Influenza

Globally, influenza detections remained low in week 40 with influenza A virus detections predominant.

In the northern hemisphere, influenza percent positivity was elevated (above 10%) in some countries in Central America and the Caribbean, Western Africa, Western, Southern, South-East and Eastern Asia. Percent positivity was over 30% in some countries in Southern and South-East Asia and in single countries in Western and Eastern Africa and Western Asia. Increases in activity were observed in some countries in Central America and the Caribbean, Western, Southern and South-East Asia and in single countries in Eastern Africa and Northern Europe.

In the southern hemisphere, influenza percent positivity was elevated (above 10%) in some countries in Tropical South America and in single countries in Temperate South America and Eastern Africa. Percent positivity was over 30% in a single country in Oceania. Increases in activity were reported in single countries in Tropical South America and Eastern Africa.

In the zones with elevated positivity, influenza A(H1N1)pdm09 was predominant in Eastern Africa, Western, Southern and South-East Asia and Oceania and influenza B was predominant in Central America and the Caribbean, Tropical and Temperate South America. Influenza A and B were codominant in Western Africa and influenza A(H1N1)pdm09 and influenza A(H3N2) were codominant in Eastern Asia.

SARS-CoV-2

Globally, SARS-CoV-2 positivity remained stable and low across most reporting countries, with elevated positivity (above 10%) reported in some countries in Central America and the Caribbean, South West and Northern Europe, and in single countries in Northern Africa, South-East and Eastern Asia. Increases in activity were observed in two countries in South West Europe and in single countries in Northern and Eastern Africa and Western Asia.

Respiratory syncytial virus (RSV)

RSV positivity was elevated (above10%) in a few countries in Central America and the Caribbean and Temperate South America and in single countries in Western Africa and Southern Asia. Small increases in activity were observed in single countries in Central America and the Caribbean and Tropical South America. RSV and influenza activity were both elevated in countries in Central America and the Caribbean, Temperate South America, Western Africa and Southern Asia.

Severity assessment

The severity assessments here are reported from countries, areas and territories. Assessments for transmissibility can be reported based on syndromic parameters and/or influenza-specific parameters. In the northern hemisphere temperate and subtropical areas, influenza-specific transmissibility was reported as below seasonal threshold in 15 countries, low in a single country and moderate in a single country; transmissibility using syndromic data was reported as below seasonal threshold in nine countries and low in two countries. In the southern hemisphere temperate and subtropical areas, influenza-specific transmissibility was reported as below seasonal threshold in a single country and low in a single country; transmissibility using syndromic data was reported as below seasonal threshold in a single country. Influenza-specific transmissibility was reported as below seasonal threshold in a single country in the tropical areas.

Current update: Global Respiratory Virus Activity: Weekly Update No. 599

All past updates: Global respiratory virus updates

Transmission remains geographically extensive. In epidemiological week 41, 44 health zones across five provinces reported confirmed cases: 19 in Ituri, 15 in North Kivu, four in Haut Uele, four in Tshopo, and two in Bas-Uele. This is an increase from 37 to 39 health zones reporting cases in each of the preceding three epidemiological weeks.

Further, provincial trends remain heterogeneous. North Kivu reported 182 confirmed cases in epidemiological week 41, 39% of all cases reported nationally. This was similar to week 40 (188 cases) but an increase compared to epidemiological weeks 38 and 39 (144 and 116 cases). Beni health zone has been the main driver in North Kivu: it reported 65 cases in epidemiological week 41, and its weekly count has increased steadily over the past month, from 38 cases in epidemiological week 36.

Figure 2: Weekly confirmed BVD cases in Beni health zone, North Kivu

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Figure 2: Weekly confirmed BVD cases in Beni health zone, North Kivu

In Ituri province, weekly incidence fell from a peak of 496 cases in mid-August and has remained consistent at about 235-290 cases per week for the past four complete epidemiological weeks. Within this plateau, the distribution of cases has shifted. Earlier hotspots such as Mangala and Komanda have declined. Mandima health zone, however, has rapidly emerged as the largest focus of transmission. It reported 199 confirmed cases in the past three complete epidemiological weeks (weeks 39–41), compared with 12 in epidemiological week 38, and had the most new cases of any health zone in epidemiological week 41. (Figure 3)

Figure 3: Weekly confirmed BVD cases in Mandima Health Zone, Ituri

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Figure 3: Weekly confirmed BVD cases in Mandima Health Zone, Ituri

Transmission also persists outside the main provinces. Tshopo reported nine confirmed cases in epidemiological week 41, its highest weekly case count since epidemiological week 38, mainly from the health zones Makiso-Kisangani and Mangobo. On 12 October, Bafwasende also reported new confirmed cases after approximately one month with no confirmed cases reported. Haut-Uele has reported 24 cases per week for the past three epidemiological weeks (weeks 39–41), mainly from Wamba and Pawa.

