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On influenza virus infection or vaccination, immune responses occur, including the production of antibodies with various functions that contribute to protection from seasonal influenza virus infection. In the current study, we attempted to identify the antibody functions that play a central role in preventing the onset of seasonal influenza by comparing the levels of several antibody titers for different antibody functions between 5 subclinically infected individuals and 16 patients infected with seasonal H3N2 virus. For antibody titers before influenza virus exposure, we found that the nAb titers and enzyme-linked immunosorbent assay titers against hemagglutinin and neuraminidase (NA) proteins in the subclinically infected individuals were significantly higher than those in the patients, whereas the NA inhibition titers and antibody-dependent cellular cytotoxicity activities did not significantly differ between subclinically infected individuals and infected patients. These results suggest that nAb and enzyme-linked immunosorbent assay titers against hemagglutinin and NA serve as correlates of symptomatic influenza infection. [ABSTRACT FROM AUTHOR]

Clinical samples from 15 amantadine-treated children were collected serially -- before, during, and/or after treatment -- and were studied to determine the actual prevalence, timing, and clinical implications of M2 mutational events. After viral RNA extraction and reverse-transcriptase polymerase chain reaction amplification of the viral RNA encoding the M2 protein, the products were cloned into plasmids, and their sequences were determined. Five mutations known to confer amantadine resistance in clinical samples were identified in 12 (80%) of 15 evaluable patients, and 9 patients had > (2-4) mutant virus. The pattern of emergence of mutant strains was clarified from the study of 6 patients with at least 4 serial samples. Although viruses with M2 mutations tended to become the dominant populations, in 2 cases, wild-type viruses became dominant after decreasing to low levels. These results suggest that resistant viruses emerge in a much higher proportion of amantadine-treated patients than has been suggested by previous studies. [ABSTRACT FROM AUTHOR]