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Journal of Virology, December 2001, p. 12070-12080, Vol. 75, No. 24
Department of Microbiology, University of
Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104
Received 4 April 2001/Accepted 19 September 2001
During latency of herpes simplex virus type 1 in sensory neurons,
the transcription of viral genes is restricted to the
latency-associated transcripts (LATs). The stable 2-kb LAT intron has
been characterized previously and has been shown to accumulate to high
levels in the nuclei of infected neurons. However, in productively
infected tissue culture cells, this unique intron is also found in the cytoplasm. Although deletion mutant analysis has suggested that the
region of the gene from which the intron is spliced plays a role in
maintenance of latency or in reactivation from latency, no well-defined
function has been ascribed specifically to the 2-kb LAT intron.
Nevertheless, previous work has shown that it associates with 50S
particles in the cytoplasm of acutely infected cells. Our studies
tested the ability of the 2-kb LAT to dissociate from cytoplasmic
protein complexes under various salt conditions. Results indicated that
this association, which had been speculated to be mRNA-like, is
actually more similar to the affinity of rRNAs for translational
complexes. Furthermore, by immunoprecipitation analysis, we demonstrate
that the 2-kb LAT associates with ribosomal as well as with splicing
complexes in infected cells. Our results suggest that the 2-kb LAT is
processed similarly to mRNAs in the nuclei of infected cells. However,
in the cytoplasm, the 2-kb LAT may play a structural role in the
ribosomal complex, similar to that of the cellular rRNAs, and therefore
affect the functioning of the translational machinery.
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.24.12070-12080.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Herpes Simplex Virus Type 1 2-Kilobase
Latency-Associated Transcript Intron Associates with Ribosomal Proteins
and Splicing Factors
*
Corresponding author. Mailing address: Department of
Microbiology, University of Pennsylvania School of Medicine,
Philadelphia, PA 19104. Phone: (215) 898-3847. Fax: (215) 898-3847. E-mail: nfraser{at}mail.med.upenn.edu.
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