Several operational indicators further support a cautious interpretation of recent trends. Deaths continued to occur predominantly in communities rather than Ebola treatment centres: community deaths made up 67% of confirmed deaths in epidemiological week 41 and between 61% and 75% in each of the past six epidemiological weeks (weeks 36–41), with no sustained improvement (Figure 4).

A review of a limited number of case narratives indicated that many affected people had sought some form of care but had not entered the appropriate referral pathway. This suggests that delayed recognition and referral, rather than an absence of care-seeking alone, may be contributing to community deaths. Weak referral pathways and delayed identification continue to drive mortality and transmission.

Figure 4: Proportion of community BVD deaths that occured in the community

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Figure 4: Proportion of community BVD deaths that occured in the community

Contact tracing performance also remained suboptimal. Although the number of contacts under follow-up had increased, a median of 8.5 were registered during the most recent two weeks. The proportion of new cases occurring among known contacts remained low, at approximately 10%, with only limited signs of recent improvement. These findings indicate that many transmission chains may still be detected retrospectively rather than through prospective surveillance and contact follow-up. Testing volume has increased over time while positivity has declined, but these positive developments should be considered alongside continuing geographic impact and weaknesses in early case identification.

Surveillance has strengthened in other respects. Weekly alerts have roughly doubled since early August, from about 9000 per week in epidemiological weeks 31–32 to about 18 400 in epidemiological week 41, and more than 99% were investigated. Test positivity declined from 22–23% in weeks 31–33 to 15% in week 41, while testing volume remained broadly stable at about 2600–3500 samples per week.

Updated modelling by the Institut National de Santé Publique (INSP) and the Institut National de Recherche Biomédicale (INRB), using data as of 12 October, estimated the risk of expansion to health zones in the Democratic Republic of the Congo which are not yet affected during the week of 13-19 October. The highest estimated probability remained in Rethy health zone, Ituri province (14%; 95% CrI 10–19%), followed by Yakusu in Tshopo (8%; 5–12%), Watsa in Haut-Uele (7%; 5–9%) and Poko in Bas-Uele (7%; 5–10%). Jiba (6%; 5–9%) and Linga (5%; 4–7%) in Ituri, and Niangara in Haut-Uele (4%; 3–6%), completed the seven health zones with the highest estimated probability.¹ Compared with the September estimates, the zones at highest risk have shifted west and north, towards Tshopo around Kisangani and further into Bas-Uele and Haut-Uele.

The outbreak also presents a continuing risk of cross-border spread. Uganda and South Sudan have been identified as the principal destinations at risk of case exportation. Detection of transmission in the province of Sud-Ubangi increased concerns regarding possible spread towards the Central African Republic. However, the confirmation of cases in Kenya shows that exportation can also occur beyond neighbouring countries. On 6 October, Kenya reported an imported case of Bundibugyo virus disease, a Kenyan national living in the Democratic Republic of the Congo who died on 5 October. A second case, a close family member of the first case and who was already under quarantine, was reported by the Kenyan Ministry of Health on 14 October.

In summary, recent epidemiological signals should be interpreted with caution: the coexistence of localized increases, community deaths, delayed identification, incomplete epidemiological linkage and expansion into new areas means that an apparent plateau may not represent sustained interruption of transmission. Priorities include strengthening alert investigation, contact identification and follow-up, referral from community and primary-care services, and preparedness in neighbouring countries. Consistent public communication is important to recognize progress without creating premature confidence that the outbreak has been brought under control.

Seasonal influenza activity

From February through August 2026, influenza activity was reported in all transmission zones. Overall detections were lower compared to the same reporting period in 2025. During the reporting period, influenza A viruses predominated in most transmission zones, apart from Northern and Western Africa, North America and Eastern Asia where influenza B viruses predominated.

