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Western equine encephalomyelitis (WEE) virus is 40 to 55 m/z in diameter (1) and apparently contains nucleic acid of the ribose type (2, 3). Although electron microscopic examination of whole mounts of tissue cultures infected with a closely related agent (Eastern equine encephalomyelitis virus) has shown viral particles both within and on the surface of cells (4,5), no studies employing thin sections have been previously reported. The purpose of this communication is to illustrate and describe the manner in which WEE virus appears to differentiate within, and gain egress from, infected tissue culture cells as revealed in thin sections by the electron microscope. Similarities in development or release among WEE virus, influenza virus, herpes simplex virus, the virus associated with erythroblastosis of chickens, Rous sarcoma virus and a mouse mammary tumor agent will be discussed. Stable human amnionic cells:A stable line of human anauionic epithelium was kindly supplied by Dr. Katherine Sprnnt. Replicate cultures were prepared in Leighton tubes without coverslip% using Eagle's basal medium with 10 per cent horse serum. The cultures were inocu-* These studies were aided

The acquired immune deficiency syndrome (AIDS), which has recently occurred at increasing rates in homosexual men, intravenous drug users, and others, is characterized by the development of Kaposi's sarcoma and several opportunistic infections including pneumonia caused by Pneumocystis carinii. Serum samples from patients with AIDS and from matched and unmatched control subjects were examined for the presence of antibodies to cell membrane antigens associated with human T-cell leukemia virus. Nineteen of 75 of the AIDS patients had antibodies directed to surface antigens of Hut 102, a reference T lymphoid cell line infected with leukemia virus, as did two of the 336 control subjects.

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Respiratory syncytial (RS) virus was grown in Vero cells and fixed for electron microscopy at various stages of maturation. Both filamentous and round or kidney-shaped particles, either with (complete) or without (incomplete) internal structure, were observed. All four morphological forms were identical with respect to their reactivity with ferritin-labeled antibody to RS virus. Freezeetching revealed a structural feature apparently unique for RS virus, namely helical striations around the core on the internal aspect of the envelope. This specific configuration was already detectable during the early stages of viral differentiation of the host cell membrane. Concentration of free virus by zonal ultracentrifugation of culture fluids onto sucrose cushions yielded predominantly filamentous forms up to 10 um in length.

After attachment, the uncoating of Sendai virus, which was accompanied by dissolution of the plasma membrane and fusion of virus to cell, proceeded quickly. Nucleoprotein filaments were found at stages of transit from virus to cytoplasm.After attachment of influenza virus to the cell, the following events have been shown to occur in rapid succession. The virion is uncoated at the cellular surface, the cytoplasmic membrane is dissolved, and the viral core ruptures with consequent release of nucleoprotein into the cytoplasm (6). It was suggested that this mechanism of entry had heretofore escaped attention simply because it occurred so quickly. Indeed, the several stages of the process were observed only when virus was allowed to adsorb to the cells at 4 C and then was studied carefully during the first 5 min after the environmental temperature was raised to 37 C. In the light of the findings with influenza virus, it was decided to investigate, by similar methods, the manner in which parainfluenza type 1 (Sendai) virus gains entry into the cell.

Concentrated Sendai virus, when adsorbed to erythrocytes at 4 C, caused invaginations in the plasma membrane. Following elevation of the temperature to 37 C, the plasma membrane became fused with the viral envelope before dissolution of the virions and rupture of the cells. Cell lysis was accompanied by rapid and total loss of hemoglobin to the extracellular space. Following aqueous pyridine extraction, the hemoglobin-free ghosts remaining were found to be devoid of N-acetylneuraminic acid and to have solubility properties different from those of normal erythrocyte ghosts. By the action of viral neuraminidase, bound N-acetylneuraminic acid was also liberated from purified virus receptor substance whose electrophoretic mobility was thereby substantially reduced. Cu++ selectively inhibited hemolysis and neuraminidase without interfering with hemagglutination and attachment. Neuraminidase appeared to be essential for Sendai virus hemolysis; viral particle size may also be a critical factor in this process.

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