Enhanced Resistance Against Junin Virus Infection Induced by Corynebacterium parvum

Abstract

The effects of intraperitoneal administration of Corynebacterium parvum on the course of Junin virus infection in mice were investigated. This treatment produced enhanced resistance to the virus infection, evidenced by an increase in both survival times and the proportion of survivors. The protective effect was dependent upon the dose of C. parvum , and 280 μg/g of body weight was found to be the optimal dose. In various experiments, about 80% of the infected animals receiving this dose survived, whereas survival ranged between 0 and 20% among untreated infected mice. Maximal protection was afforded by C. parvum when administered simultaneously with the virus. A smaller but significant degree of resistance was induced by C. parvum given 3 or 6 days after infection. C. parvum injected before infection was ineffective. Viral titers measured in the brains of C. parvum -treated and untreated mice at various times after infection were found to be comparable. In addition, there were no significant differences between circulating-antibody titers measured either by neutralization tests or by complement fixation. Depression of the reticuloendothelial system by treatment with silica particles also resulted in enhanced resistance to Junin virus infection, suggesting that the protective effect of C. parvum is not likely to be due merely to its capacity to stimulate macrophages. The present data, highlighting that the presence of high titers of Junin virus and disease do not necessarily correlated, suggest that in mice this disease is not the consequence of cell damage caused directly by the virus but of a still undefined indirect mechanism induced by the virus, not necessarily mediated by macrophages.

Enhancement of Natural Resistance to Influenza Virus in Lipopolysaccharide-Responsive and -Nonresponsive Mice by Propionibacterium acnes

“…However, it should be noted that P. acnes can also activate suppressor macrophages (10) which, in turn, may limit immunopathological damage resulting from infiltrating cytotoxic cells. Suppression of cytotoxic T-cell activity has been proposed as a mechanism for the P. acnes-induced enhancement of murine resistance to the hemorrhagic arenavirus Junin (9); however, the kinetics of the P. acnes-induced protective effects observed in our studies differ from those observed in the Junin studies.…”

“…Certain strains of propionibacteria which were formerly classified as Corynebacterium parvum have the ability to cause intense stimulation of the mononuclear phagocyte system, as manifested by enlargement of the spleen and liver and enhanced clearance of particles from the bloodstream (2, 10,24,37). Depending on the time and route of inoculation, these strains can enhance antibody production (2,10,26,37) and resistance to viral (9,11,23,28,30,35,36), bacterial (1,15,45), and protozoan (8,14) infections. The macrophage appears to be a critical element for many of the stimulatory activities induced by the propionibacteria (2), and it is believed that macrophage activation is primarily responsible for augmentation of resistance.…”

The long‐standing history ofCorynebacterium parvum, immunity, and viruses

“…Moreover, Budzko et al 32 showed a dose‐dependent response in Junin virus infection in mice: 280 mcg injected intraperitoneally uplifted the survival rate to 80% compared with 20% of the untreated animals. Naficy et al 33 reported the antiviral activity of five different C.parvum strains in comparison with simple vaccination, stressing an effective adjuvant role.…”