In Africa, influenza activity varied by transmission zone. In Northern Africa, influenza detections decreased from February and remained low during the reporting period, and influenza B viruses predominated throughout the reporting period. In Western Africa, influenza detections increased in July; influenza B viruses predominated until August when influenza A(H3N2) viruses increased and predominated. In Middle Africa, influenza detections were low throughout the reporting period with an increase in influenza A detections from July; influenza A(H3N2) viruses predominated for most of the period except in August when detections of A(H1N1)pdm09 viruses increased. In Eastern Africa, influenza detections peaked in May; influenza A viruses predominated with cocirculation of A(H1N1)pdm09 and A(H3N2) viruses throughout the reporting period. In Southern Africa, influenza detections peaked in June; influenza A viruses predominated with mostly A(H1N1)pdm09 viruses detected until April when A(H3N2) viruses predominated. 

In the Americas, influenza activity varied by transmission zone. In North America, influenza detections decreased from late February and remained low for the rest of the reporting period; influenza A virus detections predominated until mid-February and influenza B virus detections predominated from March to June. In Central America and the Caribbean, influenza virus detections decreased early in the reporting period and remained low; influenza A(H3N2) viruses accounted for the majority of detections. In Tropical South America, influenza virus detections increased in February and remained elevated until August; influenza A(H3N2) virus detections predominated until mid-June then decreased, and influenza B viruses predominated until the end of the reporting period. In Temperate South America, influenza activity increased in April, peaked in June and decreased for the remainder of the reporting period; influenza A(H3N2) viruses predominated among subtyped viruses through mid-July. Influenza B virus detections increased in June and predominated from mid-July.

In Asia, influenza activity varied by transmission zone. In Central Asia, influenza detections were very low throughout the reporting period. Most influenza detections were reported from Eastern Asia where influenza detections remained elevated throughout the reporting period; influenza A activity due to predominantly A(H3N2) viruses decreased from February to May then increased in June and A(H1N1)pdm09 virus detections increased at the end of the reporting period. Influenza B viruses remained elevated throughout the reporting period with a peak in March. In South-East Asia, influenza activity was detected throughout the reporting period and increased from May. Influenza B virus detections predominated until May; influenza A(H3N2) viruses accounted for the majority of influenza detections from May until August, and A(H1N1)pdm09 viruses predominated at the end of the reporting period. In Southern Asia, influenza detections increased throughout the reporting period; influenza A(H3N2) viruses accounted for the majority of detections until July when A(H1N1)pdm09 detections increased and predominated for the remainder of the reporting period. In Western Asia, influenza detections decreased from February and remained low until June, with predominantly A(H1N1)pdm09 virus detections reported from July. 

In Europe, influenza activity decreased early in the reporting period and remained low throughout this period in all transmission zones. Influenza A viruses predominated with very low detections of influenza B viruses; among subtyped influenza A viruses, A(H3N2) detections were higher in all transmission zones. 

In Oceania, influenza activity increased from June and remained elevated throughout the reporting period; influenza A viruses predominated with higher detections of A(H3N2) viruses among subtyped viruses. Influenza B virus detections were very low throughout the reporting period. 

Influenza A

Globally, influenza A virus detections outnumbered influenza B detections in most transmission zones during the start of the reporting period. Influenza A viruses predominated throughout most of the reporting period in Eastern and Southern Africa; Central America and The Caribbean; Temperate South America; South-East, Southern, and Western Asia; Europe and Oceania Melanesia and Polynesia. Influenza A viruses predominated until mid-June in Tropical South America and from mid-July in Eastern Asia. Among the subtyped influenza A viruses, A(H3N2) viruses predominated throughout the reporting period in most transmission zones; in South-East, Southern and Western Asia, influenza A(H1N1)pdm09 virus detections increased and predominated towards the end of the reporting period. The overall number of influenza detections was very low in Middle Africa and Central Asia.

Figure 5: Distribution of influenza virus types and subtypes by influenza transmission zone, 1 February -- 13 September 2026

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Figure 5: Distribution of influenza virus types and subtypes by influenza transmission zone, 1 February -- 13 September 2026

Influenza B

Influenza B virus detections predominated throughout most of the reporting period in Northern and Western Africa and North America, and through June in Eastern Asia, and from July in Tropical South America and August in Temperate South America. All influenza B viruses where lineage was confirmed belonged to the B/Victoria lineage.

