Involvement of the UL24 protein in herpes simplex virus 1-induced dispersal of B23 and in nuclear egress

Abstract UL24 of herpes simplex virus 1 (HSV-1) is widely conserved within the Herpesviridae family. Herein, we tested the hypothesis that UL24, which we have previously shown to induce the redistribution of nucleolin, also affects the localization of the nucleolar protein B23. We found that HSV-1-i...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2011-04, Vol.412 (2), p.341-348
Main Authors: Lymberopoulos, Maria H, Bourget, Amélie, Abdeljelil, Nawel Ben, Pearson, Angela
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Animals
B23
Biotechnology
CELL CONSTITUENTS
Cell Line
CELL NUCLEI
Computer Science
DISEASES
DNA Mutational Analysis
HERPES SIMPLEX
Herpes simplex virus 1
Herpesviridae
Herpesvirus 1, Human
Herpesvirus 1, Human - physiology
HSV-1 UL24
Humans
HYPOTHESIS
Infectious Disease
INFECTIOUS DISEASES
Life Sciences
Microbiology and Parasitology
MICROORGANISMS
Nuclear egress
Nuclear Proteins
Nuclear Proteins - metabolism
NUCLEOLI
Nucleolus
ORGANIC COMPOUNDS
PARASITES
PROTEINS
SKIN DISEASES
VIRAL DISEASES
Viral Proteins
Viral Proteins - metabolism
Virology
Virus Replication
VIRUSES
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Summary:Abstract UL24 of herpes simplex virus 1 (HSV-1) is widely conserved within the Herpesviridae family. Herein, we tested the hypothesis that UL24, which we have previously shown to induce the redistribution of nucleolin, also affects the localization of the nucleolar protein B23. We found that HSV-1-induced dispersal of B23 was dependent on UL24 . The conserved N-terminal portion of UL24 was sufficient to induce the redistribution of B23 in transient transfection assays. Mutational analysis revealed that the endonuclease motif of UL24 was important for B23 dispersal in both transfected and infected cells. Nucleolar protein relocalization during HSV-1 infection was also observed in non-immortalized cells. Analysis of infected cells by electron microscopy revealed a decrease in the ratio of cytoplasmic versus nuclear viral particles in cells infected with a UL24-deficient strain compared to KOS-infected cells. Our results suggest that UL24 promotes nuclear egress of nucleocapsids during HSV-1 infection, possibly though effects on nucleoli.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2011.01.016