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 1993-07, Vol.67 (7), p.3786-3797
Main Authors: Whealy, M.E, Card, J.P, Robbins, A.K, Dubin, J.R, Rziha, H.J, Enquist, L.W
Format: Article
Language:English
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
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Description
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
ISSN:0022-538X
1098-5514
DOI:10.1128/jvi.67.7.3786-3797.1993