Influenza H1N1pdm-specific maternal antibodies offer limited protection against wild-type virus replication and influence influenza vaccination in ferrets.

Amorsolo L Suguitan,Stephanie Gee,Paulyn Cha,Zhongying Chen,Rosemary Broome,Scott Jacobson,Hong Jin,James R Zengel,Janet Cetz

doi:10.1111/irv.12220

Abstract

ObjectiveThe objective was to study passively acquired influenza H1N1 pandemic (H1N1pdm) maternal antibody kinetics and its impact on subsequent influenza infection and vaccination in ferrets during an outbreak of the H1N1pdm.Design and main outcome measuresInfectivity of the H1N1pdm in the respiratory tract of ferrets was compared with the previous seasonal A/South Dakota/6/2007 (SD07, H1N1). Influenza-specific antibodies were quantitated and antibody-mediated protection against the homologous and heterologous H1N1 virus challenge infection was determined.ResultsH1N1pdm virus was approximately 10 times more infectious than SD07 in ferrets, replicated to higher viral titers in the upper respiratory tract and shed for a longer duration. Influenza-specific antibodies after natural infection persisted much longer in the circulation than passively acquired maternal antibodies. The protection conferred by the maternal antibodies was limited to the homologous virus strain and was ineffective against SD07 and H3N2 virus. Serum antibodies from maternal transmission or passive transfer interfered with homologous vaccine strain-mediated antibody responses in the ferret. A booster immunization was required to elicit a high level of antibody.ConclusionsThe findings support the rationale for a prime and boost immunization strategy in young children in whom maternal antibodies are present.

Highlights

Influenza virus is a significant cause of respiratory tract infections resulting in an estimated 3–5 million clinical infections and up to half million deaths annually worldwide.[1]Approximately 1 million children suffer from severe cases of influenza with 100 000 deaths annually.[2]
To determine whether the rapid spread of an influenza H1N1 pandemic (H1N1pdm)-like virus among ferrets could be explained by its high infectivity in these animals, Gil[11] H1N1pdm was compared with the seasonal South Dakota/6/2007 (SD07) H1N1 virus for infectious dose at which fifty percent of ferrets could be infected (FID50)
CA09 can grow to high titer after egg adaptation and was used to evaluate the morbidity caused by H1N1pdm infection in ferrets instead of Gil11.25 The ferrets that were infected with either CA09 or SD07 virus showed typical symptoms of influenza infection including weight loss, elevated body temperature, and lethargy

Summary

Introduction

Influenza virus is a significant cause of respiratory tract infections resulting in an estimated 3–5 million clinical infections and up to half million deaths annually worldwide.[1]. 1 million children suffer from severe cases of influenza with 100 000 deaths annually.[2] The 2009 swineorigin influenza A H1N1 pandemic (H1N1pdm) spread to more than 200 countries worldwide and caused half a million deaths during the first year of its circulation.[3] The antigenicity of this swine-origin virus is distinct from previously circulating seasonal H1N1 viruses.[4] It caused acute infection mainly in children and younger adults, while older adults were mostly resistant to H1N1pdm infection, presumably due to cross-reactive antibodies from previous exposure to antigenically related strains.[5,6,7]. The high levels of pre-existing antigen-specific maternal antibodies could significantly inhibit the immunogenicity of some vaccines.[16,17,18] immunizations are often scheduled when passively acquired antibodies have waned

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