulation and adaptive evolution of the virus in poultry remain a serious threat. In this study, we analyzed three highly pathogenic H7N9 isolates collected in China in 2022, representing two hemagglutinin (HA) gene evolutionary lineages: Group.y.2.3 (isolate 229-4, chicken origin; isolate 782-2, quail origin) and Group.y.2.4 (isolate 621, quail origin). Pathogenicity was compared through phylogenetic analysis, molecular characterization, and infection experiments in both avian and mammalian models. Group.y.2.3 isolates displayed stronger replication and pathogenicity in chickens and mice, with isolate 782-2 being the most virulent. The chicken-origin isolate 229-4 caused more severe weight loss and higher viral loads in the lungs of mice, indicating that host origin influences cross-species transmission potential. Molecular analyses revealed that all isolates possessed multiple basic cleavage sites and mutations linked to mammalian adaptation, including HA 186 V. Some isolates also harbored newly acquired glycosylation sites associated with immune evasion. Overall, our findings demonstrate that both genetic lineage and host origin shape the biological characteristics of H7N9 isolates. Group.y.2.3 isolates warrant priority in surveillance, providing critical insights for vaccine updates and risk assessment.

Source: 

Link: https://www.sciencedirect.com/science/article/pii/S0032579126002555?via%3Dihub

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#Zanamivir - #Amantadine Conjugate: A Dual-Action Agent with Broad-Spectrum Synergistic #Antiviral Efficacy

 

Abstract

Influenza A virus is a highly contagious respiratory pathogen, and its rapid and continuous adaptive mutations for immune escape have limited the efficacy of existing vaccines and antiviral drugs. Here, we report a multimechanism anti-influenza platform based on the conjugation of zanamivir (ZMV) with amantadine (Aman). Aman acts as a hydrophobic tag that promotes the degradation of neuraminidase and concurrently enhances the physicochemical properties of ZMV, leading to improved membrane permeability and a significantly prolonged half-life. Meanwhile, the ZMV moiety counteracts Aman-induced cytotoxic autophagy. The resulting conjugate, compound 7j, exhibits potent activity against a wide range of neuraminidase and M2 ion channel mutations. Notably, a single intravenous dose of 7j fully protected mice from a lethal H1N1 challenge. Our work demonstrates that the rational fusion of ZMV and Aman achieves synergistic multimechanistic antiviral activity with enhanced efficacy and safety, offering a new strategy for the development of next-generation anti-influenza drugs.

Source: 

Link: https://pubs.acs.org/doi/10.1021/acs.jmedchem.5c03547

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#Synergy between HA #cleavage site #sequence and NA-mediated #plasminogen recruitment as a virulence mechanism for low-pathogenic avian #influenza

 

ABSTRACT

An outbreak of H3N1 low-pathogenic avian influenza virus (LPAIV) in Belgium in 2019 caused unexpected levels of mortality and morbidity in poultry. These viruses possess an NA polymorphism associated with plasminogen (PLG) binding, as well as an atypical sequence around the HA cleavage site; accordingly, HA cleavage mediated by NA-driven PLG recruitment has been proposed to underlie their systemic spread and pathogenicity. To test this, we established a reverse genetics system for A/chicken/Belgium/460/2019 and created single mutations in HA (K345R) and NA (S122N) that restored the viruses to normal consensus, as well as an HA/NA double mutant. Confirming previous work, trypsin-independent spread and HA cleavage of wild-type Ck/Belgium were observed in the presence of fetal bovine serum containing PLG in vitro. Dose-dependent HA cleavage and trypsin-independent spread were also observed in the presence of purified chicken PLG. Compared to the wild-type virus, both HA cleavage and virus spread in vitro were reduced by the HA K345R mutation and further blocked by the NA mutation S122N. PLG-mediated HA cleavage was seen in a variety of avian cell lines and chicken organoids, excluding cell type-dependent effects. Furthermore, in ovo tests showed that mutant viruses unable to recruit PLG were less able to replicate systemically in chicken embryos. Bioinformatics analyses revealed other viruses that could potentially recruit PLG, including two independent outbreaks of H6N1 viruses, one of which we confirmed PLG-driven spread in vitro. We conclude that PLG recruitment by NA is a general virulence mechanism of N1 LPAIVs.

