1. The cause for the phenomenon of hemagglutination with heated PVM suspensions has been sought. 2. Evidence in wide variety indicates that the component responsible for hemagglutination is the virus particle itself. 3. The virus is capable of combining with a substance present in lung tissue of certain mammalian host species susceptible to infection by PVM. The occurrence of such combination accounts for a number of unusual properties manifested by this pneumotropic virus.

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In a previous communication (1) evidence was presented which indicated that the hemagglutination observed with heated suspensions of lungs infected with pneumonia virus of mice (PVM) was caused by the virus itself, even though the virus had been rendered non-infectious in the course of heating. From the available data it was concluded that the virus has the capacity to combine firmly not only with mouse or hamster erythrocytes but also with lung tissue particles from certain host species, and that appropriate heating serves to release the virus from combination. The occurrence of such combination with PVM appeared to account for its capacity to cause hemagglutination and for other unusual attributes of this virus.It is the purpose of this paper to present additional evidence in support of the conclusion (1) that combination between PVM and tissue particles does occur, and to elucidate further the mechanism and significance of this phenomenon. I t will be shown that the virus can be released from combination by treatment with alkali. Further evidence will be presented to demonstrate that PVM, as it exists in vivo, is not combined and that combination occurs in the process of grinding tissues infected with it. Moreover, it will be shown that free infectious virus recovered by a technique described in the preceding paper (2) is not combined and that estimates of its titer can be made directly both in vivo and in vitro. It will be shown that in demonstrating the presence of PVM or in estimating its titer the results obtained by in vitro techniques are more accurate than corresponding results obtained in vivo. Finally, evidence will be presented indicating that the virus may occur in several different states and that it possesses certain distinguishing properties in each.

The results of neutralization tests with PVM and serum obtained from numerous animal species indicate that antibodies agaiust this virus were present in the blood of all mammalian species tested, as not in that of fowls, and that their incidence in various species was widely different. They indicate, also, that in certain species, particularly the cotton rat, there were marked seasonal variations in the incidence of such antibodies; in the late winter and spring the incidence was much higher than during the summer and fall seasons. Cotton rats and hamsters which did not possess neutralizing antibodies against PVM were susceptible to manifest pulmonary infection with this virus, irrespective of the effects of previous experiments upon them, whereas those which possessed such antibodies were immune. It is suggested that circulating antibodies against PVM were present as a result of preceding infection with a latent virus; either PVM or an agent closely related to it in antigenic composition. Appropriate non-specific stimuli, e.g. the intranasal injection of suspensions of normal chick embryos, induced the development of neutralizing antibodies against PVM with significantly greater frequency in each of three species than occurred in control animals. Materials derived from patients with primary atypical pneumonia yielded results almost identical to those obtained with normal chick embryo suspensions. It is suggested that such materials, like the other non-specific stimuli employed, were effective in evoking a specific antibody response, because they unbalanced an equilibrium which previously existed between animal host and latent pneumotropic virus.

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A filterable agent was isolated from the blood and from washings of the upper respiratory passages of a young laboratory worker during a mild, acute, febrile illness. This agent was identified as a strain of Venezuelan equine encephalomyelitis virus. Circulating specific complement-fixing and neutralizing antibodies not present in sera withdrawn during the acute phase of illness were demonstrated in sera obtained during convalescence. A fellow laboratory worker who became similarly ill simultaneously also developed during convalescence specific circulating antibodies not present prior to illness.