Poly(I).poly(CU) or interferon treatment inhibited multiplication of the xenotropic baboon type C endogenous retrovirus M7 in chronically infected human AV3-M7 cells, as determined by a reverse transcriptase (RT) assay and electron microscopy. Furthermore, this polynucleotide induced 2′5′ oligoadenylate (2′5′A) synthetase activity. In contrast to interferon (IFN), poly(I).poly(CU) did not give rise to the appearance of a trapping phenomenon observable by electron microscopy. When AV3-M7 cells were treated simultaneously with poly(I).poly(CU) and anti-IFN-β/α antibodies, the induction of 2′5′A synthetase was abolished without any alteration of the inhibitory effect of RT activity. Taken together, these results suggest that different mechanisms are used by poly(I).poly(CU) and IFN in blocking type C retrovirus multiplication.


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