RT Journal Article SR Electronic(1) A1 Yoshikawa, Tomoki A1 Matsuo, Keiko A1 Matsuo, Kazutoshi A1 Suzuki, Yujiro A1 Nomoto, Akio A1 Tamura, Shin-ichi A1 Kurata, Takeshi A1 Sata, TetsutaroYR 2004 T1 Total viral genome copies and virus–Ig complexes after infection with influenza virus in the nasal secretions of immunized mice JF Journal of General Virology, VO 85 IS 8 SP 2339 OP 2346 DO https://doi.org/10.1099/vir.0.79892-0 PB Microbiology Society, SN 1465-2099, AB The kinetics of infectious virus (p.f.u.), total virus and virus–Ig complex formation following influenza A/PR8 (H1N1) viral infection was examined in the nasal secretions of naive mice and mice immunized with A/PR8, A/Yamagata (H1N1), A/Guizhou (H3N2) and B/Ibaraki influenza viruses. The total number of virus particles and the number within virus–Ig complexes, captured in advance using an anti-mouse Ig-coated plate, were determined on the basis of viral genome copy number using quantitative RT-PCR. The kinetics of infectious and total virus particle formation, the latter of which increased by 103–104-fold above infectious virus numbers, showed that virus elimination from the nasal area was earlier in A/PR8, A/Yamagata and A/Guizhou-X virus-immunized mice, in decreasing order, compared with naive mice. Early virus elimination correlated with the level of A/PR8 virus-reactive antibodies in immunized mice. Virus elimination coincided with the appearance of virus–Ig complexes shortly after infection. This result suggested that antibodies led to the formation of immune complexes in a dose-dependent manner together with a reduction in number of infectious virus particles. The fact that a large number of virus particles was observed in immune complexes for a wide range antibody levels made it difficult to detect slight differences in virus number within the immune complexes, depending on antibody level. These results suggested that the formation of virus–Ig complexes in virus-immunized mice shortly after infection is involved in early virus elimination, which is determined by the strength of protective immunity against challenge viruses., UL https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.79892-0