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Splenectomy of mice genetically susceptible to Listeria monocytogenes genetically susceptible mouse strains increased their resistance to L. monocytogenes infection but had no effect on the course of infection in L. monocytogenes-resistant mice. However, splenectomy led to a dramatic decrease in the production of colony-stimulating factor and interferon after L. monocytogenes infection in all mouse strains examined.

Our investigations of interferon induction by rotaviruses showed that only when cells were pretreated with interferon, i.e., primed, could infectious rotaviruses induce significant quantities of interferon. As little as 0.5 U of interferon provided sufficient priming for this induction. UV-irradiated rotaviruses induced significant levels of interferon, and priming only marginally enhanced the yields. Neither heat-inactivated virus nor serum-neutralized virus was able to induce interferon, even when cells were primed. When cells were treated with purified virus double-stranded RNA in the presence of DEAE-dextran to facilitate uptake, interferon was induced, although priming did not enhance yields. These results strongly implicate the viral double-stranded RNA as the effector for interferon induction. The insensitivity of rotaviruses to interferon in vitro was also studied. Results suggested that this lack of sensitivity was not due to any inherent resistance of the virus to the antiviral proteins, but rather to lack of activation of cellular enzymes exhibiting antiviral activity.

Antisera to SA11 virus proteins were prepared by immunizing rabbits with individual polypeptides separated by polyacrylamide gel electrophoresis under reducing or nonreducing conditions; the resulting antisera were characterized by four immunological methods. Results of complement fixation tests with double-shelled rotavirus particles and sera raised against reduced or unreduced proteins of the outer shell of the virus suggested the presence of common antigenic determinants in the outer capsid layers of SA11 and the Northern Ireland strain of calf rotavirus. In this test, antisera to outer shell polypeptides gp34 (O2) and gp25 (O4) cross-reacted with calf rotavirions, whereas those to p62 (O1) and p26 (O3) reacted only with the homologous virus. Antisera to the reduced outer shell proteins of the virus did not neutralize viral infectivity, nor did they possess hemagglutination inhibition activity. Evidence suggesting the presence of type-specific antigenic determinant(s) in the major inner protein p42 (I4) of SA11 virus, capable of inducing neutralizing antibody, is presented and discussed. Antisera produced against unreduced gp34 and p26 polypeptides of the virus contained type-specific neutralizing antibodies. Polypeptide gp34 was also capable of inducing hemagglutination inhibiting antibody. All of the antisera to unreduced polypeptides had agglutinating activity against double-shelled particles of homologous and heterologous rotaviruses.