RBP4 deficiency attenuates IAV replication <i>in vivo.</i>
<p>(A, B) Analysis of NP and M1 protein levels and mRNA expression or plaque assay of virus titers in BMDMs derived from WT and RBP4-deficient mice infected with IAV WSN strain (MOI = 0.5) at indicated time points. Representative immunoblotting results from two independent experiments (A) and...
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2025
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| Summary: | <p>(A, B) Analysis of NP and M1 protein levels and mRNA expression or plaque assay of virus titers in BMDMs derived from WT and RBP4-deficient mice infected with IAV WSN strain (MOI = 0.5) at indicated time points. Representative immunoblotting results from two independent experiments (A) and pooled qPCR data and virus titers (B) from three independent experiments (mean ± SD) were shown, respectively. (C) Schematic diagram of the influenza virus infection model in mice. WT and RBP4-deficient mice were intranasally infected with 1 × 10<sup>4</sup> PFU of WSN. Lungs were collected 3 days post-infection, and body weight was monitored daily for 6 days. (D) Body weight changes in mice infected with IAV WSN as described in (C) (mean ± SEM, n = 6). (E) Immunoblotting analysis of NP and M1 protein expression in lungs of mice infected with IAV as in C (n = 3). (F) Immunofluorescence of NP proteins in lung tissues from WT and RBP4-deficient mice infected IAV as described in (C). Scale bars, 100 μm. Mean fluorescence intensity was calculated from two independent experiments (right). (G-J) Plaque assay analysis of virus titers (G), qPCR analysis of M1 copy number (H) and inflammatory cytokine expression (I) in lung tissues or histopathological analysis of lung tissues from WT and RBP4-deficient mice infected with WSN at day 3 post-infection. Each dot represents an individual mouse. Scale bars, 100 μm in J. Data are representative of two independent experiments (E-J, mean ± SEM). *<i><i>p</i></i> < 0.05, **<i><i>p</i></i> < 0.01, ***<i><i>p</i></i> < 0.001 (Student’s <i>t</i>-test).</p> |
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