Cell death pathways in retroviral infection

Piacentini, Mauro; Kroemer, Guido

doi:10.1038/sj.cdd.4401655

Cited by 3 publications

(3 citation statements)

References 15 publications

(22 reference statements)

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“…Apoptosis at the late stage of the viral life cycle avails the egress of some viruses by adopting a tolerogenic type of cell death and subverting host's immune response [54] (Figure 2). Accordingly, many viruses develop strategies to promote apoptosis whenever favorable.…”

Section: Apoptosismentioning

confidence: 99%

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Orchestrated efforts on host network hijacking: Processes governing virus replication

et al. 2020

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With the high pervasiveness of viral diseases, the battle against viruses has never ceased. Here we discuss five cellular processes, namely "autophagy", "programmed cell death", "immune response", "cell cycle alteration", and "lipid metabolic reprogramming", that considerably guide viral replication after host infection in an orchestrated manner. On viral infection, "autophagy" and "programmed cell death" are two dynamically synchronized cell survival programs; "immune response" is a cell defense program typically suppressed by viruses; "cell cycle alteration" and "lipid metabolic reprogramming" are two altered cell housekeeping programs tunable in both directions. We emphasize on their functionalities in modulating viral replication, strategies viruses have evolved to tune these processes for their benefit, and how these processes orchestrate and govern cell fate upon viral infection. Understanding how viruses hijack host networks has both academic and industrial values in providing insights toward therapeutic strategy design for viral disease control, offering useful information in applications that aim to use viral vectors to improve human health such as gene therapy, and providing guidelines to maximize viral particle yield for improved vaccine production at a reduced cost. ARTICLE HISTORY

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Section: Apoptosismentioning

confidence: 99%

“…Apoptosis triggered in non-infected inflammatory or immune cells could paralyze host's innate and adaptive defense systems to foster a favorable environment for the progression of viruses and their progenies ( Figure 2) [54]. It was observed that T cells isolated from HIVinfected individuals underwent spontaneous apoptosis.…”

Section: Apoptosismentioning

confidence: 99%

Orchestrated efforts on host network hijacking: Processes governing virus replication

et al. 2020

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“…Both HIV-1 associated dementia (HAD) and a milder form of HIV-1 associated cognitive disorder, known as minor cognitive and motor disorder (MCMD) are frequent complications of the acquired immunodeficiency syndrome (AIDS) and are characterized by neuronal dysfunction and cell death caused by HIV-1 through direct and indirect mechanisms [1-4]. …”

Section: Introductionmentioning

confidence: 99%

HIV-1 Nef increases astrocyte sensitivity towards exogenous hydrogen peroxide

Masanetz

Lehmann

2011

Virol J

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BackgroundHIV-1 infected individuals are under chronic exposure to reactive oxygen species (ROS) considered to be instrumental in the progression of AIDS and the development of HIV-1 associated dementia (HAD). Astrocytes support neuronal function and protect them against cytotoxic substances including ROS. The protein HIV-1 Nef, a progression factor in AIDS pathology is abundantly expressed in astrocytes in patients with HAD, and thus may influence its functions.ResultsEndogenous expressed HIV-1 Nef leads to increased sensitivity of human astrocytes towards exogenous hydrogen peroxide but not towards TNF-alpha. Cell death of nef-expressing astrocytes exposed to 10 μM hydrogen peroxide for 30 min occurred within 4 h.ConclusionHIV-1 Nef may contribute to neuronal dysfunction and the development of HAD by causing death of astrocytes through decreasing their tolerance for hydrogen peroxide.

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New insights on the role of apoptosis and autophagy in HIV pathogenesis

Gougeon

Piacentini

2009

Apoptosis

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Viruses manipulate host cells to ensure their own survival and, at late stages of the viral life cycle, they kill the infected target cell to ensure their propagation. In addition, some viruses induce a bystander killing, a viral strategy to escape from the host's innate and cognate defense systems. In HIV-infection, the disabling of the immune system is initially due to the preferential depletion by apoptosis of virus-specific CD4(+) T cells in lymphoid tissues, followed by the destruction of non-infected bystander cells. Both the extrinsic and the intrinsic pathways are activated, and this is the consequence of systemic immune activation. This review presents recent developments showing that the gastrointestinal tract is the major reservoir of infected cells and the site of rapid and profound loss of CD4 T cells, and that microbial translocation from the gastrointestinal tract is the cause of immune activation. Furthermore, apoptosis mechanisms involved in HIV-induced neuropathological disorders are discussed, including the role of syncytia that involve the sequential activation of ATM, p38MAPK and p53. Finally, HIV-associated dementia (HAD) was recently found in monkey models to be linked to inhibition of autophagy in neurons, suggesting that homeostasis of autophagy is a reliable security factor for neurons, and challenging the development of new therapeutics aimed at boosting neuronal autophagy to prevent HAD.

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Cell death pathways in retroviral infection

Cited by 3 publications

References 15 publications

Orchestrated efforts on host network hijacking: Processes governing virus replication

Orchestrated efforts on host network hijacking: Processes governing virus replication

HIV-1 Nef increases astrocyte sensitivity towards exogenous hydrogen peroxide

New insights on the role of apoptosis and autophagy in HIV pathogenesis

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