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<p>Maternal antibodies are transferred transplacentally&#xa0;to fetuses and then through&#xa0;lactation to&#xa0;infants to protect them whilst their own immune system is still&#xa0;immature. However, these maternal&#xa0;antibodies also suppress neonatal B-cell responses, thereby impairing vaccine efficacy and leaving infants potentially vulnerable to life-threatening pathogens, such as rotaviruses. Currently available rotavirus vaccines are composed of live-attenuated viral strains administered to infants orally at&#xa0;6-8 weeks old. Although high concentrations of maternal antibodies correlate with poor production of antibodies following vaccination (i.e., seroconversion), the immunological basis of this interference is unknown. To investigate the underlying mechanisms, we here&#xa0;developed a mouse model of neonatal oral rotavirus vaccination, in which vaccination only fails to induce seroconversion if maternal antibodies are present. Such antibodies are shown to block vaccine replication, while faster maternal antibody waning is observed in vaccinated compared to unvaccinated pups. FcγRIIB deletion does not overcome interference in pups, although pup IgG levels increase when maternal antibody titers are very low. Our findings show that maternal antibody-mediated vaccine clearance is a key mechanism of interference with oral rotavirus vaccines, with a minor role for FcγRIIB in neonatal IgG responses.</p>

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Mechanisms of maternal antibody interference with rotavirus vaccination

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月14日

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  • Tawny L Chandler,
  • Sarah Woodyear,
  • Valerie Chen,
  • Tom M Lonergan,
  • Natalie Baker,
  • Katherine Harcourt,
  • Simon Clare,
  • Faraz Ahmed,
  • Sarah L Caddy

摘要

Maternal antibodies are transferred transplacentally to fetuses and then through lactation to infants to protect them whilst their own immune system is still immature. However, these maternal antibodies also suppress neonatal B-cell responses, thereby impairing vaccine efficacy and leaving infants potentially vulnerable to life-threatening pathogens, such as rotaviruses. Currently available rotavirus vaccines are composed of live-attenuated viral strains administered to infants orally at 6-8 weeks old. Although high concentrations of maternal antibodies correlate with poor production of antibodies following vaccination (i.e., seroconversion), the immunological basis of this interference is unknown. To investigate the underlying mechanisms, we here developed a mouse model of neonatal oral rotavirus vaccination, in which vaccination only fails to induce seroconversion if maternal antibodies are present. Such antibodies are shown to block vaccine replication, while faster maternal antibody waning is observed in vaccinated compared to unvaccinated pups. FcγRIIB deletion does not overcome interference in pups, although pup IgG levels increase when maternal antibody titers are very low. Our findings show that maternal antibody-mediated vaccine clearance is a key mechanism of interference with oral rotavirus vaccines, with a minor role for FcγRIIB in neonatal IgG responses.