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The present study concerns the monitoring of serum-interferon (serum-IFN) levels among 189 patients followed after and sometimes during an acute episode of malaria due mainly to Plasmodium falciparum (P. falciparum). Of these patients, 110 known to have no other parasitic or infectious disease were followed in France; 79 were from Thailand, among which 25 cases of neuromalaria were diagnosed. In a first four-month survey conducted in France, among 100 patients seen after the acute attack, serum-IFN-gamma was characterized among 87% cases for which at least two sera were controlled, whereas in a healthy population no serum-IFN was present. When efforts were concentrated on screening ten cases during the first 48 h of the febrile attack, serum-IFN-alpha was mainly characterized, whereas serum-IFN-gamma was present only once. Elevated leukocyte 2',5' oligoadenylate synthetase levels were found among several IFN-alpha positive patients of this study group. A peculiarity pertaining to the patients from Thailand was that one-third (25 cases) were cerebral malaria cases. Among these, 15 were followed under hospitalization during the first 96 h. In this study group, the onset of circulating immune interferon was found to be preceded or accompanied by that of IFN-alpha. Thus, if serum-IFN-gamma is largely characterized among malaria patients followed after the acute attack, it is possible that the onset of circulating immune interferon is generally preceded by that of IFN-alpha.

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We demonstrate that Simian Foamy viruses (SFV) types 1, 2, 4 and 10 do not induce Interferon (IFN) production in mouse and primate (simian and human) cell lines, but that their cytopathogenic effect is blocked by this viral inhibitor. The mechanisms of action of IFN seems to be different from that of other Retroviridae. No trapping of virions appears in treated cells examined by ectron microscopy. Moreover, neither precursor nor mature virus particles were observed in infected cultures submitted to IFN treatment.