What are the differences between influenza A and influenza B in the 2025‑2026 season regarding circulating strains, clinical severity, diagnostic testing, antiviral treatment, and vaccine effectiveness?

Differences Between Influenza A and Influenza B in 2025/2026

Both influenza A and B produce clinically indistinguishable illness with similar severity in hospitalized children, but influenza A evolves faster, has pandemic potential, and currently includes two subtypes (H1N1 and H3N2) while influenza B includes only the Victoria lineage after Yamagata disappeared in 2020. 1, 2, 3

Circulating Strains in 2025/2026

Influenza A Strains

• Two influenza A subtypes are currently circulating: H1N1pdm09 and H3N2, both included in the 2024-2025 trivalent vaccine 1, 2
• The H3N2 component was updated for the 2024-2025 season (A/Thailand/8/2022-like for egg-based; A/Massachusetts/18/2022-like for cell-based/recombinant), while H1N1pdm09 remains unchanged (A/Victoria/4897/2022-like for egg-based; A/Wisconsin/67/2022-like for cell-based/recombinant) 1
• H3N2 subclade K (J.2.4.1) is the predominant variant globally as of December 2025, detected in up to 50% of cases in the EU/EEA and driving a 30-year high in respiratory illness incidence in the United States 4
• H3N2-predominant seasons are associated with higher severity, increased hospitalizations, and greater mortality, particularly in young children and older adults 5

Influenza B Strains

• Only the Victoria lineage is circulating; the Yamagata lineage has not been detected globally since 2020 and has been removed from all U.S. seasonal vaccines 1
• The Victoria lineage component (B/Austria/1359417/2021-like) remains unchanged in the 2024-2025 vaccine 1
• Influenza B represented 21.32% of positive cases in recent surveillance data, with limited contribution to overall disease burden compared to influenza A 6

Virologic and Evolutionary Differences

Antigenic Variation

• Influenza A undergoes antigenic drift markedly faster than influenza B due to frequent point mutations during replication, making it the primary driver of seasonal epidemics 2
• Influenza B evolves more slowly with a reduced rate of antigenic drift 2
• Only influenza A can cause pandemics through antigenic shift—major genetic reassortment between distinct viral strains, especially between human and avian viruses 2

Viral Classification

• Influenza A viruses are categorized into subtypes based on hemagglutinin (H) and neuraminidase (N) surface antigens; 16 H subtypes and 9 N subtypes exist in nature 2
• Influenza B viruses are not divided into subtypes but are grouped into two genetic lineages (Victoria and Yamagata) 2
• H3N2 viruses have rapidly evolved since 1968, adding numerous N-linked glycans to hemagglutinin, increasing net charge, and altering receptor binding preferences 7

Clinical Severity and Presentation

Symptom Profile

• Influenza A and B produce clinically indistinguishable illness characterized by abrupt onset of fever, myalgia, headache, malaise, non-productive cough, sore throat, and rhinitis 2
• In pediatric patients, both virus types commonly cause otitis media, nausea, and vomiting 2
• Symptoms alone cannot reliably differentiate influenza A from B, requiring laboratory confirmation (RT-PCR or rapid antigen testing) for definitive diagnosis 2

Comparative Severity in Children

• A 14-year Finnish study of 391 hospitalized children found no significant differences in clinical features, outcomes, ICU treatment, or length of stay between influenza A and B infections 3
• Blood cultures were obtained from 36.2% of children with influenza A versus 34.8% with influenza B (P=0.80); lumbar puncture was performed in 5.7% versus 9.8% respectively (P=0.15) 3
• Influenza B appears to cause more illness in children aged 1-10 years than in other age groups 8

High-Risk Populations

• Children younger than 5 years (especially <2 years) and those with underlying medical conditions are at increased risk for hospitalization and complications from both virus types 1
• High-risk conditions include chronic pulmonary disease (asthma, cystic fibrosis), cardiovascular disease, immunosuppression, neurologic conditions, extreme obesity, and diabetes 1