Source: 

Link: https://journals.asm.org/doi/full/10.1128/mbio.02466-25?af=R

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#Tecovirimat for the Treatment of #Mpox

 

Abstract

Background

Tecovirimat is approved for smallpox treatment under the Food and Drug Administration Animal Rule on the basis of efficacy in nonhuman primate models of mpox (previously known as monkeypox). However, the clinical efficacy of tecovirimat against human clade II mpox is unclear.

Methods

In a phase 3, international, double-blind, randomized, placebo-controlled trial, we evaluated the efficacy of oral tecovirimat in adults with laboratory-confirmed clade II mpox. Participants were randomly assigned in a 2:1 ratio to receive tecovirimat or placebo for 14 days. The primary outcome was clinical resolution, assessed in a time-to-event analysis in participants with active skin or mucosal lesions. Secondary outcomes included reduction in pain, assessed in all participants with laboratory-confirmed mpox and in those with severe pain at baseline (pain score, 7 to 10; scale, 0 [no pain] to 10 [worst pain imaginable]); complete lesion healing (assessed in a time-to-event analysis); viral DNA clearance; and safety.

Results

Of 412 participants who underwent randomization (275 to tecovirimat and 137 to placebo), 344 had laboratory-confirmed mpox, and 336 had active skin or mucosal lesions and were included in the primary analysis. By day 29, the estimated cumulative incidence of clinical resolution was 83% with tecovirimat and 84% with placebo; the competing-risks hazard ratio for clinical resolution was 0.98 (95% confidence interval [CI], 0.74 to 1.31; P=0.89). No substantial between-group differences were seen in pain reduction among participants with severe pain (difference, 0.1 point; 95% CI, −0.8 to 1.0), in complete lesion healing (competing-risks hazard ratio, 0.97; 95% CI, 0.75 to 1.26), or in viral DNA clearance. The incidence of adverse events of grade 3 or higher was similar in the two groups (4% with tecovirimat and 3% with placebo).

Conclusions

This trial showed no evidence that tecovirimat therapy shortened the time to clinical resolution, reduced pain, or increased viral clearance among adults with clade II mpox. (Funded by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health; STOMP/A5418 ClinicalTrials.gov number, NCT05534984.)

Source: 

Link: https://www.nejm.org/doi/full/10.1056/NEJMoa2506495?af=R&rss=currentIssue

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#Wastewater #Surveillance for #SARS-CoV-2 in Rural #Kentucky, 2021–2023

 

Abstract

Wastewater testing for SARS-CoV-2 provided useful public health information during the COVID-19 pandemic yet was underutilized in rural communities. We addressed this gap by implementing wastewater surveillance and assessing its performance in 10 communities in Eastern Kentucky. We collected wastewater samples 1–2 times weekly at 10 wastewater treatment plants (WWTPs) from May 2021 until April 2023 and measured SARS-CoV-2 RNA concentrations using polymerase chain reaction testing. We calculated time-lagged correlations between wastewater concentrations and county-level reported COVID-19 cases by site. We developed a generalized linear model to estimate COVID-19 incidence from wastewater SARS-CoV-2 concentrations. The 10 participating WWTPs served 2430 to 35,575 customers, and 90% were in rural counties. We cumulatively analyzed 818 wastewater samples. Correlations between wastewater SARS-CoV-2 concentrations and COVID-19 cases were significant at seven of the WWTPs and were strongest during the Delta variant period. The incidence density model predicted more COVID-19 cases during the latter study period (May 2022–April 2023) than were officially reported. Wastewater surveillance data in these rural communities corroborated clinical case data and may have more accurately described community disease levels later in the pandemic.

