By C. Howe, J. E. Coward, T. W. Fenger (auth.), Hein Fraenkael-Conrat, Robert R. Wagner (eds.)
The time turns out ripe for a serious compendium of that phase of the organic universe we name viruses. Virology, as a technology, having handed only in the near past via its descriptive part of naming and num bering, has most likely reached that degree at which particularly few new actually new-viruses may be stumbled on. prompted by means of the highbrow probes and methods of molecular biology, genetics, biochemical cytology, and excessive answer microscopy and spectroscopy, the sphere has skilled a real info explosion. Few severe makes an attempt were made to chronicle those occasions. This entire sequence, as a way to include a few 6000 pages in a complete of approximately 18 volumes, represents a dedication by means of a wide staff of energetic investigators to research, digest, and expostulate at the nice mass of information with regards to viruses, a lot of that is now amorphous and disjointed, and scattered all through a large literature. during this manner, we are hoping to put the whole box in viewpoint, and to increase an invalua ble reference and sourcebook for researchers and scholars in any respect degrees. This sequence is designed as a continuum that may be entered anyplace, yet which additionally offers a logical development of constructing proof and built-in concepts.
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Extra info for Comprehensive Virology: Vol. 16: Virus-Host Interactions: Viral Invasion, Persistence, and Disease
5) (Silverstein and Dales, 1968). Rotaviruses are biologically akin to reoviruses because of their double-stranded RNA core; they have a particular tropism for intes- Chapter I 18 40 b Fig. 4. Murine A9 cells infected with minute virus of mice. (a) Stages in viral uptake into coated vesicles by invagination (right and left) and formation of "autonomous" coated vesicles (center). Clusters of virions are seen between the plasma membrane surface and the edge of the filopodium . (b) A filopodium bearing a patch of virions is folded into the cytoplasm forming a channel which contains two viral particles.
Sendai, NOV) in which intramembranal cleavage of F glycoprotein (to yield F 1 ) is prerequisite to infectivity. Accordingly, there is also striking homology between HA2 and Fl in N-terminal amino acid sequences, the region which in each of these molecules is apparently involved in viral penetration infection (Choppin and Scheid, 1980). Studies with electron spin resonance have indicated that there is an increase in the fluidity of the lipid bilayer of chicken erythrocytes on primary reaction of influenza virus with surface glycoprotein receptors (Lyles and Landsberger, 1976).
Responding cell receptors. As with paramyxoviruses, however, RS virus appears to be capable of fusing with the cell membrane and thus introducing its genome into the cytoplasm (Fig. 13). , 1974). Along with the characteristic endofusion which occurs during active infection (Bachi and Howe, 1973), these findings constitute suggestive evidence for the presence in the viral envelope of a "fusion factor" analogous to the F 1 protein of Sendai and the F protein of measles virus, respectively. 5. , 1970; Cohen and Summers, 1974) or the G envelope protein (Schloemer and Wagner, 1975) of molecular weight 69,000 (Morrison and McQuain, 1978) which contains NANA.