The pathogenesis of pneumonia virus of mice (PVM) and human respiratory syncytial virus (HRSV) in BALB/c mice were investigated by using in situ hybridization to detect virus mRNA in fixed lung sections. Following intranasal inoculation with 120 p.f.u. PVM the pattern of hybridization showed that virus mRNA was initially detected within 2 days in alveolar cells. As the infection progressed the number of hybridizing alveolar cells increased and signal was also detected in cells lining the terminal bronchioles. By days 4 to 5 post-infection areas of morphological abnormality could be seen, particularly in the strongly hybridizing regions of the lung, and this correlated with the appearance of clinical signs of infection. In animals which survived the infection virus-specific mRNA could not be detected 10 days post-infection. Mice infected with 1500 p.f.u. HRSV showed significant differences in the distribution of virus-specific mRNA when compared to the pattern seen with PVM. HRSV mRNA was detected over large areas, but predominantly in peribronchiolar and perivascular regions of the lungs 5 days post-infection. The yield of PVM from infected mouse lungs was considerably higher than that of HRSV. The possible implications of these results for the use of the mouse model for pneumovirus infections are discussed.


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