Source: 

Link: https://www.mdpi.com/1999-4915/18/3/282

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Re-infection with #SARS-CoV-2 is associated with increased #antibody breadth and potency against diverse #sarbecovirus strains

 

ABSTRACT

The ease with which emerging SARS-CoV-2 variants escape neutralizing antibodies limits the protection afforded by a prior exposure, be it infection or vaccination. While rare, broadly neutralizing antibodies with activity toward diverse sarbecoviruses have been detected in convalescent serum. Motivated by findings that plasma responses show increased neutralization breadth and potency with continued antigen exposure, we isolated monoclonal antibodies (mAbs) after a SARS-CoV-2 re-infection and compared them to those isolated 1 year prior, after the first breakthrough infection. Among clonal lineage members identified at both time points, mAbs from the later time point showed improved neutralization potency and breadth. One mAb isolated after re-infection, C68.490, targets a conserved region in the receptor binding domain and shows remarkable activity not only against SARS-CoV-2 variants, but also diverse sarbecoviruses from more distant clades present in animal reservoirs. These findings suggest that a focus on individuals with diverse and repeated antigen exposure could lead to the identification of antibodies with therapeutic utility not just toward current and future SARS-CoV-2 variants, but also distant sarbecoviruses in the event of a future spillover.

Source: 

Link: https://journals.asm.org/doi/full/10.1128/mbio.03612-25?af=R

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#Mpox Multi-country external #situation #report no. 63, published 24 February 2026 (#WHO, summary)

 

Highlights   

• Transmission of mpox continues in sexual networks, affecting both women and men, and in some historically endemic areas. 

- All clades of monkeypox virus (MPXV) continue to circulate. 

- Unless mpox outbreaks are rapidly contained and human-to-human transmission is interrupted, there is a risk of sustained community transmission. 

• In January 2026, 50 countries across all WHO regions reported a total of 1334 new confirmed mpox cases, including three deaths (case fatality ratio [CFR] 0.2%). 

- Of these cases, 66% were reported in the African Region. 

• Four regions observed a decline in confirmed cases in January, compared to December 2025, while the European Region reported an increase in confirmed cases.

• Twenty countries in Africa reported active transmission of mpox in the last six weeks (5 January – 15 February 2026), with 1142 confirmed cases, including four deaths (CFR 0.4%). 

- Countries reporting the highest number of cases in this period are the Democratic Republic of the Congo, Guinea, Madagascar, Liberia and Ghana. 

• One country, Comoros, and one territory, La Réunion (Overseas Department of France), have reported mpox due to clade Ib MPXV for the first time.   

• Outside Africa, reports of community transmission of clade Ib MPXV continue in France, Portugal and Spain, including in sexual networks of men who have sex with men.  

• WHO conducted a global mpox rapid risk assessment in February 2026; the overall global public health risk associated with the mpox multi-country outbreak was assessed as moderate. 

• India has reported a case of mpox with the clade Ib /IIb recombinant MPXV. 

- The strain sequenced is closely related to the first clade Ib / IIb recombinant strain reported by the United Kingdom of Great Britain and Northern Ireland in December 2025. 

- As both cases are travel-related, these case reports suggest wider transmission of the recombinant strain, implicating four countries in three WHO regions. 

(...)

