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Updated: Aug 16, 2026

Cellular Redox Profiling Using High-content Microscopy
Published on: May 14, 2017
HIV-1 triggers mitochondrion death
Damien Arnoult1, Laurence Viollet, Frédéric Petit
1NIH/NINDS, Biochemistry Section, Bldg 10, room 4N258, Bethesda, MD 20892, USA.
Abstract:
Apoptosis, a phenotype of programmed cell death involved in development and tissue homeostasis of multicellular organisms, brings into two major pathways and implies a central sensor: the mitochondria. Abnormalities in the cell death control can lead to a variety of diseases and many pathogenic agents target the mitochondria, especially affecting its permeability in order to induce cell death. HIV infection is linked to progressive CD4 T cell depletion. Among the different hypothesis that may explain T cell depletion, apoptosis is one of the main described mechanisms. This review provides current knowledge in HIV-mediated mitochondrial damage due to (i) HIV-specific proteins, (ii) death-by-neglect and (iii) side effects of the HIV drugs.
Insights
Human immunodeficiency virus (HIV) infection causes CD4 T cell depletion through apoptosis, a programmed cell death pathway. This review examines how HIV proteins, neglect, and drug side effects damage mitochondria, leading to cell death.
Area of Science:
- Cell Biology
- Immunology
- Virology
Background:
- Apoptosis, or programmed cell death, is crucial for multicellular organism development and tissue homeostasis.
- Mitochondria act as central sensors in apoptosis, with their permeability alterations often inducing cell death.
- Dysregulation of cell death pathways is implicated in various diseases, and pathogens frequently target mitochondria.
Purpose of the Study:
- To review current knowledge on HIV-mediated mitochondrial damage.
- To explore the mechanisms contributing to CD4 T cell depletion in HIV infection.
- To consolidate understanding of apoptosis as a key factor in HIV pathogenesis.
Main Methods:
- Literature review of scientific articles and research papers.
- Analysis of studies investigating HIV-specific proteins and their apoptotic effects.
- Examination of research on "death-by-neglect" mechanisms in HIV.
- Review of studies on the mitochondrial side effects of antiretroviral therapies.
Main Results:
- HIV infection is strongly associated with progressive CD4 T cell depletion.
- Apoptosis is a primary mechanism contributing to T cell loss in HIV.
- HIV-specific proteins, cellular neglect, and antiretroviral drug toxicity all contribute to mitochondrial dysfunction and apoptosis.
Conclusions:
- Mitochondrial damage and subsequent apoptosis are central to CD4 T cell depletion in HIV infection.
- Understanding these mechanisms is vital for developing therapeutic strategies against HIV.
- Further research into HIV-induced mitochondrial pathways can elucidate disease progression and treatment outcomes.
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