Coronavirus induction of class I major histocompatibility complex expression in murine astrocytes is virus strain specific

infected glial cell cultures is not a direct consequence of infection, but is instead due to the release of a soluble factor into the medium that requires continual virus production (33, 53, 54) . The presence of a non-IFN-like soluble factor was demonstrated in supernatants from A59-infected glial cells that had been exposed to UV light to inactivate the virus. Similarly, our data show that UV-inactivated A59 and A59like recombinant coronavirus strains are not able to induce class I activity in purified astrocytes (Table 4 ). Virus inactivation in the UV-treated virus preparations was confirmed by plaque assay using DBT cells (data not shown). However, class I-inducing activity was not detected in the supernatants collected on days 3 and 7 p.i. from A59-infected astrocytes and exposed to UV light to inactivate the virus (Fig. 5) , while supernatants that were not exposed to UV light and thus, contained infectious virus, were able to induce class I. Induction was not inhibited by the addition of antibodies specific for IFN-'y or IFN-ot/~ to the astrocytes before A59 infection (Table 5 ). Finally, there was no evidence of the presence of TNF-ot in UV-treated supernatants of A59-infected astrocytes (data not shown). These data suggest that class I induction is a direct consequence of A59 infection itself, and does not occur indirectly as a result of the release of a soluble class I inducer into the astrocyte medium. Data are also included for uninfected astrocytes exposed to IFN-y (100 U/ml) for 48 h before assay on day 3 p.i. A and B are two experiments that are representative of four experiments yielding similar results.