Virus of Bats Antigenically Related to Group B Arthropod-Borne Encephalitis Viruses

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Abstract
A neurotropic virus from bats was isolated in mice and a potent hemagglutinin (> 1:10240) for this isolate was prepared from infected brains of suckling mice. The capabilities of this virus to yield a hemagglutinin on the basis of temperature of incubation (4 C, 25 C or 37 C.) and rigid requirements of pH (6.4 to 6.6 for freshly prepared hemagglutinin, and 6.0 to 6.5 after 35 days of ripening) suggest that the antigen is derived from a virus that is a member of Casals'' B group of arthropod-borne viruses. Hemagglutination-inhibition tests demonstrate that the hemagglutinin of bat virus is inhibited by antiserums for St. Louis encephalitis (SLE), Japanese B encephalitis (JBE), and West Nile (WN) at low titers, but that it reacts best with its homologous antiserum. Results of reciprocal complement-fixation tests suggest that the bat virus shares an antigen in common with St. Louis encephalitis virus, as indicated by fixation of complement with St. Louis encephalitis antiserum in the presence of bat antigens. The fixation is of low order, and it is not reciprocal. No immunologic relationship between the bat virus and other neurotropic viruses (Eastern equine encephalomyelitis, Western equine encephalo-myelitis, Venezuelan equine encephalitis, Japanese B encephalitis, lymphocytic choriomeningitis, or rabies) could be demonstrated by complement-fixation tests. Further evidence that the bat virus is immunologically related to, but distinct from, St. Louis encephalitis virus is obtained from the fact that this agent is neutralized by St. Louis encephalitis hyperimmune serum, without any evidence of reciprocal activity. Additional neutralization studies with the bat virus (1410-19) demonstrate a distinct crossing with hyperimmune serums prepared against the viruses of West Nile, Murray Valley (MVE) and Japanese B encephalitis. Immune serums prepared against the bat virus neutralize the homologous virus, and, in addition, are protective against Ntaya virus; therefore, on the basis of neutralization tests, it would seem that there is a closer interrelation between Ntaya and the bat salivary gland viruses than that which exists for the viruses of WN, MVE, JBE, and SLE. Hyperimmune serums for Western equine encephalomyelitis, Eastern equine encephalomyelitis, Venezuelan equine encephalitis, lymphocytic choriomeningitis, encephalomyocarditis, and rabies viruses have no neutralizing effect against the bat virus. Inasmuch as the hemagglutination-inhibition test seems to be the more sensitive serologic technic for demonstrating antigenic relationship between broadly related arthropod-borne viruses, the failure to obtain identical titers of inhibition (with the antiserums prepared against the bat virus and those of St. Louis, West Nile, and Japanese B encephalitis) suggests that the bat salivary gland virus is probably a distinct, new entity.
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