Antibody-mediated neutralization of human rhinovirus 14 explored by means of cryoelectron microscopy and X-ray crystallography of virus-Fab complexes.

The structures of three different human rhinovirus 14 (HRV14)-Fab complexes have been explored with X-ray crystallography and cryoelectron microscopy procedures. All three antibodies bind to the NIm-IA site of HRV14, which is the beta-B-beta-C loop of the viral capsid protein VP1. Two antibodies, Fab17-IA (Fab17) and Fab12-IA (Fab12), bind bivalently to the virion surface and strongly neutralize viral infectivity whereas Fab1-IA (Fab1) strongly aggregates and weakly neutralizes virions.

WIN 52035-dependent human rhinovirus 16: assembly deficiency caused by mutations near the canyon surface.

Three drug-dependent mutants of human rhinovirus 16 (HRV16) were characterized by sequence analyses of spontaneous mutant isolates and were genetically reconstructed from a parental cDNA plasmid. These mutants formed plaques in the presence but not in the absence of the selecting antiviral drug, WIN 52035, which binds to the capsid of wild-type virus and inhibits its attachment to the host cell. The drug-dependent phenotype of each mutant was caused by a single amino acid substitution in the VP1 coat protein.

The refined structure of human rhinovirus 16 at 2.15 A resolution: implications for the viral life cycle.

Background: Rhinoviruses belong to the picornavirus family and are small, icosahedral, non-enveloped viruses containing one positive RNA strand. Human rhinovirus 16 (HRV16) belongs to the major receptor group of rhinoviruses, for which the cellular receptor is intercellular adhesion molecule-1 (ICAM-1). In many rhinoviruses, one of the viral coat proteins (VP1) contains a hydrophobic pocket which is occupied by a fatty acid-like molecule, or so-called 'pocket factor'.

Complete replication of an animal virus and maintenance of expression vectors derived from it in Saccharomyces cerevisiae.

Here we describe the first instances to our knowledge of animal virus genome replication, and of de novo synthesis of infectious virions by a nonendogenous virus, in the yeast Saccharomyces cerevisiae, whose versatile genetics offers significant advantages for studying viral replication and virus-host interactions. Flock house virus (FHV) is the most extensively studied member of the Nodaviridae family of (+) strand RNA animal viruses. Transfection of yeast with FHV genomic RNA induced viral RNA replication, transcription, and assembly of infectious virions.