UMMS Affiliation

Department of Medicine; Center for Infectious Disease and Vaccine Research

Publication Date


Document Type



Animals; Antibodies, Monoclonal; Antibodies, Viral; Antigen-Presenting Cells; Antigens, Viral; Cell Line; Cross Reactions; Humans; Influenza A virus; Influenza, Human; Male; Mice; Mice, Inbred BALB C; Neuraminidase; Neutralization Tests; Receptors, Fc


Life Sciences | Medicine and Health Sciences


Antibody-dependent enhancement of the uptake of influenza A virus by Fc receptor-bearing cells was analyzed by using virus strains of the three human influenza A virus subtypes, A/PR/8/34 (H1N1), A/Japan/305/57 (H2N2), and A/Port Chalmers/1/73 (H3N2). Immune sera obtained from mice following primary infection with an H1N1, H2N2, or H3N2 subtype virus neutralized only virus of the same subtype; however, immune sera augmented the uptake of virus across subtypes. Immune sera from H1N1-infected mice augmented uptake of the homologous (H1N1) and H2N2 viruses. Antisera to the H2N2 virus augmented the uptake of virus of all subtypes (H1N1, H2N2, or H3N2). Antisera to the H3N2 virus augmented the uptake of the homologous (H3N2) and H2N2 viruses. These results show that subtype cross-reactive, nonneutralizing antibodies augment the uptake of influenza A virus strains of different subtypes. Antibodies to neuraminidase may contribute to the enhanced uptake of viruses of a different subtype, because N2-specific monoclonal antibodies augmented the uptake of both A/Japan/305/57 (H2N2) and A/Port Chalmers/1/73 (H3N2) viruses.


J Virol. 1994 Jun;68(6):3499-504.

Journal/Book/Conference Title

Journal of virology

Related Resources

Link to Article in PubMed

PubMed ID