scholarly journals Adenovirus VA1 Noncoding RNA Can Inhibit Small Interfering RNA and MicroRNA Biogenesis

2004 ◽  
Vol 78 (23) ◽  
pp. 12868-12876 ◽  
Author(s):  
Shihua Lu ◽  
Bryan R. Cullen
Keyword(s):  
Gene Product ◽  
Nuclear Export ◽  
Noncoding Rna ◽  
Viral Gene ◽  
Rna Duplexes ◽  
Direct Binding ◽  
Viral Gene Product ◽  
Infected Cells ◽  
Short Hairpin Rnas ◽  
Interfering Rna

ABSTRACT Although inhibition of RNA interference (RNAi) by plant virus proteins has been shown to enhance viral replication and pathogenesis in plants, no viral gene product has as yet been shown to inhibit RNAi in vertebrate cells. Here, we present evidence demonstrating that the highly structured ∼160-nucleotide adenoviral VA1 noncoding RNA can inhibit RNAi at physiological levels of expression. VA1, which is expressed at very high levels in adenovirus-infected cells, potently inhibited RNAi induced by short hairpin RNAs (shRNAs) or human microRNA precursors but did not affect RNAi induced by artificial short interfering RNA duplexes. Inhibition appeared to be due both to inhibition of nuclear export of shRNA or premicro-RNA precursors, competition for the Exportin 5 nuclear export factor, and inhibition of Dicer function by direct binding of Dicer. Together, these data argue that adenovirus infection can result in inhibition of RNAi and identify VA1 RNA as the first viral gene product able to inhibit RNAi in human cells.

Systemic immunity against a murine colon tumor (CT-26) produced by immunization with syngeneic cells expressing a transfected viral gene product

1989 ◽  
Vol 43 (5) ◽  
pp. 823-827 ◽  
Author(s):  
Hans K. Schackert ◽  
Toshiyuki Itaya ◽  
Gabriele Schackert ◽  
Eric Fearon ◽  
Bert Vogelstein ◽  
...  
Keyword(s):  
Gene Product ◽  
Viral Gene ◽  
Colon Tumor ◽  
Systemic Immunity ◽  
Viral Gene Product ◽  
Murine Colon

scholarly journals Expression in transgenic plants of a viral gene product that mediates insect transmission of potyviruses.

1989 ◽  
Vol 86 (21) ◽  
pp. 8402-8406 ◽  
Author(s):  
P. H. Berger ◽  
A. G. Hunt ◽  
L. L. Domier ◽  
G. M. Hellmann ◽  
Y. Stram ◽  
...  
Keyword(s):  
Transgenic Plants ◽  
Gene Product ◽  
Viral Gene ◽  
Viral Gene Product ◽  
Insect Transmission

scholarly journals Immune activation, viral gene product expression and neurotoxicity in the HIV-1 transgenic rat

2012 ◽  
Vol 247 (1-2) ◽  
pp. 16-24 ◽  
Author(s):  
Walter Royal ◽  
Li Zhang ◽  
Ming Guo ◽  
Odell Jones ◽  
Harry Davis ◽  
...  
Keyword(s):  
Gene Product ◽  
Immune Activation ◽  
Viral Gene ◽  
Transgenic Rat ◽  
Product Expression ◽  
Viral Gene Product ◽  
Hiv 1

scholarly journals Large-Scale, High-Throughput Validation of Short Hairpin RNA Sequences for RNA Interference

2006 ◽  
Vol 11 (3) ◽  
pp. 236-246 ◽  
Author(s):  
Laurence H. Lamarcq ◽  
Bradley J. Scherer ◽  
Michael L. Phelan ◽  
Nikolai N. Kalnine ◽  
Yen H. Nguyen ◽  
...  
Keyword(s):  
High Throughput ◽  
Large Scale ◽  
Strong Support ◽  
Gc Content ◽  
Rapid Identification ◽  
Hairpin Rna ◽  
Rna Sequences ◽  
Short Hairpin ◽  
Short Hairpin Rnas ◽  
Interfering Rna