Detailed information by country of the extent of seasonal influenza activity and type/subtype of viruses worldwide is available on the WHO website: https://www.who.int/tools/flunet. Detailed information on zoonotic influenza activity, including the genetic and antigenic characteristics of zoonotic influenza viruses, is available on the WHO website: https://www.who.int/teams/global-influenza-programme/vaccines/who-recommendations.

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

Influenza A(H1N1)pdm09 viruses 

Since February 2026, A(H1N1)pdm09 viruses circulated globally but did not predominate in any regions except for Western Asia. The haemagglutinin (HA) genes of viruses that were genetically characterized belonged to subclades D.3.1, D.3.1.1, C.1.9 and C.1.9.3.⁵ Viruses from subclade D.3.1.1 predominated worldwide, with cocirculation of subclade D.3.1 and very small proportions of subclades C.1.9 and C.1.9.3 being detected in a few countries in the Region of the Americas, the Eastern Mediterranean Region and the Africa Region.

During this reporting period, the majority of A(H1N1)pdm09 viruses sequenced globally belonged to subclade D.3.1.1, characterized by R113K, A139D, E283K and K302E. Genetic diversity of the HA in subclade D.3.1.1 viruses increased during this reporting period. Emerging viruses within subclade D.3.1.1 with an additional substitution of G155E increased in recent weeks and belonged to several genetic groups characterized by different combinations of additional amino acid substitutions. Viruses from subclade D.3.1 with substitutions T120A, I372V, I460T and V520A still predominated in South Africa and circulated in minor proportions in some countries in Central America, Africa, Asia and Oceania.

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 February 2026 showed that post-infection ferret antisera raised against viruses from subclade D.3.1 (e.g., A/Missouri/11/2025) recognized most recently circulating viruses well. However, post-infection ferret antisera raised against viruses from subclades C.1.9.3, D.3.1 and D.3.1.1 showed reductions in recognition of some viruses from subclade D.3.1.1 with additional substitutions including G155E.

Human serology studies used seven serum panels from children (under 10 years), adults (18 to 64 years) and older adults (65 years and older) who had received egg-propagated inactivated (standard or adjuvanted) or cell culture-propagated inactivated vaccines with SH 2026 influenza vaccine formulations. SH 2026 egg-based vaccines contained A/Missouri/11/2025 (H1N1)pdm09-like, A/Singapore/GP20238/2024 (H3N2)-like and B/Austria/1359417/2021-like virus antigens. Cell culture-propagated vaccines contained A/Missouri/11/2025 (H1N1)pdm09-like, A/Sydney/1359/2024 (H3N2)-like and B/Austria/1359417/2021-like virus antigens. 

Recent A(H1N1)pdm09 viruses with HA genes from subclade D.3.1.1 were analysed in HI assays using these human serum panels. When compared to the post-vaccination geometric mean titres (GMTs) to egg- or cell culture-propagated A/Missouri/11/2025 (H1N1)pdm09-like vaccine reference viruses, post-vaccination GMTs were significantly reduced for some recently circulating viruses from subclade D.3.1.1 with amino acid substitutions Q54H, D139N, G155E, or D139N, V152I, G155E, or D139N, V152I, S157L, S190G in several serum panels.

Of 1029 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 alone or in combination with S247N substitution and eight had S247N combined with I223V, I223T or Q136K substitutions. Of 1101 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) viruses⁶ collected since February 2026 showed that the majority of circulating viruses globally belonged to subclade K (characterized by K2N, T135K, S144N [a potential addition of an N-glycosylation site], N158D, I160K, Q173R, T328A and S378N). There were still low proportions of viruses circulating from J.2 subclades, notably J.2.2 (characterized by S124N) in Asia, J.2.3 (characterized by N158K, K189R and S378N) in the Americas, J.2.4 (characterized by T135K [a potential loss of an N-glycosylation site] and K189R) in Asia and J.2.4.2 (characterized by F79V, T135K, S144N [a potential addition of an N-glycosylation site], N158D, I160K and T328A) in most regions.   Post-infection ferret antisera raised against cell culture-propagated A/Sydney/1359/2024-like and egg-propagated A/Singapore/GP20238/2024-like J.2.4 viruses, representing the A(H3N2) component for the SH 2026 influenza vaccines, recognized most J.2.4 viruses and many subclade J.2.4.2 and K viruses well. However, subclade J.2.4.2 and K viruses 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 recently circulating A(H3N2) viruses with HA genes from subclades J.2.3, J.2.4.2 and K. When compared to titres against cell-propagated A/Sydney/1359/2024-like and egg-propagated A/Singapore/GP20238/2024-like vaccine reference viruses, post-vaccination HI GMTs or VN GMTs against many of the recent viruses in J.2.3, J.2.4.2 and K subclades tested were significantly reduced in many serum panels.

