Deletion of the fiber gene induces the storage of hexon and penton base proteins in PML/Sp100-containing inclusions during adenovirus infection

Citation
F. Puvion-dutilleul et al., Deletion of the fiber gene induces the storage of hexon and penton base proteins in PML/Sp100-containing inclusions during adenovirus infection, BIO CELL, 91(8), 1999, pp. 617-628
Citations number
53
Categorie Soggetti
Cell & Developmental Biology
Journal title
BIOLOGY OF THE CELL
ISSN journal
02484900 → ACNP
Volume
91
Issue
8
Year of publication
1999
Pages
617 - 628
Database
ISI
SICI code
0248-4900(199911)91:8<617:DOTFGI>2.0.ZU;2-V
Abstract
The present study has documented changes in the in situ distribution of vir al DNA and capsid proteins in 293 cells infected with fiber gene-deleted ad enoviruses. It shows that infection results in the intense production of pr ogeny viruses which appear morphologically intact although they are devoid of fiber-coding sequence in their genome and hence of fiber protein in thei r capsid. The data confirm, therefore, that fiber protein is not essential for the assembly of progeny viruses. The main contribution of our observati ons concerns specific intranuclear structures induced by infection with eit her wild-type or fiber gene-deleted viruses. These clear amorphous inclusio ns contain two cellular proteins, PML and Sp100, which in non-infected cell s co-localize to a special type of nuclear bodies. PML and Sp100 nuclear bo dies appear to directly modulate or to be altered in a wide variety of situ ations including viral infections, cell death and transformation. In cells infected with fiber gene-deleted viruses, the clear amorphous inclusions no w accumulate non-used hexon and Fenton base proteins, whereas the absence o f fiber protein prevents the assembly of capsid proteins in crystallin arra ys. Taken together, the data suggest that the clear amorphous inclusions ma y correspond to storage sites of structural and regulatory proteins. Conseq uently, these virus-induced structures may promote the productive cycle of adenoviruses by regulating the amount of over-produced viral proteins and t he shutoff of the host cell metabolism. (C) 1999 Editions scientifiques et medicales Elsevier SAS.