Lassa fever as it was first noticed early in 1969 in three missionary nurses in Nigeria will be described by Frame et al. The disease later affected two laboratory workers at the Yale Arbovirus Research Unit (YARU) in New Haven. Two of the nurses and one of the laboratory workers died.
Studies at YARU have been concerned with attempts to isolate and establish the aetiological agent in experimental hosts, cell cultures and mice and with its antigenic characterization. A detailed account of this work will be published elsewhere, but the current interest In this virus seems to warrant an advance summary.
Sixteen virus isolates, subsequently proved to be alike, were obtained from the following materials : serum taken between days 6 and I2 after onset from the two nurses and laboratory worker who died ; serum and pleural fluid taken between days 5 and 14 from the surviving nurse; and serum (days 7 and 9), throat washings (days 9 and 14) and urine (days 9, 17 and 32) of the surviving laboratory worker. (The infection in this last patient will be described elsewhere).
The isolations of Lassa virus were done in Vero cells. A cytopathic effect appeared as early as 4 days after inoculation, and in some instances progressed to complete destruction of the cell sheet within 5-8 days. In addition, distinct plaques measuring 2 mm in diameter were observed 5-8 days after inoculation. Both the cytopathic effect and the production of plaques were speciflcally inhibited by convalescent serum from the two patients who survived.
Infected Vero cells stained with Giemsa showed basophilic pleomorphic aggregates localized in the cytoplasm; the aggregates were similar in appearance to those described for Junin virus. Electron microscopy revealed spheroid particles closely resembling those reported for lymphocytic choriomeningitis (LCM) virus. Lassa virus failed to infect Singh's Aedes aegypti and A. albopictus cell lines.
Lassa virus was propagated by intracerebral inoculation to 1 day old mice, which showed no signs of illness but later had antibody in their serum at the same time that virus was detected in their urine. In contrast, young adult mice similarly inoculated became ill, developed convulsions and died. This combined picture is reminiscent of LCM virus infection in mice.
Lassa virus is inactivated by sodium deoxycholate and by betapropiolactone. It appears to contain RNA, as determined by incorporation of 5-bromodeoxyuridino into the medium. As calculated by flltration, the virus has a diameter between 70 and 150 nm.
Complement-fixing antigens could be prepared from infected Vero cells and from infected newborn mouse brain tissuo harvested 7 days after inoculation. In serological studies involving large-scale complement-fixing tests as well as haemagglutination-inhibition and plaque reduction neutralization tests, Lassa virus was found to be distinct from more than 200 viruses, including most known arboviruses. By complement-fixing test, a reprcducible, low-level relationship was shown between Lassa and LCM wiruses and also some members of the Tacaribe group.