HIV-1 Infection Dysregulates Cell Cycle Regulatory Protein p21 in CD4+ T Cells Through miR-20a and miR-106b Regulation

2016 ◽  
Vol 117 (8) ◽  
pp. 1902-1912 ◽  
Author(s):  
Debjani Guha ◽  
Allison Mancini ◽  
Jessica Sparks ◽  
Velpandi Ayyavoo
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
Cd4 T Cells ◽  
Regulatory Protein ◽  
Cell Cycle Regulatory Protein ◽  
Hiv 1

scholarly journals IL-7 differentially regulates cell cycle progression and HIV-1-based vector infection in neonatal and adult CD4+ T cells

2001 ◽  
Vol 98 (16) ◽  
pp. 9277-9282 ◽  
Author(s):  
V. Dardalhon ◽  
S. Jaleco ◽  
S. Kinet ◽  
B. Herpers ◽  
M. Steinberg ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
Cd4 T Cells ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Hiv 1

scholarly journals Expression of the c-myc Proto-oncogene Is Essential for HIV-1 Infection in Activated T Cells

1999 ◽  
Vol 189 (9) ◽  
pp. 1391-1398 ◽  
Author(s):  
Yu Sun ◽  
Edward A. Clark
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
Nuclear Import ◽  
Antisense Oligonucleotide ◽  
Cd4 T Cells ◽  
Apoptotic Cell ◽  
Activated T Cells ◽  
Cell Cycle Entry ◽  
Phosphorothioate Oligodeoxynucleotides ◽  
Hiv 1

We previously found that activation of primary CD4+ T cells via both the T cell antigen receptor (TCR) and CD28 is required for HIV-1 DNA to be translocated from the cytoplasm to the nucleus. Here we report that expression of c-Myc protein in CD4+ T cells is induced only after such costimulation. In addition, cyclosporin A not only inhibits nuclear import of HIV-1 DNA but also inhibits expression of c-Myc protein. Because of these correlations, we tested whether c-Myc is necessary for nuclear import of HIV-1 DNA. Specific c-myc antisense, but not sense or non-sense, phosphorothioate oligodeoxynucleotides selectively induced the accumulation of two NH2-terminally truncated c-Myc proteins and abolished HIV-1 genome entry into host nuclei. Consequently, both virus replication and HIV-1–induced apoptotic cell death were inhibited. Synthesis of viral full-length DNA was not affected. Specific c-myc antisense oligonucleotide inhibited HIV-1 infection under conditions that did not affect cell cycle entry or proliferation. Thus, c-Myc appears to regulate HIV-1 DNA nuclear import via a mechanism distinct from those controlling entry into the cell cycle.

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