Abstract
Rickettsia prowazekii Madrid E established persistent infections in cultures of growing L-929 cells. Although some L-929 cells died, the cultures survived, remained infected with rickettsiae, and continued to grow. R. prowazekii Madrid E also induced interferon in L-929 cell cultures, and this interferon modulated rickettsial growth. Production of interferon (anti-viral activity) by cultures of R. prowazekii-infected L-929 cells was directly related to the initial rickettsial infection and was blocked by erythromycin. The media collected from R. prowazekii-infected L-929 cells suppressed not only the replication of vesicular stomatitis virus but also the growth of R. prowazekii in fresh L-929 cells. Both anti-viral and anti-rickettsial activities in the media were neutralized by antibodies against murine interferons-alpha and -beta, but not by antibodies against murine interferon-gamma. In addition, a commercial preparation of virus-induced interferons-alpha and -beta also suppressed rickettsial growth in L-929 cells. The combination of treating L-929 cells with this virus-induced interferon and infecting them with R. prowazekii killed some of the L-929 cells.
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