A method for high-throughput cloning and analysis of short hairpin RNAs (shRNAs) is described. Using this approach, 464 shRNAs against 116 different genes were screened for knockdown efficacy, enabling rapid identification of effective shRNAs against 74 genes. Statistical analysis of the effects of various criteria on the activity of the shRNAs confirmed that some of the rules thought to govern small interfering RNA (siRNA) activity also apply to shRNAs. These include moderate GC content, absence of internal hairpins, and asymmetric thermal stability. However, the authors did not find strong support for positionspecific rules. In addition, analysis of the data suggests that not all genes are equally susceptible to RNAinterference (RNAi).

scholarly journals Patterns of accumulation of miRNAs encoded by herpes simplex virus during productive infection, latency, and on reactivation

2014 ◽  
Vol 112 (1) ◽  
pp. E49-E55 ◽  
Author(s):  
Te Du ◽  
Zhiyuan Han ◽  
Guoying Zhou ◽  
Bernard Roizman
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Cultured Cells ◽  
Viral Gene Expression ◽  
The Body ◽  
Productive Infection ◽  
Viral Gene ◽  
Infected Cells ◽  
Simplex Virus ◽  
Portal Of Entry

The key events in herpes simplex virus (HSV) infections are (i) replication at a portal of entry into the body modeled by infection of cultured cells; (ii) establishment of a latent state characterized by a sole latency-associated transcript and microRNAs (miRNAs) modeled in murine peripheral ganglia 30 d after inoculation; and (iii) reactivation from the latent state modeled by excision and incubation of ganglia in medium containing anti-NGF antibody for a timespan of a single viral replicative cycle. In this report, we examine the pattern of synthesis and accumulation of 18 HSV-1 miRNAs in the three models. We report the following: (i) H2-3P, H3-3P, H4-3P, H5-3P, H6-3P, and H7-5P accumulated in ganglia harboring latent virus. All but H4-3P were readily detected in productively infected cells, and most likely they originate from three transcriptional units. (ii) H8-5P, H15, H17, H18, H26, and H27 accumulated during reactivation. Of this group, only H26 and H27 could be detected in productively infected cells. (iii) Of the 18 we have examined, only 10 miRNAs were found to accumulate above background levels in productively infected cells. The disparity in the accumulation of miRNAs in cell culture and during reactivation may reflect differences in the patterns of regulation of viral gene expression during productive infection and during reactivation from the latent state.

scholarly journals Control of adenovirus early gene expression: posttranscriptional control mediated by both viral and cellular gene products.

1981 ◽  
Vol 1 (9) ◽  
pp. 807-813 ◽  
Author(s):  
M G Katze ◽  
H Persson ◽  
L Philipson
Keyword(s):  
Gene Product ◽  
Messenger Rna ◽  
Adenovirus Type ◽  
Negative Regulator ◽  
Early Gene ◽  
In Vitro Translation ◽  
Mapping Technique ◽  
Cellular Gene ◽  
Infected Cells ◽  
Adenovirus Type 5

An adenovirus type 5 host range mutant (hr-1) located in region E1A and phenotypically defective in expressing viral messenger ribonucleic acid (RNA) from other early regions (Berk et al., Cell 17:935-944, 1979) was analyzed for accumulation of viral RNA in the presence of protein synthesis inhibitors. Nuclear RNA was transcribed from all early regions at the same rate, regardless of whether the drug was present or absent. As expected, low or undetectable levels of RNA were found in the cytoplasm of hr-1-infected cells compared with the wild-type adenovirus type 5 in the absence of drug. When anisomycin was added 30 min before hr-1 infection, cytoplasmic RNA was abundant from early regions E3 and E4 when assayed by filter hybridization. In accordance, early regions E3 and E4 viral messenger RNA species were detected by the S1 endonuclease mapping technique only in hr-1-infected cells that were treated with the drug. Similar results were obtained by in vitro translation studies. Together, these results suggest that this adenovirus type 5 mutant lacks a viral gene product necessary for accumulation of viral messenger RNA, but not for transcription. It is proposed that a cellular gene product serves as a negative regulator of viral messenger RNA accumulation at the posttranscriptional level.

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