Source: 

Link: https://www.who.int/publications/m/item/multi-country-outbreak-of-mpox--external-situation-report--63---24-february-2026

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#Argentina - #Influenza A #H5 viruses of high pathogenicity (Inf. with) (non-poultry including wild birds) (2017-) - Immediate notification

 

{A Coscoroba Swan. By Charles J. Sharp - Own work, from Sharp Photography, sharpphotography.co.uk, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=179069673}

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{A Black-Necked Swan. By Charles J. Sharp - Own work, from Sharp Photography, sharpphotography.co.uk, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=178158764}

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{A Fulvous Whistling Duck. By JeffreyGammon - Own work, CC BY 4.0, https://commons.wikimedia.org/w/index.php?curid=158156460}

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{A Brown-Hooded Gull. By Charles J. Sharp - Own work, from Sharp Photography, sharpphotography.co.uk, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=179073441}

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Contact with wild migratory birds present in the area is presumed to be the likely source of infection. Virological analysis has identified the presence of the H5 subtype of high pathogenicity avian influenza (HPAI). The determination of the neuraminidase subtype is pending in order to complete the characterisation of the pathogenic agent. Further information is provided in the epidemiological comments of the outbreak.

Source: 

Link: https://wahis.woah.org/#/in-review/7291

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#Argentina - High pathogenicity avian #influenza #H5 viruses (Inf. with) (#poultry) - Immediate notification

 

At a heavy breeding poultry farm located in the province of Buenos Aires, an increase in mortality and the presence of clinical signs consistent with high pathogenicity avian influenza (HPAI) were observed. Given the clinical suspicion, official intervention was carried out, including a health inspection and the collection of diagnostic samples for processing. Laboratory analyses confirmed a positive result for high pathogenicity avian influenza subtype H5 (HPAI H5).

The event occured on a farm raising heavy breeding stock. On 21/02/2026, the National Service of Agri-Food Health and Quality (SENASA) received a notification concerning mortality and clinical signs consistent with high pathogenicity avian influenza (HPAI) which began on 19/02/2026, as reported by the reporting person. On 22/02/2026, the suspicion was officially addressed with the restriction of the establishment and taking of samples for official diagnosis. On 23/02/2026, the samples tested positive for HPAI H5. All the birds on the establishment will be culled. We will update the population data in subsequent follow-up reports.

Source: 

Link: https://wahis.woah.org/#/in-review/7290

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#Report on #influenza viruses received and tested by the #Melbourne #WHO CC for #Reference and Research on #Influenza during 2024

 

Abstract

As part of its role in the World Health Organization (WHO) Global Influenza Surveillance and Response System (GISRS), the WHO Collaborating Centre for Reference and Research on Influenza in Melbourne received 12,180 human influenza-positive samples during 2024. Viruses were analysed for their antigenic, genetic, and antiviral susceptibility properties. Selected viruses were propagated in qualified cells or embryonated hens’ eggs for potential use in seasonal influenza virus vaccines. During 2024, influenza A(H1N1)pdm09 and A(H3N2) viruses predominated, accounting for 33% and 42%, respectively, of all viruses received, compared to 5% for influenza B/Victoria. Of note, one influenza A(H5N1) virus was also received in 2024. The majority of A(H1N1)pdm09 (98%), A(H3N2) (88%) and influenza B (100%) viruses analysed at the Centre were found to be antigenically and genetically similar to the respective WHO recommended vaccine strains for the Southern Hemisphere in 2024. Of 4,007 samples tested for susceptibility to the neuraminidase inhibitors oseltamivir and zanamivir, twelve A(H1N1)pdm09 viruses and one B/Victoria virus showed highly reduced inhibition against oseltamivir or zanamivir. Of 3,294 total samples sequenced for baloxavir susceptibility, 18 of the 1,825 A(H3N2) samples were identified with genetic evidence of reduced susceptibility to baloxavir marboxil in the PA gene.

