Alveolar macrophages from PRRSV-infected and naïve pigs were placed into culture and infected with PRRSV laboratory strain SD-23983. Permissiveness increased with time in culture, and macrophages from infected pigs could be superinfected. Addition of actinomycin D, an inhibitor of mRNA synthesis, blocked infection. Interferon-γ reduced infection in cultures, while the addition of tumor necrosis factor-α or interleukin (IL)-10 did not affect permissiveness. IL-4 produced a marginal increase in the percentage of infected cells, but without a detectable increase in virus yield. These results suggest that the PRRSV-permissive population of cells in culture arises from a non-permissive precursor population and depends on new mRNA synthesis.
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