Tumor necrosis factor alpha selectively sensitizes human immunodeficiency virus-infected cells to heat and radiation.

Wong, Grace; McHugh, Thomas M.; Weber, Richard F.; Goeddel, David V.

doi:10.1073/pnas.88.10.4372

Cited by 81 publications

(33 citation statements)

References 32 publications

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“…This absence of correlations does not exclude the participation of TNF␣ in causing oxidative stress in patients with hepatitis C. Although the induction of Mn-SOD by TNF␣ occurs in most cells, there are some human tumors cells lines and HIV-infected T lymphocytes where Mn-SOD is not induced by TNF␣. 31,33 On the other hand, it should be considered that Mn-SOD expression is modulated by a diversity of cytokines and proinflammatory mediators in addition to TNF␣.…”

Section: Discussionmentioning

confidence: 99%

Superoxide Dismutase in Patients With Chronic Hepatitis C Virus Infection

Larrea

Beloqui

Muñoz-Navas

et al. 1998

Free Radical Biology and Medicine

110

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Abstract-It has been reported that hepatitis C virus (HCV) may cause oxidative stress in infected cells. Patients with chronic hepatitis C exhibit an increased production of tumor necrosis factor-␣ (TNF␣), a cytokine that can produce oxidative stress by stimulating the generation of reactive oxygen species (ROS). Cell defense against ROS includes overexpression of Mn-superoxide dismutase (SOD), an inducible mitochondrial enzyme. To investigate cell defense against oxidative stress in HCV infection, we analyzed Mn-SOD mRNA in liver and in peripheral blood mononuclear cells (PBMC) from patients with chronic hepatitis C. Mn-SOD expression in PBMC was significantly increased in patients with HCV infection. Patients with sustained virological and biochemical response after therapy showed significantly lower Mn-SOD than patients with positive viremia. By contrast, Mn-SOD expression was not enhanced in the liver of patients with chronic hepatitis C. The values of Mn-SOD mRNA did not correlate with TNF␣ mRNA expression, viral load, or liver disease activity. Our results indicate that in HCV infection an induction of Mn-SOD was present in PBMC but absent in the liver, suggesting that this organ could be less protected against oxidative damage. Oxidative stress could participate in the pathogenesis of HCV infection.

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Section: Discussionmentioning

confidence: 99%

Superoxide Dismutase in Patients With Chronic Hepatitis C Virus Infection

Larrea

Beloqui

Muñoz-Navas

et al. 1998

Free Radical Biology and Medicine

110

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“…It has been proposed that oxidative stress induced by reactive oxygen species (ROS) may play a role in the stimulation of HIV viral replication, speci®cally by activating the nuclear factor (NF)-KB (Duh et al, 1989), which is thought to be necessary for HIV replication (Nabel & Baltimore, 1987). ROS have been implicated in the development of immunode®ciency (Wong et al, 1991) and oxidative stress has also been causally linked to AIDS dementia complex (Bjugstad et al, 1998;Vincent et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

A preliminary open label dose comparison using an antioxidant regimen to determine the effect on viral load and oxidative stress in men with HIV/AIDS

et al. 2001

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Objective: To investigate the effect of antioxidant supplementation on viral load and the antioxidantareactive oxygen species system in people with HIV. Design: Single centre, prospective, dose comparison study. Setting: Outpatient clinic specializing in HIV care. Subjects: Sixty-six participants were sequentially recruited by advertisement, and 48 subjects completed the study. Interventions: A recommended dose antioxidant regimen (5450 IU vitamin A as b-carotene, 250 mg vitamin C, 100 IU vitamin E, 100 mg selenium, 50 mg coenzyme Q10) or a high-dose antioxidant regimen (21 800 IU vitamin A as b-carotene, 1000 mg vitamin C, 400 IU vitamin E, 200 mg selenium, 200 mg coenzyme Q10) for a 12 week period. Results: Using repeated measures analysis of variance, the changes over treatment time were signi®cant for selenium, glutathione, glutathione peroxidase and lipid peroxides (P`0.03). Changes in allantoin, uric acid and viral load were not signi®cant (Pb0.05). The main effects for group and the interaction effects were not signi®cant for any of the parameters measured (P ! 0.05).

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“…The hypothesis that oxidative stress may be a mediator of apoptosis during HIV infection is supported by the broad-based loss of antioxidant defences and excess production of reactive oxygen species (ROS) during HIV disease [11]. Low levels of antioxidant lead to rapid generation of free radicals which in turn render T cells susceptible to apoptotic death [12]. Hyperthermia may also induce cell damage [12], and concomitant increases in ROS levels.…”

Section: Discussionmentioning

confidence: 99%

“…Low levels of antioxidant lead to rapid generation of free radicals which in turn render T cells susceptible to apoptotic death [12]. Hyperthermia may also induce cell damage [12], and concomitant increases in ROS levels. When this occurs in MCD, apoptosis with a similar increase in cellsurface hsp70 may occur, so explaining an apparent reduction of T cell numbers.…”

Section: Discussionmentioning

confidence: 99%

“…Oxidative stress may be a mediator of the apoptosis associated with HIV infection and this is correlated with the broad-based loss of antioxidant defences and excess production of reactive oxygen species (ROS) during disease [11]. The low levels of antioxidant render T cells in HIV infection susceptible to death by hyperthermia [12], a prevalent oxidative stress in clinical medicine [11]. We hypothesized that hyperthermia-induced T cell apoptosis may be an important feature in MCD.…”

Section: Introductionmentioning

confidence: 99%

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Heat shock-enhanced T cell apoptosis with heat shock protein 70 on T cell surface in multicentric Castleman's disease

Ishiyama¹,

Koike²,

Akimoto³

et al. 1996

Clinical and Experimental Immunology

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SUMMARYWe report here that T cells from patients with multicentric Castleman's disease (MCD) are sensitive to hyperthermia. T cells from two of three patients with MCD revealed DNA ladder formation and chromatin condensation following heat shock (30 min at 41 . 58C). Peripheral blood mononuclear cells (PBMC) from the same MCD patients exhibited high levels of spontaneous apoptosis after 72 h in culture and elevated apoptosis after heat shock, as evaluated by a quantitative flow cytometric assay. Heat shock protein 70 (hsp70) was detected on the cell surface of T cells in all three patients after heat shock. Furthermore, hsp70 was detected on T cells in the two MCD patients with apoptosis even in the absence of heat shock. T cells from normal samples did not show either heat-shock-induced expression of cell-surface hsp70 or apoptosis. Thus, heat shock treatment augmented hsp70 expression on the cell surface of T cells and enhanced apoptosis. Our studies suggest that hyperthermia may influence the clinical course of MCD.

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Tumor necrosis factor alpha selectively sensitizes human immunodeficiency virus-infected cells to heat and radiation.

Abstract: We report here that infection of the human

Cited by 81 publications

References 32 publications

Superoxide Dismutase in Patients With Chronic Hepatitis C Virus Infection

Superoxide Dismutase in Patients With Chronic Hepatitis C Virus Infection

A preliminary open label dose comparison using an antioxidant regimen to determine the effect on viral load and oxidative stress in men with HIV/AIDS

Heat shock-enhanced T cell apoptosis with heat shock protein 70 on T cell surface in multicentric Castleman's disease

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