The present study demonstrates the inhibitory effect of human recombinant interferons (r-Hu-IFN) alpha and gamma, and that of highly purified natural human interferon beta on the replication of simian foamy virus type 1 (SFV1) in human AV3-cell cultures. All IFN led to strong inhibition of the SFV1 cytopathic effect. Electron microscopy showed a 70 to 95% decrease in viral particles. Significant inhibition of virus-associated reverse transcriptase activity was found in supernatant fluids of infected IFN-treated cultures. Metabolic labelling of the virus confirmed the inhibition of extracellular release of SFV1. PAGE analysis of immunoprecipitates indicated a reduction in viral-specific protein bands. Altogether, these results indicate that the mechanism of inhibition of Spumavirinae infection by interferon differs from that described for the other Retroviridae, and particularly for types B, C and D viruses. Our data is of therapeutic interest since Spumavirinae have been linked to pathological processes such as de Quervain thyroiditis.

The effects of Plasmodium falciparum proteins released in asexual blood stage culture supernatants on human T-lymphocytes from malaria non-immune donors were examined. Supernatants from several plasmodial strains stimulated both CD+4 and CD+8 T-lymphocytes to proliferate and secrete interferon gamma in vitro. Active moieties were predominantly released during the final stages of the parasite cycle. They were enriched by gel filtration and were further purified by anion-exchange and Superose 12 column fast protein liquid chromatography. Three active fractions of apparent 250, 70 and 18 kilodaltons were identified. The parasitic origin of the predominant 70-kilodaltons protein(s) was shown by biosynthesis experiments with radioactive amino acid precursors and was also demonstrated by in vitro translation of parasitic mRNA species. Interestingly, antibodies to the 70-kilodalton exoprotein(s) also reacted to a schizont protein of similar molecular weight.

Three cell lines tera I, tera II, and PA1, derived from human teratocarcinomas were tested for their capacity to produce interferon (IFN) and for their sensitivity to both human IFN-alpha and IFN-beta. When treated with Newcastle disease virus or Sendai virus, or a synthetic polyribonucleotide, poly(rI):poly(rC), tera I cells produced no IFN and the 2',5'-oligoadenylate (2-5A) synthetase enzymatic pathway was not activated, although there was an increase in protein kinase. In contrast, tera II and PA1 cells produced IFN and both enzymatic activities were detected. IFN treatment has no effect on the growth of any of the cell lines. Tera I and PA1 cells did not develop resistance to challenge with vesicular stomatitis virus or encephalomyocarditis virus, but the growth of a type-C baboon retrovirus was inhibited. Tera II cells were protected against all three viruses. It appears that human teratocarcinoma cell lines can thus differ greatly in their ability to produce IFN and to respond to it.