Maternally-derived antibodies do not inhibit swine influenza virus replication in piglets but decrease excreted virus...

Area of Science:

• Veterinary Immunology
• Virology
• Swine Health

Background:

• Maternally-derived antibodies (MDA) confer passive immunity to piglets against swine influenza A virus (H1N1).
• However, MDA can interfere with active immune responses and vaccine efficacy, raising questions about protection after passive immunity wanes.
• Understanding MDA's impact is crucial for optimizing H1N1 control strategies in piglets.

Purpose of the Study:

• To investigate the influence of varying residual MDA levels on H1N1 virus excretion and immune responses in piglets.
• To assess the impact of MDA on protection against a secondary homologous H1N1 infection.
• To compare responses in piglets from vaccinated (MDA+) versus unvaccinated (MDA-) sows.

Main Methods:

• Piglets from vaccinated (MDA+) and unvaccinated (MDA-) sows were infected with H1N1 at 5, 7, or 11 weeks of age.
• Virus excretion, clinical signs, and humoral (HI, neutralizing, anti-NP/M) and cellular (T cell proliferation) immune responses were monitored.
• Protection against a homologous H1N1 challenge four weeks post-primary infection was evaluated.

Main Results:

• MDA- piglets exhibited clinical signs and virus shedding, with age-dependent variations in severity and duration.
• MDA+ piglets showed increased clinical signs correlating with lower MDA levels; virus shedding was not prevented but viral particles from younger MDA+ piglets were less infectious.
• MDA significantly impacted humoral responses (HI, neutralizing) but less so anti-NP/M and T cell proliferation; all piglets, regardless of MDA status, were protected from reinfection.

Conclusions:

• Piglet responses to H1N1 are influenced by both the piglet's physiological development at the time of infection and the level of MDA.
• MDA can modulate but does not abrogate protective immunity against subsequent H1N1 infection.
• These findings highlight the complex interplay between passive immunity and active immune development in H1N1-infected piglets.