Revisiting Regulated Cell Death Responses in Viral Infections

Rex, Devasahayam Arokia Balaya; Prasad, T. S. Keshava; Kandasamy, Richard K.

doi:10.3390/ijms23137023

Cited by 28 publications

(11 citation statements)

References 276 publications

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“…For instance, the ability to delay or prevent apoptosis provides viruses with more time and opportunities to replicate and assemble viral particles and promotes long-term survival of viruses in the host cell as well as their spread to surrounding hosts cells, which can lead to persistent infection. Thus, apoptosis induced by HIV-1 contributes, among many mechanisms, to the gradual T cell decline that occurs in HIV-infected patients, and programmed cell death of uninfected bystander T lymphocytes, including CD4 + and CD8 + T cells ( Rex et al 2022 ). The same is true for cellular senescence, often considered a part of the host cell response to fight viruses ( Baz-Martínez et al 2016 ; Kelley et al 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Interactomics: Dozens of Viruses, Co-evolving With Humans, Including the Influenza A Virus, may Actively Distort Human Aging

Teulière

Bernard

Bonnefous

et al. 2023

Molecular Biology and Evolution

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Some viruses (e.g. HIV-1, SARS-CoV-2) have been experimentally proposed to accelerate features of human ageing and of cellular senescence. These observations, along with evolutionary considerations on viral fitness, raised the more general puzzling hypothesis that, beyond documented sources in human genetics, ageing in our species may also depend on virally-encoded interactions distorting our ageing to the benefits of diverse viruses. Accordingly, we designed systematic network-based analyses of the human and viral protein interactomes, which unraveled dozens of viruses encoding proteins experimentally demonstrated to interact with proteins from pathways associated with human ageing, including cellular senescence. We further corroborated our predictions that specific viruses interfere with human ageing using published experimental evidence and transcriptomic data; identifying influenza A virus (subtype H1N1) as a major candidate age-distorter, notably through manipulation of cellular senescence. By providing original evidence that viruses may convergently contribute to the evolution of numerous age-associated pathways through co-evolution, our network- and bipartite network-based methodology supports an ecosystemic study of ageing, also searching for genetic causes of ageing outside a focal ageing species. Our findings, predicting age-distorters and targets for anti-ageing therapies amongst human viruses, could have fundamental and practical implications for evolutionary biology, ageing study, virology, medicine and demography.

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Section: Discussionmentioning

confidence: 99%

Interactomics: Dozens of Viruses, Co-evolving With Humans, Including the Influenza A Virus, may Actively Distort Human Aging

Teulière

Bernard

Bonnefous

et al. 2023

Molecular Biology and Evolution

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“…Lymphopenia may be caused by cell-in-cell (CIC) structures, which are phenomena referring to lymphocytes internalized in IECs [ 41 , 120 , 137 ]. CIC structures, commonly found in cancer, can be driven by mitosis and potentially tumor-induced autophagy [ 138 ]. Interestingly, lymphopenia has been associated with mitochondrial dysfunction [ 139 ].…”

Section: Microbial Translocationmentioning

confidence: 99%

Long COVID as a Tauopathy: Of “Brain Fog” and “Fusogen Storms”

Sfera

Rahman

Campo

et al. 2023

IJMS

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Long COVID, also called post-acute sequelae of SARS-CoV-2, is characterized by a multitude of lingering symptoms, including impaired cognition, that can last for many months. This symptom, often called “brain fog”, affects the life quality of numerous individuals, increasing medical complications as well as healthcare expenditures. The etiopathogenesis of SARS-CoV-2-induced cognitive deficit is unclear, but the most likely cause is chronic inflammation maintained by a viral remnant thriving in select body reservoirs. These viral sanctuaries are likely comprised of fused, senescent cells, including microglia and astrocytes, that the pathogen can convert into neurotoxic phenotypes. Moreover, as the enteric nervous system contains neurons and glia, the virus likely lingers in the gastrointestinal tract as well, accounting for the intestinal symptoms of long COVID. Fusogens are proteins that can overcome the repulsive forces between cell membranes, allowing the virus to coalesce with host cells and enter the cytoplasm. In the intracellular compartment, the pathogen hijacks the actin cytoskeleton, fusing host cells with each other and engendering pathological syncytia. Cell–cell fusion enables the virus to infect the healthy neighboring cells. We surmise that syncytia formation drives cognitive impairment by facilitating the “seeding” of hyperphosphorylated Tau, documented in COVID-19. In our previous work, we hypothesized that the SARS-CoV-2 virus induces premature endothelial senescence, increasing the permeability of the intestinal and blood–brain barrier. This enables the migration of gastrointestinal tract microbes and/or their components into the host circulation, eventually reaching the brain where they may induce cognitive dysfunction. For example, translocated lipopolysaccharides or microbial DNA can induce Tau hyperphosphorylation, likely accounting for memory problems. In this perspective article, we examine the pathogenetic mechanisms and potential biomarkers of long COVID, including microbial cell-free DNA, interleukin 22, and phosphorylated Tau, as well as the beneficial effect of transcutaneous vagal nerve stimulation.

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“…Apoptosis, as well as two forms of regulated necrosis—necroptosis and pyroptosis, are considered as the main ways of virus associated cell death [ 28 , 29 ]. cfDNA can also originate from neutrophil extracellular traps (NETs), web-like structures formed due to the programmed death of neutrophils called NETosis in response to infections or cancer [ 30 ]. Brinkmann et al [ 31 ] for the first time reported that NETs are composed of decondensed chromatin complexed with neutrophil proteins (e.g., neutrophil elastase and myeloperoxidase) which are able to capture, neutralize, and kill microbes.…”

Section: Brief Overview Of Cell-free Dnamentioning

confidence: 99%

The Diagnostic, Prognostic, and Therapeutic Potential of Cell-Free DNA with a Special Focus on COVID-19 and Other Viral Infections

Hovhannisyan,

Harutyunyan,

Aroutiounian

et al. 2023

IJMS

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Cell-free DNA (cfDNA) in human blood serum, urine, and other body fluids recently became a commonly used diagnostic marker associated with various pathologies. This is because cfDNA enables a much higher sensitivity than standard biochemical parameters. The presence of and/or increased level of cfDNA has been reported for various diseases, including viral infections, including COVID-19. Here, we review cfDNA in general, how it has been identified, where it can derive from, its molecular features, and mechanisms of release and clearance. General suitability of cfDNA for diagnostic questions, possible shortcomings and future directions are discussed, with a special focus on coronavirus infection.

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Revisiting Regulated Cell Death Responses in Viral Infections

Cited by 28 publications

References 276 publications

Interactomics: Dozens of Viruses, Co-evolving With Humans, Including the Influenza A Virus, may Actively Distort Human Aging

Interactomics: Dozens of Viruses, Co-evolving With Humans, Including the Influenza A Virus, may Actively Distort Human Aging

Long COVID as a Tauopathy: Of “Brain Fog” and “Fusogen Storms”

The Diagnostic, Prognostic, and Therapeutic Potential of Cell-Free DNA with a Special Focus on COVID-19 and Other Viral Infections

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