Both necrosis and apoptosis contribute to HIV-1-induced killing of CD4 cells

Plymale, Douglas R.; Tang, Derek S. Ng; Comardelle, Alla M; Fermin, César D.; Lewis, Dorothy E.; Garry, Robert F.

doi:10.1097/00002030-199910010-00004

Cited by 62 publications

(37 citation statements)

References 43 publications

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“…Thus, in both cases, virus indeed use spermatozoa as a vehicle. Damages in the neck observed in Figures 2a and 3a indicate that the mitochondria related structure could have been seriously affected, which is consistent with the earlier observations [6]; namely that HIV infected patients (with HAART) show signals of mitochondrial necrosis, one of the controlled mechanisms of cell death [11]. The situation from the morphological point of view has been worsening after HAART.…”

Section: Discussionsupporting

confidence: 89%

Use of Atomic Force Microscopy to Reveal Sperm Ultrastructure in Hiv-Patients on Highly Active Antiretroviral Therapy

Barboza

Medina

Hernández

et al. 2004

Archives of Andrology

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Section: Discussionsupporting

confidence: 89%

Use of Atomic Force Microscopy to Reveal Sperm Ultrastructure in Hiv-Patients on Highly Active Antiretroviral Therapy

Barboza

Medina

Hernández

et al. 2004

Archives of Andrology

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“…NFB has been shown to be involved with HIV-1 Tat and host cellular factors, such as positive transcription elongation factor B, in promoting elongation of transcription of integrated HIV-1 proviral DNA (37,38). Triggering through Toll receptor pathways as well as viral replication have lethal cytopathic effects on host cells (25,26). Nevertheless, in the studies reported herein, a significantly high viability (Ն95%) was observed during a 10-wk period of productive infection in CBMC (Fig.…”

Section: Discussionmentioning

confidence: 63%

“…Acute HIV-1 infection of CD4 ϩ T cells leads to active viral replication, which causes death of both infected and uninfected bystander cells by multiple apoptotic and necrotic mechanisms (24,25). In addition, apoptotic signaling pathways have also been shown to be triggered by activation through TLR-mediated pathways (26).…”

Section: Tlr Agonists or Viral Replication Do Not Induce Apoptosismentioning

confidence: 99%

Signaling through Toll-Like Receptors Triggers HIV-1 Replication in Latently Infected Mast Cells

Sundstrom

Little

Villinger

et al. 2004

The Journal of Immunology

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Evidence that human progenitor mast cells are susceptible to infection with CCR5-tropic strains of HIV-1 and that circulating HIV-1-infected FcεRIα+ cells with a similar progenitor phenotype have been isolated from AIDS patients has led to speculation that mast cells may serve as a potential reservoir for infectious HIV-1. In this study, progenitor mast cells, developed in vitro from CD34+ cord blood stem cells, were experimentally infected with the CCR5-tropic strain HIV-1Bal after 28 days in culture as they reached their HIV-1-susceptible progenitor stage. HIV-1 p24 Ag levels were readily detectable by day 7 postinfection (PI), peaked at 2–3 wk PI as mature (tryptase/chymase-positive) HIV-1 infection-resistant mast cells emerged, and then steadily declined to below detectable limits by 10 wk PI, at which point integrated HIV-1 proviral DNA was confirmed by PCR quantitation in (∼34% of) latently infected mast cells. Stimulation by ligands for Toll-like receptor (TLR) 2, TLR4, or TLR9 significantly enhanced viral replication in a dose- and time-dependent manner in both HIV-1-infected progenitor and latently infected mature mast cells, without promoting degranulation, apoptosis, cellular proliferation, or dysregulation of TLR agonist-induced cytokine production in infected mast cells. Limiting dilution analysis of TLR activated, latently infected mature mast cells indicated that one in four was capable of establishing productive infections in A301 sentinel cells. Taken together, these results indicate that mast cells may serve both as a viral reservoir and as a model for studying mechanisms of postintegration latency in HIV infection.

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“…10 It was then concluded that HIV-1 infection resulted in profound disorders in the immune system with a loss of CD4 + T cells and a reduction of the CD4 + /CD8 + T cell ratio. 11 However, the pathogenic mechanism responsible for these consequences remains elusive.…”

Section: Cd4mentioning

confidence: 99%

Comparison of Transcriptional Profiles Between CD4⁺ and CD8⁺ T Cells in HIV Type 1-Infected Patients

Ye²,

Han³

et al. 2014

AIDS Research and Human Retroviruses

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The CD4+ /CD8 + T cell ratio is altered when HIV-1 infects the human immune system. However, the exact mechanisms of how CD4+ and CD8 + T cells participate in HIV infection are still unknown. This study used bioinformatics methods to compare the transcriptional profiles between CD4+ and CD8 + T cells in HIV-1-infected patients in order to explore the potential molecular mechanisms of CD4 + and CD8 + T cells in HIV-1 infection. We found that expression patterns of differentially expressed genes (DEG) in CD4 + T cells were dramatically different from those in CD8 + T cells. We also constructed protein-protein interaction (PPI) networks to extract functional modules at each stage, and found that some of the important genes such as BRCA1 were central hubs of the modules. Finally, we applied functional annotation to the modules and found that CD4 + /CD8 + T cells played critical roles in regulating the cell cycle and other cellular pathways. Thus, this study would greatly further our understanding of the roles of T cells in HIV infection, and provide potential clues for developing AIDS vaccines in the future.

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Both necrosis and apoptosis contribute to HIV-1-induced killing of CD4 cells

Abstract: Both necrosis and apoptosis contribute to HIV-1-induced killing of CD4 cells.

Cited by 62 publications

References 43 publications

Use of Atomic Force Microscopy to Reveal Sperm Ultrastructure in Hiv-Patients on Highly Active Antiretroviral Therapy

Use of Atomic Force Microscopy to Reveal Sperm Ultrastructure in Hiv-Patients on Highly Active Antiretroviral Therapy

Signaling through Toll-Like Receptors Triggers HIV-1 Replication in Latently Infected Mast Cells

Comparison of Transcriptional Profiles Between CD4⁺ and CD8⁺ T Cells in HIV Type 1-Infected Patients

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Both necrosis and apoptosis contribute to HIV-1-induced killing of CD4 cells

Abstract: Both necrosis and apoptosis contribute to HIV-1-induced killing of CD4 cells.

Cited by 62 publications

References 43 publications

Use of Atomic Force Microscopy to Reveal Sperm Ultrastructure in Hiv-Patients on Highly Active Antiretroviral Therapy

Use of Atomic Force Microscopy to Reveal Sperm Ultrastructure in Hiv-Patients on Highly Active Antiretroviral Therapy

Signaling through Toll-Like Receptors Triggers HIV-1 Replication in Latently Infected Mast Cells

Comparison of Transcriptional Profiles Between CD4+ and CD8+ T Cells in HIV Type 1-Infected Patients

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Comparison of Transcriptional Profiles Between CD4⁺ and CD8⁺ T Cells in HIV Type 1-Infected Patients