Diagnostic Testing

Laboratory Methods

• Both influenza A and B require the same diagnostic approaches: RT-PCR (gold standard) or rapid antigen testing 2
• Subtyping is performed to distinguish H1N1 from H3N2 within influenza A, and lineage determination (Victoria vs. Yamagata) for influenza B 1
• Real-time reverse transcriptase-polymerase chain reaction assays are used for detection and subtyping in surveillance networks 6

Transmission Characteristics

• Both viruses spread primarily via respiratory droplets expelled during coughing and sneezing 2
• The incubation period is 1-4 days (average ≈2 days) for both types 2
• Adults are infectious from one day before symptom onset through approximately five days after onset for either virus type 2
• Children may remain infectious for more than 10 days after symptom onset for both virus types 2

Antiviral Treatment

Treatment Recommendations

• Antiviral treatment recommendations have been simplified for the 2024-2025 season and do not differ based on whether the infection is influenza A or B 1
• Neuraminidase inhibitors (oseltamivir, zanamivir) are effective against both influenza A and B 1
• Most seasonal influenza A (H1N1) strains have developed resistance to oseltamivir, though current treatment guidelines remain unchanged 2
• Treatment decisions may be influenced by local strain circulation patterns and resistance profiles 5

Vaccine Effectiveness

Overall Effectiveness by Type

• Vaccine effectiveness varies significantly by strain and season, with recent seasons showing VE ranging from 9% against A(H3N2) to 76% against influenza B/Victoria in children 5
• During the 2016/2017 season, the H3N2 component exhibited poor protective efficacy (28-42%) against co-circulating strains 7
• Influenza vaccination prevented an estimated 116 deaths in children 6 months through 17 years during the 2022-2023 season 1

Age-Specific Effectiveness

• In children 6 months to 8 years, VE ranged from 23-59% for H1N1pdm09, 23-34% for H3N2, and 39-51% for B/Victoria across recent seasons 1
• In children 9-17 years, VE was lower: -20 to 29% for H1N1pdm09, 29-40% for H3N2, and 34-43% for B/Victoria 1
• Historically, up to 80% of influenza-associated pediatric deaths occurred in unvaccinated or incompletely vaccinated children 1

Protection Against Severe Outcomes

• Overall VE against influenza-associated death in all children was 65% (95% CI, 54-74%) and 51% (95% CI, 31-67%) in children with underlying conditions 1
• Even in mismatched seasons, vaccination provides 50-60% effectiveness in preventing hospitalization/pneumonia and 80% effectiveness in preventing death 9
• Vaccination reduced the risk of life-threatening influenza illness by three-quarters in a 2010-2012 case-control study 1

Cross-Protection Limitations

• Antibodies generated against one influenza type provide limited or no protection against the other type due to distinct surface antigens 2
• Within the same type, antibodies to one antigenic variant may not protect against newly emerging variants of the same subtype or lineage 2
• The shift to trivalent vaccines (removing Yamagata) does not represent reduced protection but reflects the global disappearance of that lineage 9

Key Clinical Pitfalls

Vaccination Coverage Gaps

• Only 53.9% of children 6 months to 17 years were vaccinated during the 2023-2024 season, more than 8.5 percentage points lower than May 2020 1
• Non-Hispanic Black children had the lowest coverage (49.1%), and rural children had significantly lower coverage (39.9%) than suburban (53.7%) or urban (59.5%) children 1

Surveillance Importance

• Check the CDC's FluView Interactive dashboard for weekly updated surveillance data on circulating strains by region and state 5
• Contact local health departments for real-time influenza surveillance reports to track predominant strains and activity levels 5
• Influenza activity typically peaks between December and February but can occur as late as April or May 5

Treatment Timing

• Vaccination should not be delayed to obtain a specific product or formulation—timely vaccination with any available age-appropriate vaccine is the priority 9
• Coadministration with other recommended immunizations, including nirsevimab, is emphasized 1