scholarly journals Molecular Characterization of the Human T Cell Lymphotropic Virus Type 2 Long Terminal Repeat Region: A Discussion about Possible Influences at Viral Gene Expression

2014 ◽  
Vol 30 (1) ◽  
pp. 92-96 ◽  
Author(s):  
Fernanda K. Barreto ◽  
Felipe F.A. Rego ◽  
Loianna M. Fonseca ◽  
Bernardo Galvão-Castro-Filho ◽  
Thessika H.A. Araújo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Long Terminal Repeat ◽  
Viral Gene Expression ◽  
Viral Gene ◽  
Repeat Region ◽  
Human T Cell ◽  
Long Terminal Repeat Region ◽  
Terminal Repeat Region

scholarly journals Characterization of HPV integration, viral gene expression and E6E7 alternative transcripts by RNA-Seq: A descriptive study in invasive cervical cancer

Genomics ◽  
2019 ◽  
Vol 111 (6) ◽  
pp. 1853-1861 ◽  
Author(s):  
Ayslan C. Brant ◽  
Albert N. Menezes ◽  
Shayany P. Felix ◽  
Liz M. de Almeida ◽  
Michael Sammeth ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cervical Cancer ◽  
Invasive Cervical Cancer ◽  
Viral Gene Expression ◽  
Descriptive Study ◽  
Viral Gene ◽  
Rna Seq ◽  
Alternative Transcripts

scholarly journals An Interferon Regulatory Factor Binding Site in the U5 Region of the Bovine Leukemia Virus Long Terminal Repeat Stimulates Tax-Independent Gene Expression

1998 ◽  
Vol 72 (7) ◽  
pp. 5526-5534 ◽  
Author(s):  
Véronique Kiermer ◽  
Carine Van Lint ◽  
Delphine Briclet ◽  
Caroline Vanhulle ◽  
Richard Kettmann ◽  
...  
Keyword(s):  
Gene Expression ◽  
Long Terminal Repeat ◽  
Binding Site ◽  
Bovine Leukemia Virus ◽  
Transcription Initiation ◽  
Leukemia Virus ◽  
Viral Gene Expression ◽  
Terminal Repeat ◽  
Viral Gene ◽  
Enhancer Activity

ABSTRACT Bovine leukemia virus (BLV) replication is controlled by bothcis- and trans-acting elements. The virus-encoded transactivator, Tax, is necessary for efficient transcription from the BLV promoter, although it is not present during the early stages of infection. Therefore, sequences that control Tax-independent transcription must play an important role in the initiation of viral gene expression. This study demonstrates that the R-U5 sequence of BLV stimulates Tax-independent reporter gene expression directed by the BLV promoter. R-U5 was also stimulatory when inserted immediately downstream from the transcription initiation site of a heterologous promoter. Progressive deletion analysis of this region revealed that a 46-bp element corresponding to the 5′ half of U5 is principally responsible for the stimulation. This element exhibited enhancer activity when inserted upstream or downstream from the herpes simplex virus thymidine kinase promoter. This enhancer contains a binding site for the interferon regulatory factors IRF-1 and IRF-2. A 3-bp mutation that destroys the IRF recognition site caused a twofold decrease in Tax-independent BLV long terminal repeat-driven gene expression. These observations suggest that the IRF binding site in the U5 region of BLV plays a role in the initiation of virus replication.

scholarly journals Mouse Hepatitis Virus Type 2 Enters Cells through a Clathrin-Mediated Endocytic Pathway Independent of Eps15

2008 ◽  
Vol 82 (16) ◽  
pp. 8112-8123 ◽  
Author(s):  
Yinghui Pu ◽  
Xuming Zhang
Keyword(s):  
Gene Expression ◽  
Virus Type ◽  
Hepatitis Virus ◽  
Mouse Hepatitis Virus ◽  
Viral Gene Expression ◽  
Dominant Negative ◽  
Endocytic Pathway ◽  
Dominant Negative Mutant ◽  
Viral Gene

ABSTRACT It has recently been shown that cell entry of mouse hepatitis virus type 2 (MHV-2) is mediated through endocytosis (Z. Qiu et al., J. Virol. 80:5768-5776, 2006). However, the molecular mechanism underlying MHV-2 entry is not known. Here we employed multiple chemical and molecular approaches to determine the molecular pathways for MHV-2 entry. Our results showed that MHV-2 gene expression and infectivity were significantly inhibited when cells were treated with chemical and physiologic blockers of the clathrin-mediated pathway, such as chlorpromazine and hypertonic sucrose medium. Furthermore, viral gene expression was significantly inhibited when cells were transfected with a small interfering RNA specific to the clathrin heavy chain. However, these treatments did not affect the infectivity and gene expression of MHV-A59, demonstrating the specificity of the inhibitions. In addition, overexpression of a dominant-negative mutant of caveolin 1 did not have any effect on MHV-2 infection, while it significantly blocked the caveolin-dependent uptake of cholera toxin subunit B. These results demonstrate that MHV-2 utilizes the clathrin- but not caveolin-mediated endocytic pathway for entry. Interestingly, when the cells transiently overexpressed a dominant-negative form (DIII) of Eps15, which is thought to be an essential component of the clathrin pathway, viral gene expression and infectivity were unaffected, although DIII expression blocked transferrin uptake and vesicular stomatitis virus infection, which are dependent on clathrin-mediated endocytosis. Thus, MHV-2 entry is mediated through clathrin-dependent but Eps15-independent endocytosis.

scholarly journals HTLV-1 Rex is required for viral spread and persistence in vivo but is dispensable for cellular immortalization in vitro

Blood ◽  
2003 ◽  
Vol 102 (12) ◽  
pp. 3963-3969 ◽  
Author(s):  
Jianxin Ye ◽  
Lee Silverman ◽  
Michael D. Lairmore ◽  
Patrick L. Green
Keyword(s):  
Gene Expression ◽  
Interleukin 2 ◽  
Viral Gene Expression ◽  
Viral Gene ◽  
Viral Oncoprotein ◽  
Cell Leukemia Virus Type ◽  
Viral Spread ◽  
Human T Cell

Abstract Human T-cell leukemia virus type 1 (HTLV-1) is associated with leukemia/lymphoma and neurologic disorders. Although the viral transcriptional activator Tax is the critical viral oncoprotein, Rex, which regulates the expression of the viral structural and enzymatic genes, is essential for efficient viral replication. Herein, we investigate the contribution of Rex in HTLV-1 immortalization of primary T cells in vitro and viral survival in an infectious rabbit animal model. A Rex-deficient HTLV-1 (HTLVRex-) was constructed and characterized for viral gene expression, protein production, and immortalization capacity. Cells transiently transfected with the HTLVRex- proviral clone produced low detectable levels of p19 Gag. 729HTLVRex- stable transfectants produced functional Tax, but undetectable levels of Rex or p19 Gag. Coculture of irradiated 729HTLVRex- cells with peripheral blood mononuclear cells (PBMCs) resulted in sustained interleukin-2 (IL-2)-dependent growth of primary T lymphocytes. These cells carried the HTLVRex- genome and expressed tax/rex mRNA but produced no detectable Rex or p19 Gag. Rabbits inoculated with irradiated 729HTLVRex- cells or 729HTLVRex- cells transiently transfected with a Rex cDNA expression plasmid failed to become persistently infected or mount a detectable antibody response to the viral gene products. Together, our results provide the first direct evidence that Rex and its function to modulate viral gene expression and virion production is not required for in vitro immortalization by HTLV-1. However, Rex is critical for efficient infection of cells and persistence in vivo.

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