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 learn sequence covers a various variety of in-depth studies offering a precious assessment of the present box of virology. This eclectic quantity includes six studies masking issues in terms of plant viruses, evolution of viruses with hosts and cellphone popularity by way of viruses. Six finished experiences on: * Varicella Virus - Mononuclear phone interplay * Evolution of mobilephone popularity by way of Viruses: A resource of organic Novelty with scientific Implications * Infectious Pancreatic Necrosis Virus: Biology, Pathogenesis and Diagnostic tools * constructions of Picrona-like plant viruses: Implications and functions * Cucumoviruses * Co-Evolution of Viruses with Hosts and Vectors and attainable Paleontology

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Almost all strains described to date require interactions with two molecules on the cell surface. One of them acts as an attachment receptor, with which viral glycoprotein gp120 interacts. This interaction promotes conformational changes that expose the fusogenic peptide of gp41, which, in turn interacts with the fusion receptor. This is essential for the fusion of viral and cellular membranes and therefore allows the viral capsid to enter the host cell. The group of cellular molecules involved in lentivirus fusion are referred to as coreceptors.

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. There is no strict requirement that surface residues involved in receptor recognition be entirely shielded from immune attack.

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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