Advances in Virus Research, Vol. 62 by Karl Maramorosch, Frederick A. Murphy, Aaron J. Shatkin

By Karl Maramorosch, Frederick A. Murphy, Aaron J. Shatkin

The Advances in Virus study sequence covers a various variety of in-depth reports offering a worthwhile evaluate of the present box of virology. This eclectic quantity comprises six studies overlaying themes in relation to plant viruses, evolution of viruses with hosts and mobilephone acceptance via viruses. Six finished stories on: * Varicella Virus - Mononuclear cellphone interplay * Evolution of phone reputation via Viruses: A resource of organic Novelty with scientific Implications * Infectious Pancreatic Necrosis Virus: Biology, Pathogenesis and Diagnostic equipment * buildings of Picrona-like plant viruses: Implications and functions * Cucumoviruses * Co-Evolution of Viruses with Hosts and Vectors and attainable Paleontology

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EVOLUTION OF CELL RECOGNITION BY VIRUSES 25 TABLE I BIOLOGICAL RELEVANCE OF QUASISPECIES DYNAMICS FOR RNA VIRUSESa Relevant parameters 1. Average number of mutations per genome found in a viral population: typically it ranges from 1 to 100 2. Virus population size: very variable but can reach 109 to 1012 in some infections in vivo 3. Genome length: 3 to 33 kb, with compact genetic information 4. Mutations needed for a phenotypic change: one or few mutations, as documented amply in the text for changes in receptor recognition specificity Examples of phenotypic changes in RNA viruses dependent on one or few mutations 1.

Genetic variation to escape from selective constraints is generally reflected in the survival of subpopulations of genomes that may show little alteration in replication capacity (fitness) or, despite a reduction of fitness, may still replicate to generate new mutant distributions of higher fitness. B. , 2001; Eigen and Biebricher, 1988). , 1976; Drake and Holland, 1999), values that imply the continuous generation of dynamic mutant distributions in a replicating RNA virus population. These high mutation rates in RNA genomes would be incompatible with maintenance of the genetic information contained in large viral or cellular DNA genomes (Eigen and Biebricher, 1988).

1985). , 1995). It may be predicted that when receptor-binding sites and neutralizing antibody-binding sites overlap at the virus surface, amino acid replacements needed for antibody escape may be deleterious as they affect receptor recognition. However, in line with the dynamics of RNA virus populations (Section II,B), this conflict is just one of the several instances in which negative selection may act to maintain variants at low levels and to rescue fit viruses through compensatory mutations.

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