Increase of cellular murine leukemia virus reverse transcriptase in interferon-treated cells.

The addition of mouse interferon (IFN) to AKR murine leukemia virus (MuLV)-producing NIH3T3 cells inhibited the extracellular appearance of AKR MuLV when assayed for reverse transcriptase activity or infectious virus production. IFN treatment had no detectable effect on proviral DNA formation during infection nor on the level of viral RNA in virus-producing cells. However, addition of IFN did alter the level of cellular viral reverse transcriptase activity. Chromatography of extracts from virus-producing cells on poly(G)-Sepharose columns revealed two peaks of reverse transcriptase activity. Peaks I and II eluted at 0.45 M and 0.65 M NaCl, respectively, while the cellular DNA polymerase beta eluted earlier at 0.3 M NaCl. IFN treatment of these chronic virus producer cells resulted in a 5-fold increase in peak I whereas peak II and polymerase beta remained essentially unchanged. When reverse transcriptase from purified virions was similarly chromatographed on poly(G)-Sepharose, all of the enzymatic activity eluted as peak I. Thus, the reverse transcriptase in peak I from cell extracts appears to be the form which is present in mature virions. Contrary to the results with chronic virus-producing cells, IFN treatment prior to exogenous infection with MuLV did not alter levels of reverse transcriptase peaks I and II or polymerase beta. These results provide further evidence that the major effect of IFN occurs at the level of MuLV maturation and assembly.