SUMMARYThe virus of Tanapox isolated from the lesions of patients during an outbreak of mild disease in Africa has been found to be indistinguishable in its biological and serological properties from a virus isolated from outbreaks of a pox virus infection in monkeys in primate centres in America. The natural hosts of this virus are believed to be African monkeys and ‘Tanapox virus’ is proposed as a suitable designation for the virus.

In the present studies ten common species of Western North American mosquitoes have been tested for their ability to act as vectors of Japanese B encephalitis virus (see summary Table XII). The strain of Japanese B encephalitis virus which was used was adapted to direct mouse brain passage, probably a disadvantage, but no freshly isolated strain was available. Of the ten species of mosquitoes tested, seven were demonstrated to be laboratory vectors. These seven species represent three genera (Culex, Aedes, and Culiseta). In previously reported work Japanese and Russians had only incriminated five species of two genera (Aedes and Culex) (1–3). Transmission was made to mice 21 times and to a chicken once. Two attempts to infect mosquitoes from an infected chicken were unsuccessfui, but no significance is attached to so few experiments. Repeated tests for virus in the eggs, or in imagines reared from eggs of infected female mosquitoes have been negative. In this we failed to confirm results claimed by Japanese investigators (5, 6). These data, in addition to the published accounts by Japanese and Russian workers of the natural epidemiology of this disease lead us to believe that this virus might well establish itself in North America, especially if introduced in those areas where our native encephalitides are now endemic. These studies also indicate that species of mosquitoes (Culex tarsalis, Culex pipiens, See PDF for Structure Aedes dorsalis, and Culiseta inornata) now known to be fully incriminated vectors of the Western equine or St. Louis encephalitis viruses can also serve as laboratory vectors of the Japanese B virus. Methods for the effective abatement of these species should be further developed and put into practice if future epidemics of encephalitis of the Western equine, St. Louis, or Japanese B types in Western North America are to be prevented or brought under control.

Isolates of virus from the brain tissue of two naturally occurring cases of progressive multifocal leukoencephalopathy in rhesus monkeys (Macaca mulatta) have been characterized. Both isolates were demonstrated to be simian virus 40 (SV40) by serological tests and analysis of cleavage fragments of viral deoxyribonucleic acid produced by restriction endonuclease from Haemophilus influenzae. SV40 virions and the nonvirion T antigen were demonstrated in the brain lesions of one monkey by the fluorescent antibody staining technique. SV40 was not demonstrated in the brain of normal rhesus monkeys from the same colony with use of the same methods of viral isolation or demonstration of antigen.

Simian hemorrhagic fever (SHF) was induced in three species of monkeys (Macaca mulatta, M. radiata and M. fascicularis) using plasma from animals that died with SHF in the 1967 outbreak at the California Primate Research Center. The disease was uniformly fatal in all three species with death occurring by day 5 in M. radiata and M. fascicularis and by day 7 in M. mulatta. Serial studies of hemostasis were consistent with the occurrence of disseminated intravascular coagulation, particularly in the M. mulatta. Studies of pathology were typical of previously reported findings in SHF and support the possibility of intravascular coagulation. The role of intravascular coagulation in the pathogenesis and outcome of SHF remains uncertain but studies of the influence of heparin on the disease are in progress.

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