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Influence of Type and Concentration of Sera in vitro on Susceptibility of Genetically Resistant Cells to Mouse Hepatitis Virus

Department of Pathobiology, The Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland 21205, U.S.A.

The type and concentration of sera used to support macrophages was found to influence the in vitro destruction of macrophages from genetically resistant C3H mice by the PRINCETON strain of mouse hepatitis virus, and the accompanying conversion of mouse hepatitis virus (PRINCETON) to the variant virus, mouse hepatitis virus (C3H). Cells incubated in 20% horse serum were more susceptible to destruction than those in 90% horse serum. Susceptibility was greatest in the presence of 10% foetal calf serum, while cells in 10% mouse sera were the most resistant. Differences in susceptibility were as great as 10,000 TCD 50. The sera had no direct effect upon either mouse hepatitis virus (PRINCETON) inoculum virus or the released variant virus, but appeared to influence intracellular adaptation of virus. In plaque titrations using reduced concentration of horse sera, mouse hepatitis virus (PRINCETON) produced small plaques on C3H cells. The variant virus, mouse hepatitis virus (C3H), produced both large plaques characteristic of mouse hepatitis virus (C3H) and small plaques characteristic of mouse hepatitis virus (PRINCETON). The results suggest that a fraction of mouse hepatitis virus (PRINCETON) virus multiplies in resistant C3H cells, and is then converted to mouse hepatitis virus (C3H), and that mouse hepatitis virus (PRINCETON) continues to be carried in stocks of mouse hepatitis virus (C3H) during passage in C3H cells. The outcome of infection of genetically resistant C3H macrophages with mouse hepatitis virus (PRINCETON) was greatly influenced by the type and concentration of sera used to support macrophages.

^* Present address: National Institute of Allergy and Infectious Diseases, Rocky Mountain Laboratory, Hamilton, Montana 59840, U.S.A.

Received 20 April 1970; accepted 20 April 1971.