Impact of mitochondrial regulation of apoptosis on the pathogenesis and treatment of HIV-1-induced immunodeficiency

Eric J. Buenz, Andrew David Badley

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

HIV-1 infection causes the depletion of CD4 T cells, which results in AIDS. There are numerous potential mechanisms by which this cell death can occur, and a majority of the molecular mechanisms involve the mitochondria. Furthermore, current HIV therapies also have an impact on mitochondrial stability. The alteration in apoptotic homeostasis induced by HIV, HIV proteins, the host response to HIV infection and/or HIV therapies either promote apoptosis or inhibit apoptotic signals depending on the cellular context. Latent HIV reservoirs prevent the eradication of the virus because these cells are resistant to apoptosis: a change potentially induced at the level of the mitochondria. Many of the novel treatment strategies aimed at eradicating the virus involve alterations of mitochondrial regulation of apoptosis.

Original languageEnglish (US)
Pages (from-to)235-254
Number of pages20
JournalMitochondrion
Volume4
Issue number2-3
DOIs
StatePublished - Jul 2004

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HIV-1
HIV
Apoptosis
HIV Infections
Mitochondria
Viruses
Human Immunodeficiency Virus Proteins
Acquired Immunodeficiency Syndrome
Homeostasis
Cell Death
T-Lymphocytes
Therapeutics

Keywords

  • Apoptosis
  • HIV
  • Mitochondria

ASJC Scopus subject areas

  • Biophysics

Cite this

Impact of mitochondrial regulation of apoptosis on the pathogenesis and treatment of HIV-1-induced immunodeficiency. / Buenz, Eric J.; Badley, Andrew David.

In: Mitochondrion, Vol. 4, No. 2-3, 07.2004, p. 235-254.

Research output: Contribution to journalArticle

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