Differential regulation of host cellular genes by HIV-1 viral protein R (Vpr): cDNA microarray analysis using isogenic virus

Janket, Michelle L.; Manickam, Pachiappan; Majumder, Biswanath; Thotala, Dineshkumar; Wagner, M.; Schafer, Elizabeth A.; Collman, Ronald G.; Srinivasan, Alagarsamy; Ayyavoo, Velpandi

doi:10.1016/j.bbrc.2004.01.008

Cited by 17 publications

(12 citation statements)

References 24 publications

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“…Collectively, these proteins appear to manipulate host cell biology to ensure a favorable cellular environment for viral replication, transmission, dissemination, and immune evasion (Malim & Emerman, 2008). One of them in particular, the 14-kDa HIV-1 viral protein R (Vpr), down-regulates the expression of genes involved in cell cycle/proliferation, DNA repair, tumor antigen presentation by the host cell, and immune activation factors, and upregulates many ribosomal and structural proteins required for viral propagation (Janket et al, 2004;Levy et al, 1994;Wu et al, 1995, Sherman et al, 2000. These changes can occur in the absence of other viral gene products, suggesting that Vpr can mediate its proviral effects partially, or perhaps solely, through modulation of the target cell environment (Ayyavoo et al, 1997a).…”

Section: Viral Protein R Potentiates the Effect Of Glucocorticoid Recmentioning

confidence: 99%

“…Glucocorticoids are among the most commonly prescribed drugs worldwide due to their profound anti-inflammatory and immunosuppressive activity (Herold et al, 2006;Kim et al, 2001;Janket et al, 2004). They control homeostasis of T cell monocytes/macrophages, osteoclasts, and dendritic cells by inducing their apoptosis or inhibiting maturation.…”

Section: Role Of Glucocorticoid Receptor In Immune Resonance Retrovimentioning

confidence: 99%

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The Glucocorticoid Receptor in Retroviral Infection

Fouty¹,

Solodushko²

2011

Viral Gene Therapy

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Section: Viral Protein R Potentiates the Effect Of Glucocorticoid Recmentioning

confidence: 99%

Section: Role Of Glucocorticoid Receptor In Immune Resonance Retrovimentioning

confidence: 99%

The Glucocorticoid Receptor in Retroviral Infection

Fouty¹,

Solodushko²

2011

Viral Gene Therapy

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“…[2][3][4][5] Specific HIV-1 gene products including Tat, Nef, gp120, and Vpr were examined to dissect their role in modifying transcription of cellular genes. [6][7][8][9] Some of these differentially expressed cellular genes may play a role in host defense or pathology of the host cell.…”

mentioning

confidence: 99%

Knockdown of ERM Family Member Moesin in Host Cells Increases HIV Type 1 Replication

Capalbo

Mueller-Kuller

Marković

et al. 2011

AIDS Research and Human Retroviruses

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Moesin is a member of the ERM (ezrin, radixin, moesin) family of cytoskeleton/membrane structure organizing and signal transduction proteins. Previously, we found an increased expression of moesin during HIV-1 infection. Moesin was also reported to be incorporated into HIV-1 virions. To analyze whether moesin is a host factor affecting the replication cycle of human immunodeficiency virus type 1 (HIV-1), we used small interfering RNAs (siRNAs) to evaluate the effect of moesin knockdown on HIV-1 replication in P4-CCR5 cells. Moesin's knockdown did not affect the cell viability or cell phenotype. Interestingly, we observed a marked increase in viral replication, as demonstrated by enhanced HIV-1 RNA, p24 antigen, and ß-galactosidase reporter expression. Moesin-dependent enhancement of HIV-1 replication was confirmed in lymphocytic host cells (Jurkat). These results suggest an overall rather restrictive role of moesin for HIV-1 replication in host cells in vitro.

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“…7 Specific HIV-1 gene products including Tat, Nef, gp120, and Vpr were examined to dissect their role in modifying transcription of cellular genes. [8][9][10][11] In general, some of the differentially expressed cellular genes may play a role in host defense mechanisms and/or facilitate HIV-1 replication, infectivity, and species propagation or survival. As HIV-1 replication hinges on a multitude of HIV-1 dependency factors (HDF), [12][13][14] it is assumed that HIV-1 redirects the cellular machinery favoring cellular factors that support its replication and interfering with cellular factors that inhibit viral replication.…”

mentioning

confidence: 99%

Inhibition of X4-Tropic HIV Type 1 Replication by Knockdown of the Cellular Protein LEREPO4

Capalbo

Müller-Kuller²,

Dietrich³

et al. 2010

AIDS Research and Human Retroviruses

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Human immunodeficiency virus 1 (HIV-1) and host cell factors show important mutual interactions. We found that HIV-1 infection induced expression of a likely ortholog of mouse immediate early response erythropoietin 4 (LEREPO4) in vitro. When LEREPO4 expression was suppressed by siRNA in P4-CCR5 cells, HIV-1 replication showed significantly reduced HIV-1 transcript and p24 protein levels as measured by quantitative PCR and ELISA, respectively. The LEREPO4 knockdown also had an inhibitory effect on HIV-1-LTR-driven reporter plasmid expression of β-galactosidase. Furthermore, the inhibitory effect of LEREPO4 silencing on HIV-1 replication was confirmed in Jurkat T cells. The up-regulation of LEREPO4 by HIV-1 and the inhibition of HIV-1 replication mediated by knockdown of LEREPO4 may point to an important functional role of LEREPO4 as a novel HIV-1 dependency factor.

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Differential regulation of host cellular genes by HIV-1 viral protein R (Vpr): cDNA microarray analysis using isogenic virus

Cited by 17 publications

References 24 publications

The Glucocorticoid Receptor in Retroviral Infection

The Glucocorticoid Receptor in Retroviral Infection

Knockdown of ERM Family Member Moesin in Host Cells Increases HIV Type 1 Replication

Inhibition of X4-Tropic HIV Type 1 Replication by Knockdown of the Cellular Protein LEREPO4

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