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Titolo:
HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 RNA EXPRESSION BY 4 CHRONICALLY INFECTED CELL-LINES INDICATES MULTIPLE MECHANISMS OF LATENCY
Autore:
BUTERA ST; ROBERTS BD; LAM L; HODGE T; FOLKS TM;
Indirizzi:
CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,DIV VIRAL & RICKETTSIALDIS,RETROVIRUS DIS BRANCH ATLANTA GA 30333 CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,DIV HIV-AIDS,IMMUNOL BRANCH ATLANTA GA 30333
Titolo Testata:
Journal of virology
fascicolo: 4, volume: 68, anno: 1994,
pagine: 2726 - 2730
SICI:
0022-538X(1994)68:4<2726:HTREB4>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
VIRAL MESSENGER-RNA; GENE-EXPRESSION; HIV-1 LATENCY; REV; REQUIRES; MODEL; CLONE; DNA; RRE;
Tipo documento:
Note
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
29
Recensione:
Indirizzi per estratti:
Citazione:
S.T. Butera et al., "HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 RNA EXPRESSION BY 4 CHRONICALLY INFECTED CELL-LINES INDICATES MULTIPLE MECHANISMS OF LATENCY", Journal of virology, 68(4), 1994, pp. 2726-2730

Abstract

Recent information has suggested that posttranscriptional mechanisms,whereby human immunodeficiency virus type 1 (HIV-1) RNA exists as multiply spliced transcripts without promoting an accumulation of the larger messages, are responsible for maintaining a stable state of nonproductive viral expression or viral latency. To test the universality ofthese observations, we compared the patterns of viral RNA splicing and the frequencies of cells actually harboring HIV-1 RNA in four chronically HIV-1-infectcd cell lines (U1 [promonocytic], ACH-2 [T lymphocytic], OM-10.1 [promyelocytic], and J1.1 [T lymphocytic]). In uninduced U1 and ACH-2 cultures, a high frequency of cells (approximately one insix) contained HIV-1 RNA but mainly as multiply spliced transcripts, again supporting a posttranscriptional mechanism maintaining viral latency. In sharp contrast, only 1 in 50 cells in uninduced OM-10.1 and J1.1 cultures contained HIV-1 RNA, indicating a primary transcriptionalmechanism controlling viral expression in these cells. Furthermore, those OM-10.1 and J1.1 cells that did contain viral RNA were in a stateof productive HIV-1 expression marked by the presence of both splicedand unspliced transcripts. Even though the total absence of viral RNAin the majority of OM-10.1 and J1.1 cells indicated a state of absolute latency, treatment with tumor necrosis factor alpha induced transcription of HIV-1 RNA in nearly 100% of the cells in all four of the chronically infected cultures. Tumor necrosis factor alpha induction of U1,ACH-2, and OM-10.1 cultures resulted in an initial accumulation of multiply spliced HIV-1 RNA followed by a transition to the larger unspliced viral RNA transcripts. This RNA splice transition was less apparent in the J1.1 cell line. These results demonstrate that host cell-specific transcriptional and posttranscriptional mechanisms are importantfactors in the control of HIV-1 latency.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 23:59:41