Of 2350 influenza A(H3N2) viruses examined by genetic and/or phenotypic analyses, one virus showed evidence of reduced susceptibility to NAIs with an NA S331R substitution. Of 2462 A(H3N2) viruses examined by genetic and/or phenotypic analyses, one virus showed evidence of reduced susceptibility to the endonuclease inhibitor baloxavir marboxil, with a polymerase acidic (PA) K34R substitution.

Influenza B viruses

Since February 2026, influenza B viruses were detected in all WHO regions, and all those characterized belonged to the B/Victoria/2/87 lineage. There have been no confirmed detections of circulating B/Yamagata lineage viruses after March 2020.

All influenza B/Victoria lineage viruses collected since February 2026 with available HA sequences belonged to subclades C. 3 and C.5.⁷ Viruses which shared a D197E substitution are classified as subclade C. 5 which has undergone further diversification of HA genes resulting in subclades C.5.1 (characterized by E183K), C.5.6 (characterized by D129N), C.5.6.1 (characterized by T37I, E128D, and T199A in addition to D129N), and C.5.7 (characterized by E183K and E128G). Circulating viruses derived from subclade C. 3 (characterized by E128K and A154E) include subclades C.3.1 (characterized by D197N with potential gain of N-glycosylation) and C.3.3 (characterized by substitutions S208P, S255P, I267V, and D197N with potential gain of N-glycosylation). There were differences in subclade circulation and predominance between and within regions based on currently available data. Subclade C.3.1 viruses predominated in the Americas, subclade C.3.3 viruses predominated in Eastern Asia and subclade C.5.6 predominated in Africa, Europe, South East Asia and Oceania.

Antigenic analysis showed that post-infection ferret antisera raised against B/Austria/1359417/2021-like viruses (subclade C), representing the B component for the SH 2026 influenza vaccines, recognized viruses within the C. 5 subclades well. In contrast, viruses with the HA substitution D197N from C. 3 subclades were recognized poorly. Post-infection ferret antisera raised against cell culture-propagated B/Pennsylvania/14/2025-like viruses (C.3.1), representing cell-based vaccine viruses for the NH 2026-27 influenza season, recognized recently circulating viruses from C. 3 and C. 5 subclades well. Post-infection ferret antisera raised against egg-propagated B/Tokyo/EIS13-175/2025-like viruses (C.3.1), representing egg-based vaccine viruses for the NH 2026-27 influenza season, recognized most viruses from the C. 5 subclades well but showed reduced recognition of C. 3 subclades compared to that of the cell equivalent.

In human serology studies, recently circulating B/Victoria lineage viruses with HA genes from subclades C.3.1, C.3.3, C.5.6 and C.5.6.1 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 viruses, titres against many viruses with HA genes from subclades C.5.6 and C.5.6.1 were not significantly reduced in most serum panels; however, titres against subclade C.5.6.1 viruses with the amino acid substitution P241Q were significantly reduced in some panels. In contrast, titres against many viruses with HA genes from subclades C.3.1 and C.3.3 were significantly reduced in most serum panels.

Of 2598 influenza B/Victoria lineage viruses examined by genetic and/or phenotypic analyses, five showed evidence of reduced or highly reduced susceptibility to NAIs: one had an NA D197G substitution, one had an NA N294S substitution, one had an NA G407S substitution, one had an NA G407R substitution and one had an NA M464T substitution. Of 2387 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 2027 southern hemisphere influenza season

Since February 2026, A(H1N1)pdm09 viruses circulated globally. The majority of viruses had HA genes belonging to subclades D.3.1 and D.3.1.1, with D.3.1.1 viruses predominating. Post-infection ferret antisera raised against the southern hemisphere (SH) 2026 and the northern hemisphere (NH) 2026/2027 A/Missouri/11/2025-like A(H1N1)pdm09 vaccine viruses recognized most D.3.1 and D.3.1.1 viruses well. In human serology studies, post-vaccination haemagglutination inhibition (HI) geometric mean titres (GMTs) were significantly reduced for some recently circulating A(H1N1)pdm09 viruses when compared to the responses to egg- or cell culture-propagated A/Missouri/11/2025-like vaccine reference viruses.

