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Mumps virions of the Enders' strain were examined for polymerase activity in vitro. An RNA-dependent RNA polymerase was found to be associated with the virion. The general properties of the reaction appear to be similar to those described for other paramyxoviruses.

SummaryThe multiplication cycles of Sendai, mumps, and Newcastle disease viruses were compared with that of influenza A virus in regard to site of antigen production in the cell. Single-cycle infections were followed using fluorescent antibodies prepared from infection-convalescent immune sera shown to contain anti-S and anti-V antibodies. In cells infected with influenza A virus antigen was first detectable in the nucleus and became abundant there by the time antigen appeared in the cytoplasm. In cells infected with Sendai, mumps, or Newcastle disease viruses earliest detectable antigen was found as small granules scattered throughout the cytoplasm. Antigen granules increased in size and number to form large cytoplasmic aggregates and masses. Multiplication of Sendai, mumps, or Newcastle disease viruses did not include production of antigen in the nucleus detectable by fluorescent antibody at any stage of the cycle.

The simian sarcoma virus type 1 (SSV-1) and its associated virus (SSAV-1), C-type RNA viruses, were found to possess a 60 to 70S RNA and a RNA-dependent DNA polymerase. Endogenous enzyme activity requires magnesium and is inhibited by ribonuclease. The enzyme utilizes the 60 to 70S RNA as a template and the product of this enzyme consists of DNA, as shown by physical and chemical methods. The product DNA specifically hybridizes to the SSV-1/SSAV-1 60 to 70S RNA.

Three hundred and fifty-six bone marrow tissues obtained from patients of a general hospital were tested for spontaneous production after cultivation in vitro of interferon-like substances (ILS). Seventeen percent of the tissues produced ILS that protected human, but not chick, embryo cell cultures against the cytopathic effects of challenge virus infection. The incidence of ILS did not correlate with leukemia or other neoplastic diseases, or with any non-neoplastic disease.

Walker, Duard L. (University of Wisconsin Medical School, Madison), Ping-Ping Chang, Robert L. Northrop, and Harry C. Hinze . Persistent, noncytocidal viral infection: nonsynchrony of viral and cellular multiplication. J. Bacteriol. 92: 983–989. 1966.—In cultures of human conjunctive cells persistently infected with mumps virus (C-M cultures), the degree to which viral multiplication is linked to cell multiplication was examined. First, cell multiplication was inhibited. This resulted in a 10-fold increase in virus-excreting cells in the culture and an 80-fold increase in virus in the medium as compared with vigorously growing control cultures. Second, by use of elevated incubation temperature, virus multiplication was inhibited without slowing multiplication of the cells, and uninfected cells that appeared in the culture were protected by virus antiserum. This resulted in accumulation of antigen-free cells and, in one experiment, in elimination of the virus. Evidence indicated that uninfected cells accumulated as a result of dilution of virus by repeated cell divisions, but not as a result of selection of uninfected cells. These data indicate that viral multiplication in the C-M system is not closely linked to cell multiplication and that each can proceed at a rate different from the other.

SummarySendai strain of parainfluenza 1 virus previously passed in embryonated eggs was found to be adaptable to the stable line of human conjunctiva cells. Evidence for its multiplication in these cells was based on its capacity to produce typical CPE in 5–7 days throughout 17 serial passages, on its ability to initiate macroscopic plaque formation and on the nature of its single step growth cycle. The adapted virus could be cultivated in either conjunctiva cells or chick embryos. The former was more sensitive to viral infection (ratios of PFU:EIU up to 27) whereas higher virus titers were obtained from the latter.

SummaryMucoproteins known to be inhibitors of viral agglutination inhibited agglutination of rabbit erythrocytes by the wax bean hemagglutinin (WBH). Pretreatment of red blood cells with influenza (PR 8) or Newcastle Disease virus reduced susceptibility of such cells to agglutination. The enzymatic release of sialic acid from rabbit serum by a receptor-destroying enzyme prepared from Cl. perfringens was accompanied by a loss in inhibitory activity of serum against WBH agglutination. These and related observations suggest that the site of reaction of WBH with erythrocytes is similar, if not identical, to that of the viral receptor site on the surface of the cell.

Mumps virus was grown in embryonated chicken eggs in the presence of radioactive seleno-( 75 Se)-methionine. Virus in the allantoic and amniotic fluids was concentrated in a sucrose density gradient, and a peak of viral material coincided with a significant peak of 75 Se-radioactivity. The radioactivity was acid-insoluble and remained associated with the virus after purification by erythrocyte adsorption and elution and centrifugation on a second sucrose density gradient. After amino-acid hydrolysis of the radioactive virus, only 75 Se-methionine was recovered by chromatographic analysis. These results demonstrate that the radioactive 75 Se-methionine was incorporated into protein of infectious mumps virus.

Electron microscopic examination of a renal biopsy from a 58-year-old man with persistent proteinuria revealed paramyxovirus-like filaments within glomerular endothelial cells and virus-like particles morphologically identical to mumps virus within the glomerular basement membranes. Complement fixation titers of mumps “S” antibody in the patient’s serum suggested the possibility of a recent or active infection with mumps virus; however, neither infectious virus nor viral antigen could be demonstrated in a subsequent renal biopsy. These observations support the thesis that similar glomerular endothelial filaments found in patients with systemic lupus erythematosus may be viral in origin and emphasize the need for exhaustive virologic and serologic investigation of similar cases.