Specific pseudorabies virus infection of the rat visual system requires both gI and gp63 glycoproteins

Transneuronal transport of pseudorabies virus (PRV) from the retina to visual centers that mediate visual discrimination and reflexes requires specific genes in the unique short region of the PRV genome. In contrast, these same viral genes are not required to infect retinorecipient areas of the brai...

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Bibliographic Details
Published in:	Journal of Virology Vol. 67; no. 7; pp. 3786 - 3797
Main Authors:	Whealy, M.E, Card, J.P, Robbins, A.K, Dubin, J.R, Rziha, H.J, Enquist, L.W
Format:	Journal Article
Language:	English
Published:	Washington, DC American Society for Microbiology 01-07-1993
Subjects:	Animals APARATO GOLGI APPAREIL DE GOLGI Biological and medical sciences Cells, Cultured DNA Mutational Analysis Fundamental and applied biological sciences. Psychology GANGLION NERVEUX GANGLIOS Genes, Viral Genetics GLICOPROTEINAS GLYCOPROTEINE Herpesvirus 1, Suid - growth & development Herpesvirus 1, Suid - pathogenicity HERPETOVIRIDAE Hypothalamus - microbiology In Vitro Techniques Male METABOLISME DES PROTEINES METABOLISMO PROTEICO Microbiology MUTACION INDUCIDA MUTANT MUTANTES MUTATION PROVOQUEE NERF NERVIOS Neurons - microbiology OEIL OJOS PATHOGENESE PATOGENESIS PROTEINAS PROTEINE pseudorabies virus RAT RATA Rats Rats, Sprague-Dawley RETICULO ENDOPLASMATICO RETICULUM ENDOPLASMIQUE Retina - microbiology Swine TEJIDOS ANIMALES TISSU ANIMAL Viral Envelope Proteins - physiology Viral Structural Proteins - genetics Virology VIRUS DE LOS ANIMALES VIRUS DES ANIMAUX Virus Replication Visual Pathways - microbiology Molecular processing Rat Herpesviridae Alphaherpesvirinae Rodentia Central nervous system Retina Biosynthesis Structure function relationship Eye Virus Aujeszky virus Vertebrata Mammalia Visual pathway Infectivity Molecular complex Neurotropism Mutation Virus envelope
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Summary:	Transneuronal transport of pseudorabies virus (PRV) from the retina to visual centers that mediate visual discrimination and reflexes requires specific genes in the unique short region of the PRV genome. In contrast, these same viral genes are not required to infect retinorecipient areas of the brain involved in circadian rhythm regulation. In this report, we demonstrate that viral mutants carrying defined deletions of the genes encoding glycoprotein gI or gp63, or both, result in the same dramatic transport defect. Efficient export of either gI or gp63 from the endoplasmic reticulum to the Golgi apparatus in a fibroblast cell line requires the presence of both proteins. We also show that gI and gp63 physically interact, as demonstrated by pulse-chase and sucrose gradient sedimentation experiments. Complex formation is rapid compared with homodimerization of PRV glycoprotein gII. We suggest that gI and gp63 function in concert to affect neurotropism in the rat visual circuitry and that a heterodimer is likely to be the unit of function
Bibliography:	9425938 L73 ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0022-538X 1098-5514
DOI:	10.1128/jvi.67.7.3786-3797.1993