Since February 2026, A(H3N2) viruses circulated and predominated in many regions. The vast majority of A(H3N2) viruses analysed had HA genes from subclade K. Post-infection ferret antisera raised against SH 2026 influenza season A(H3N2) vaccine viruses (cell culture-propagated A/Sydney/1359/2024-like and egg-propagated A/Singapore/GP20238/2024-like J.2.4 viruses) recognized subclade J.2.4 and many subclade J.2.4.2 and K viruses well; however, post-infection ferret antisera raised against NH 2026-27 A(H3N2) subclade K vaccine viruses (cell culture-propagated A/Darwin/1415/2025-like and egg-propagated A/Darwin/1454/2025-like viruses) showed improved recognition of subclade J.2.4.2 and K viruses. When compared to titres against cell culture-propagated A/Sydney/1359/2024-like and egg-propagated A/Singapore/GP20238/2024-like vaccine reference viruses, human post-vaccination HI GMTs or virus neutralization (VN) GMTs against many of the recent viruses in subclades J.2.3, J.2.4.2 and K were significantly reduced. 

Since February 2026, influenza B viruses cocirculated globally but at different levels among regions. All influenza B viruses characterized belonged to the B/Victoria/2/87 lineage and had HA genes belonging to subclades C. 3 and C. 5. Post-infection ferret antisera raised against B/Austria/1359417/2021-like subclade C viruses, representing the B component of vaccine viruses for the SH 2026 influenza season, recognized viruses within the C. 5 subclades (C.5.6, C.5.6.1, C.5.7) well, but C. 3 subclade viruses (C.3.1, C.3.3) with HA substitution D197N were recognized poorly. Post-infection ferret antisera raised against cell culture-propagated NH 2026-27 vaccine viruses (B/Pennsylvania/14/2025-like C.3.1 viruses) recognized recently circulating C. 3 and C. 5 subclades well. Egg-propagated NH vaccine viruses (B/Tokyo/EIS13-175/2025-like C.3.1 viruses) acquired egg-adaptive mutations that removed the potential N-glycosylation site at HA 197 to 199, and post-infection ferret antisera raised against these viruses showed reduced recognition of viruses from C. 3 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 C. 5 subclades were not significantly reduced when compared to titres against egg- or cell culture-propagated B/Austria/1359417/2021-like vaccine reference viruses. Titres against viruses with HA genes from C. 3 subclades were significantly reduced in most serum panels.

For vaccines for use in the 2027 southern 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 together with candidate vaccine viruses (CVVs) suitable for use in the development and production of human influenza vaccines and lists of reagents for vaccine standardization are available on the WHO website⁸.

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).
• Influenza Research Center, National Institute of Infectious Diseases, Japan Institute for Health Security, 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).
• 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 a weekly update⁹ of global influenza activity. Other information about influenza surveillance, risk assessment, preparedness and response can be found on the WHO Global Influenza Programme website¹⁰.

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; Fred Hutch Cancer Center, Nextstrain, Previr and University of Cambridge for quantitative analyses; 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 EpiFlu^TM database and other sequence databases which were used to share gene sequences and associated information; and the Global Influenza Vaccine Effectiveness (GIVE) Collaboration for sharing estimates of influenza vaccine effectiveness on a confidential basis. 

Annex 1

Declarations of interest

The WHO recommendation on the composition of influenza vaccines for use in the 2027 southern hemisphere influenza season was made through a WHO Consultation with relevant WHO Collaborating Centres on Influenza (CCs) and Essential Regulatory Laboratories (ERLs).

In accordance with WHO policy, directors and experts of the relevant WHO CCs and ERLs, in their capacity as representatives of their respective institutions (“Advisers”), completed the WHO form for Declaration of Interests for WHO experts before being invited to the consultation. At the start of the consultation, the interests declared by the Advisers were disclosed to all participants.

The Advisers declared the following personal current or recent (within the past four years) financial or other interests relevant to the subject of work:

Based on the WHO assessment, the interests declared by Drs Engelhardt, Kondor, Lewis, Reading and Webby were determined not to present a conflict of interest with the objectives of the WHO consultation. Therefore, it was concluded that with disclosure at the beginning of the consultation to all participants, Drs Engelhardt, Kondor, Lewis, Reading and Webby should continue to serve as Advisers.