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ARS Home » Research » Publications at this Location » Publication #119598
Title: IMMUNITY TO INFLUENZA A H9N2 VIRUSES INDUCED BY INFECTION AND VACCINATION

Author
item LU,, XIUHUA - CDC - ATLANTA, GEORGIA
item RENSHAW,, MARY - CDC - ATLANTA, GEORGIA
item Tumpey, Terrence
item KELLY,, GLORIA - CDC - ATLANTA, GEORGIA
item HU-PRIMMER,, JEAN - CDC - ATLANTA, GEORGIA
item KATZ,, JACQUELINE - CDC - ATLANTA, GEORGIA

Submitted to: Journal of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/20/2001
Publication Date: 5/1/2001
Citation: N/A

Interpretive Summary: In 1999 in Hong Kong, two human cases of respiratory illness were caused by an avian influenza A H9N2 virus. The H9 influenza subtype virus had not previously been known to cause respiratory illness in humans. The introduction of H9N2 viruses into humans raised concerns about the potential of these viruses to cause a pandemic. The identification of a human influenza vaccine for H9N2 viruses is considered a high priority in pandemic preparedness. We have used the BALB/c mouse to better understand the pathogenesis of and immunity to the H9N2 viruses in a mammalian model. The viruses were placed into two antigenic groups and it was determined that infection with either virus induced similar protection against challenge with the same or different H9N2 virus. The immunization of mice with a purified inactivated vaccine resulted in protection against challenge with the same virus but only partial protection against the different H9 virus.

Technical Abstract: Avian influenza A H9N2 viruses are widespread among domestic poultry in Asia and were recently isolated from humans with respiratory illness in Hong Kong. Since H9N2 viruses were previously isolated only from avian species, their emergence into a largely serologically naive human population raises concerns regarding the pandemic potential of these viruses. Two antigenically and genetically distinct groups of H9N2 viruse (G1 and G9) are prevalent in China. To evaluate a strategy of vaccination, we compared the G1 and G9 group viruses for their relative immunogenicity and cross-protective efficacy. H9N2 viruses replicated efficiently in the lungs of BALB/c mice, but caused no morbidity or mortality. Infection of mice with a G9 group virus induced substantially higher hemagglutination-inhibition (HI) antibody responses compared with infection of mice with a G1 group virus. Mice administered inactivated G1 group whole virus vaccine intramuscularly were completely protected from challenge with either group of H9N2 virus. Although mice administered inactivated G9 group vaccine elicited higher titers of HI antibody completely protected from challenge with homologous virus, only partial protection against the G1 group virus was observed. These results have implications for the development of human vaccines against H9N2 viruses.