Source: 

Link: https://ojs.cdi.cdc.gov.au/index.php/cdi/article/view/3449

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Longitudinal #assessment of functional #antibodies to a novel #influenza virus strain across age groups

 

Abstract

Newly emerging influenza virus strains pose a constant threat as they encounter a population lacking neutralizing antibodies against the new strain. However, cross-reactive non-neutralizing antibodies (nnABs) may be present and assist in mitigating disease symptoms via various effector mechanisms, including antibody-dependent cellular cytotoxicity (ADCC). Although nnABs to influenza virus have received more attention lately, little information is available on their age-related prevalence, steady-state levels, functional properties, and changes in these parameters over time. Using longitudinal samples from adolescents, adults, and older adults, collected before and after the 2009 swine flu pandemic, we comprehensively characterized the specificity and functionality of nnAB responses against H1N1 pandemic 2009 (H1N1pdm09) virus. Remarkably, all participants exhibited cross-reactive antibodies to this virus before having encountered it through infection or vaccination, with the highest baseline levels observed in older adults. The levels of these IgG antibodies showed a strong correlation with engagement of fragment crystallizable γ receptor IIIa (FcγRIIIa) and ADCC activity, both of which were notably lower in adolescents compared to adults and older adults. Without infection or vaccination, average amounts of H1N1pdm09-reactive antibodies remained relatively stable on population level over the 5-year study period. However, on an individual level, substantial increases and decreases occurred. H1N1pdm09 infection or vaccination significantly enhanced specific antibody levels and the FcγRIIIa-engaging capacity of these antibodies in all age groups. ADCC-mediating antibodies increased however only in adolescents, reaching the same level as observed in the adult groups. Taken together, our results demonstrate the presence of cross-reactive, non-neutralizing, functional, and boostable antibodies against a never-encountered influenza virus strain across all age groups. These antibodies can potentially contribute to protection from severe disease. Accordingly, in case of a newly emerging virus, their further enhancement by vaccination could be beneficial as an immediate protective measure before a strain-specific vaccine becomes available.

Competing Interest Statement

The authors have declared no competing interest.

Funding Statement

This study did not receive any funding

Source: 

Link: https://www.medrxiv.org/content/10.64898/2026.02.21.26346781v1

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Evaluating #primer and #probe #mismatch tolerance in an #Influenza A #matrix gene RT #qPCR using contemporary human and zoonotic strains

 

Abstract

Background: 

Genetic drift and host-associated adaptation in influenza A viruses threaten the long-term reliability of RT-qPCR-based diagnostics, particularly when nucleotide mismatches arise within primer and probe binding regions. Conventional assay evaluations often emphasize sequence conservation but rarely assess functional mismatch tolerance across divergent subtypes and hosts. 

Methods: 

We performed an in silico evaluation of a matrix (M) gene–targeted RT-qPCR assay by aligning primer and probe binding regions against 22 H1N1 isolates and representative H3N2 and H5N1 reference strains, including recent zoonotic isolates from avian and bovine hosts. Nucleotide mismatches were identified, quantified, and mapped relative to assay components and oligonucleotide termini. Mismatch burden was summarized by subtype and assay region. 

Results: 

H1N1 isolates exhibited complete conservation across primer and probe regions. In contrast, H3N2 and H5N1 strains demonstrated subtype-specific sequence variability, with a total of eleven mismatches identified across seven non-H1N1 isolates (mean mismatch per isolate = 2.43). Probe mismatches predominated (63.6%), occurring primarily at internal positions, while primer mismatches were infrequent and largely avoided 3′ terminal nucleotides. Recent H5N1 isolates (2023–2024) shared conserved internal mismatches in the probe and forward primer, whereas a historical H5N1 isolate (2016) exhibited a distinct profile including a terminal probe mismatch. Despite this variability, mismatch patterns were consistent with preserved amplification potential. 

Conclusion: 

This study demonstrates that the evaluated influenza A M gene RT-qPCR assay exhibits inherent mismatch tolerance across human and zoonotic subtypes. By shifting diagnostic evaluation from strict sequence identity to functional resilience, our findings provide a framework for designing and maintaining robust molecular assays suitable for surveillance and pandemic preparedness amid ongoing viral evolution.

Source: 

Link: https://www.biorxiv.org/content/10.64898/2026.02.23.707407v1

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