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SUMMARYTwenty-one monoclonal antibodies reactive with Junin virus structural proteins were produced and characterized. Using radioimmunoprecipitation and Western blot assays, 13 were found to react with the nucleoprotein, seven with the surface glycoprotein and one failed to react, but showed a fluorescent antibody staining pattern consistent with other glycoprotein-specific antibodies. In radioimmunoprecipitation assays, glycoprotein-specific monoclonal antibodies reacted not only with the 35K

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Guinea pigs infected with Argentine hemorrhagic fever virus (Junin) were treated with pooled, homologous convalescent sera. Use of 15,000 or 5,000 therapeutic units of immune sera prevented all signs of illness when administered within 24 hr of infection. We could also prevent illness and death in infected guinea pigs as late as 6 days after infection if we used more antisera (30,000 therapeutic units/kg). In some treatment groups, surviving animals developed a late neurological syndrome with prominent rear-limb paralysis. Treated animals typically expressed higher viral titers in the brain than in any other organ. There appeared to be no acute exacerbation of disease by antibody administration. Our data suggest that, after replicating peripherally, Junin virus infects the brain where circulating immunoglobulins may not eliminate viable virus. Subsequent replication of virus in the brain may generate a neurological phase of the illness. Histological examination of brains from guinea pigs in treatment groups favoring the neurological phase of illness showed encephalitis, meningitis, and swollen astrocytes, suggestive of neuronal degeneration. There is likely a delicate balance among presence of virus in the brain, the amount of antibody transported into the central nervous system, and the occurrence of this late neurological aspect of experimental Argentine hemorrhagic fever. Further study of this model may elucidate factors relevant in understanding the continuing problem of the late neurological syndrome seen in some human cases of Argentine hemorrhagic fever treated with immune plasma.

Nine patients with laboratory-acquired Rocky Mountain spotted fever were seen during the period 1971 to 1976. Investigation of each case revealed either definite or probable exposure to an aerosol containing infectious rickettsiae; in no case was there evidence of parenteral exposure either by accidental self-inoculation or by tick bite. These illnesses are believed to represent infection acquired via the respiratory route. This report emphasizes the aerosol hazard of Rickettsia rickettsii in the laboratory and discusses the possibility of respiratory transmission of Rocky Mountain spotted fever in nature. The illness occurred only in personnel who had received either no vaccination or the primary series of the commercial (Lederie) vaccine against this infection. Other personnel who had received the primary series with multiple booster vaccinations demonstrated increased immunity as measured by humoral antibody titers and rickettsial antigen-induced lymphocyte transformation; no cases of clinical disease developed in these multiply-vaccinated personnel.