Velma C. Chambers

The prolonged persistence of Western equine encephalomyelitis virus in cultures of strain L cells

Abstract Inoculation of cultures of strain L cells with Western equine encephalomyelitis (WEE) virus was followed by multiplication of virus and varying degrees of cellular degeneration. Large viral inocula frequently caused less degeneration than smaller inocula. Surviving cells proliferated and eventually produced thickly populated cultures. Some of these cultures continued to produce virus over a period of many months. As long as virus persisted in cultures, the cells were immune to mass destruction by superinfection from newly added virus. After virus disappeared from cultures, either spontaneously or following a period of exposure to antiserum, cultures reverted to increased susceptibility to small inocula. The hypothesis proposed to explain these observations postulates that noninfectious virus, either inactivated or incomplete, protected cells in infected cultures by autointerference. Periodic loss of interfering activity presumably rendered individual cells susceptible to infection from time to time, thereby providing a continuing supply of susceptible cells in infected cultures over long periods of time.

Rabbit kidney vacuolating virus: Ultrastructural studies☆

Abstract The ultrastructure of the rabbit kidney vacuolating (RKV) virus, grown in secondary cultures of rabbit kidney cells, was studied by electron microscopy of (1) sectioned cells and (2) negatively stained virus particles. Abundant intracellular virus particles were observed in thin sections of tissue culture cells harvested on the 6th and 7th days after inoculation with RKV virus. The RKV virus particles consisted of a dense, 38-mμ core and an outer capsid. The capsid was approximately 47 mμ in its outer diameter and was composed of capsomeres about 50 A in diameter. Elongated forms with a surface structure composed of capsomeres were observed in negatively stained preparations. Filaments or tubules of smaller diameter than the elongated forms were sometimes seen in close association with linear arrays of intracellular virus particles. Negative staining often revealed clusters of virus particles in which one to several particles were enclosed within a membrane.

Growth of Neurotropic Viruses in Extraneural Tissues. I. MM Virus in the Feet of Hamsters

Summary and Conclusion After inoculation into the pad of the hind foot of a hamster, MM virus increases in amount in the local tissue. Subsequent increases in virus in the blood and viscera are in turn followed by appearance of the virus in the central nervous system. It appears certain that the virus grows in the foot. Whether the growth occurs in subcutaneous tissue, muscles, or nerve endings was not determined in these experiments.

Neurotropic Viruses in Extraneural Tissues. III. MM Virus in Human and Murine Testicular Tissues.

Conclusions MM virus multiplied extensively in 9 serial passages in mouse testicular tissue in vitro and in 4 serial passages in human testicular tissue in vitro. Fluid from the last tissue of each series represented a 10-13 dilution of original inoculum. These experiments do not exclude the possibility that the virus may have multiplied in the very minute amounts of muscle tissue present in the cultures. The virus multiplied more slowly and persisted longer in human tissue than in mouse tissue.