Influenza B viruses are members of the Orthomyxoviridae family and consist of enveloped, segmented, negative‑sense RNA viruses. Unlike influenza A viruses, they primarily infect humans and seals and are responsible for seasonal influenza epidemics rather than pandemics.
Virology & Pathogenesis
Influenza B viruses possess an eight‑segment negative‑sense RNA genome and replicate in the nuclei of infected respiratory epithelial cells. They lack the extensive host range of influenza A viruses and are not divided into subtypes; instead they are classified into two antigenically and genetically distinct lineages, B/Victoria and B/Yamagata. Both lineages co‑circulate and evolve through antigenic drift, accumulating mutations in the hemagglutinin and neuraminidase proteins over time. Influenza B viruses cause annual epidemics along with influenza A viruses, but they have not been associated with pandemics, likely because they primarily infect humans and lack an extensive animal reservoir. After inhalation, the virus binds sialic acid residues via its hemagglutinin, enters host cells through endocytosis, and undergoes replication. Viral shedding begins before symptom onset, contributing to community spread. Infection typically results in fever, cough, myalgia and malaise; children are disproportionately affected and may experience otitis media or febrile seizures. Immunity from infection or vaccination is strain‑specific and wanes over time, necessitating periodic vaccination.
Lineages and clinical impact
The B/Victoria and B/Yamagata lineages differ antigenically, leading to incomplete cross‑protection between them. Quadrivalent influenza vaccines include representatives of both lineages, whereas older trivalent formulations contained only one. Seasonal dominance varies: the B/Yamagata lineage predominated in the late 1990s, while B/Victoria surged in the 2000s and co‑circulation has persisted since. Influenza B epidemics can be severe, particularly in school‑aged children and adolescents, and they occasionally cause large outbreaks on college campuses and in military recruits. Despite the absence of antigenic shift, reassortment within the lineage contributes to genetic diversity. Antiviral drugs such as neuraminidase inhibitors (oseltamivir and zanamivir) and baloxavir marboxil are active against influenza B, but early initiation is necessary for clinical benefit.
Influenza B viruses contribute substantially to seasonal flu burden, particularly in children and adolescents. Their limited host range and slower antigenic evolution reduce the risk of pandemics, but ongoing surveillance and vaccination remain important for controlling outbreaks.
Related Terms: Orthomyxoviridae, B/Victoria lineage, B/Yamagata lineage, Antigenic drift, Influenza A virus