Document Detail


Activation of human immunodeficiency virus by herpes simplex virus.
MedLine Citation:
PMID:  1354237     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Heterologous viruses have been examined for their ability to accelerate the course of infection with the human immunodeficiency virus (HIV) type 1. In this study, ACH-2 cells persistently infected with HIV-1 exhibited augmented HIV-1 replication as a result of superinfection with herpes simplex virus (HSV) type 1. Using HSV-1 mutants with deletions in the genes encoding immediate-early proteins ICP0, ICP4, and ICP27, it was found that ICP0 and ICP27, but not ICP4, were essential for up-regulation of HIV replication. Northern blot analysis showed that this activation of HIV was characterized by an initial rise in the level of the small, subgenomic (2.0 and 4.3 kb) mRNA species, followed by an increase in the level of unspliced genomic (9.2 kb) mRNA. Such a shift in transcriptional phase recapitulates the early-to-late transition seen in single-step growth curves of acute HIV-1 infection. Thus, HSV can activate HIV-1 from latency in ACH-2 cells, this activation of HIV is independent of productive HSV replication since the delta ICP4 deletion mutant is replication-incompetent, and this activation is evident as an increase in the steady-state levels of HIV transcripts.
Authors:
M P Golden; S Kim; S M Hammer; E A Ladd; P A Schaffer; N DeLuca; M A Albrecht
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of infectious diseases     Volume:  166     ISSN:  0022-1899     ISO Abbreviation:  J. Infect. Dis.     Publication Date:  1992 Sep 
Date Detail:
Created Date:  1992-09-17     Completed Date:  1992-09-17     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0413675     Medline TA:  J Infect Dis     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  494-9     Citation Subset:  AIM; IM; X    
Affiliation:
Division of Infectious Diseases, New England Deaconess Hospital, Boston, MA 02215.
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MeSH Terms
Descriptor/Qualifier:
CD4-Positive T-Lymphocytes / cytology,  microbiology
HIV-1 / genetics,  growth & development*
Humans
Kinetics
Mutation
RNA, Viral / biosynthesis
Simplexvirus / genetics,  physiology*
Tumor Cells, Cultured
Virus Activation*
Virus Replication
Grant Support
ID/Acronym/Agency:
AI-01015/AI/NIAID NIH HHS; AI-30897/AI/NIAID NIH HHS; HL-43510/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/RNA, Viral

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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