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. 2005 May 26;102(23):8275–8280. doi: 10.1073/pnas.0408589102

Fig. 4.

Fig. 4.

Susceptibility of transgenic mice to HCoV-229E-37. Mice with the indicated genotype were infected by different routes (oral, intragastric, intranasal, and i.p.) with HCoV-229E-37. At the indicated times postinfection, lung, intestine, spleen, and liver tissues were collected, and virus titers were determined by using a plaque assay. (A) The results shown represent medium values of titers in the lungs of the different mouse strains. (B) Virus growth in different tissues of hAPN+/+Stat1-/- mice infected with HCoV-229E-37. Virus growth could not be detected in the tissues of nontransgenic animals. To simplify the figure, only nontransgenic lung is shown. (C) RT-PCR analysis of HCoV-229E-37 growth in different tissues from the indicated transgenic mice by studying the expression of HCoV-229E S gene mRNA. The position of the expected amplified DNA is indicated. ST-hAPN, swine testis cells transformed with the gene encoding hAPN; S+ and S-, Stat1+/+ and Stat1-/-mice, respectively; Stat1 (+) and (-), presence or absence of functional Stat1 alleles; hAPN (+) and (-), presence or absence of homozygous hAPN transgenes; MM, molecular markers in bp. (D) Hematoxylin/eosin-stained lung sections 8 days after HCoV-229E-37 infection. Global severe inflammatory reactions with massive neutrophilic infiltrations were prominent in the lung of hAPN+/+Stat1-/- mice (3 and 4), whereas no histopathological changes could be detected in the lung of nontransgenic mice (1 and 2). (Scale bars: 1 and 3, 100 μm; 2 and 4, 200 μm.)