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Polypeptide structural analyses were performed by tryptic peptide mapping to assess the relationship between isolates of Ebola virus obtained in Sudan and Zaire. The results of these analyses indicate (1) that the Sudan and Zaire isolates are unique viral agents, (2) that multiple isolates within each group bear close resemblance to one another, (3) that suggestive evidence exists of conservation of homologous structure in the VP-2 (virion protein no. 2) nucleocapsid proteins of these viruses, and (4) that protein differences between the two Ebola virus subtypes appear to reside in the VP-1 and VP-3 virion polypeptides.

As a model for the pathogenesis of Lassa fever in humans, nine rhesus monkeys were inoculated with Lassa virus. Three monkeys had had a previous asymptomatic experimental infection with Mozambique virus, a closely related arenavirus; these monkeys were protected from illness and viremia and manifested only mild pathologic lesions. The other animals developed severe disease and viremia. At necropsy, hepatocellular necrosis, interstitial pneumonia, a unique pulmonary arteritis, adrenal gland necrosis, encephalitis, and uveitis were prominent pathologic lesions which correlated with the organ titers of virus. One animal infected with Lassa virus developed prolonged viremia, a typical immune response, and sudden onset of lower limb paralysis after recovery; at necropsy chronic proliferative arteritis of the spinal cord, brain, and heart was evident. Similarities and differences in the pathologic lesions in this model and Lassa fever in humans indicate that care must be taken in interpreting the results of experiments concerning immune prophylaxis, pathogenesis, and treatment in rhesus monkeys.

Ebola viruses isolated during outbreaks of acute hemorrhagic fever in Africa from 1976 to 1979 were examined by T1 oligonucleotide mapping of virion RNA. Two Ebola virus subtypes distinguishable by their oligonucleotide patterns were involved in the outbreaks of the disease during this three-year period. The first type was isolated in Zaire in 1976 and again in 1977; the second type caused outbreaks in Sudan in 1976 and again in 1979. Oligonucleotide patterns of the two groups of Ebola viruses (Zaire and Sudan) were remarkably similar within the group but differed between groups by approximately 60 oligonucleotides. We can conclude from this study (1) that the outbreaks of hemorrhagic fever which occurred concurrently in 1976 in Zaire and Sudan were caused by viruses that are genetically distinct; (2) that compared with other RNA viruses there was an unusually high genetic stability among viruses within Zaire and Sudan over two- and three-year periods, respectively; and (3) that the two genetic subtypes probably evolved from a common ancestor since they share common oligonucleotides.