Membrane Effects of Certain Viruses

It has been known for some time that different viruses have different effects on cell membranes. In particular, the enveloped viruses can cause early cell fusion as they enter the host cell or late cell fusion after replication of the virus. These phenomena apply particularly to the paramyxoviruses and have been dubbed fusion from without and fusion from within (Bratt and Gallaher, 1969). Other enveloped viruses can produce similar but usually less striking effects on cell fusion. Nonenveloped viruses can also cause drastic changes in cell membranes, usually resulting in alteration in the permeability barrier of the cell membrane. Still other viruses, or the same viruses under different conditions, can alter in a more subtle way the active or passive transport mechanisms of cells. Under some conditions, some viruses even stimulate the formation of cell membranes by inducing augmented synthesis of cellular membrane lipids. 

The membranes of negative-strand viruses lacking an identifiable fusion factor can also fuse with interacting cell membranes but to a much lesser extent than the paramyxoviruses. Influenza A and B 

Virus-Induced Alterations in Membrane Permeability and Transport 

It has been known for some time that infection with various types of viruses impairs the permeability barrier function of the host cell cytoplasmic membrane, allowing ordinarily impermeable large molecules to enter the cell from the surrounding medium and allowing particulate intracellular material to leak out. A good example of this is penetration of supravital dyes, such as trypan blue, to enter cells, usually late after viral infection as a criterion of cell death. In addition, certain viral infections induce earlier and more subtle changes by altering membrane transport of small ions into or out of the infected cell. A few selected examples of altered membrane permeability of the cytoplasmic membrane are cited here as an example of readily measured cytopathic effects of well-known virulent viruses. 

The paramyxoviruses, largely because of their profound cell-fusing activity, have served as an important model of membrane perturbation by viruses. During Sendai virus-mediated fusion of mouse ascites cells, Pasternak and Micklem (1973) detected loss of intracellular metabolites coincident with inhibition of their accumulation from the medium. This failure to maintain selective permeability did not occur at 0°C and was unaffected by cytochalasin B which inhibits fusion by the virus. Chick embryo fibroblasts infected with Newcastle disease virus were found to release cellular enzymes, such as lactate dehydrogenase, glutamic oxaloacetic transaminase, and lysosomal enzymes (Katzman and Wilson, 1974). These cells also became 

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