Interplay between the DNA damage response and the life cycle of DNA tumor viruses

Studstill, Caleb J.; Mac, Michelle; Moody, Cary A.

doi:10.1016/j.tvr.2023.200272

Cited by 4 publications

(4 citation statements)

References 197 publications

(286 reference statements)

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“…Together with EBNA-LP, it can replace the intracellular part of Notch, repressing the regulatory signaling and escaping from the innate immune system [ 33 ]. Common to all DNA tumor viruses, they can interfere with the cell’s DNA damage-repair mechanism (DDR), promoting the disruption of the host cells’ integrity and making possible oncogenic mutations [ 65 ].…”

Section: Viral Infectionsmentioning

confidence: 99%

“…This antigen is the critical modulator of viral persistence in cells, which is typical for this infection [ 73 ]. LANA directly interacts with p53 and Rb, disrupting genomic repair mechanisms [ 65 ]. Another viral protein, vIRF1, negatively regulates the ATM-dependent activation of p53 [ 65 ].…”

Section: Viral Infectionsmentioning

confidence: 99%

“…LANA directly interacts with p53 and Rb, disrupting genomic repair mechanisms [ 65 ]. Another viral protein, vIRF1, negatively regulates the ATM-dependent activation of p53 [ 65 ]. The critical element of latent HHV8 infection is through the DNA damage-response (DDR) modulation.…”

Section: Viral Infectionsmentioning

confidence: 99%

“…This negative regulation alters the cell’s ability to repair detected DNA damage, which is required for viral persistence. However, disrupting these mechanisms makes the B-cells more susceptible to acquiring additional mutations and survival, which is a critical first step of malignant clone evolution [ 65 ]. The KSHV/HHV8 positive DLBCL is a rare entity that accounts for 0.1% of DLBCL cases [ 19 ].…”

Section: Viral Infectionsmentioning

confidence: 99%

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The Possible Role of Pathogens and Chronic Immune Stimulation in the Development of Diffuse Large B-Cell Lymphoma

Gergely,

Udvardy,

Illes

2024

Biomedicines

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Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma. The disease is very heterogeneous, with distinct genetic alterations in subtypes. The WHO 2022 5th edition classification identifies several minor groups of large B-cell lymphoma where the pathogenetic role of viruses (like EBV and HHV-8) is identified. Still, most cases fall into the group of DLBCL not otherwise specified (NOS). No review focuses only on this specific lymphoma type in the literature. The pathogenesis of this entity is still not fully understood, but several viruses and bacteria may have a role in the development of the disease. The authors review critical pathogenetic events in the development of DLBCL (NOS) and summarize the data available on several pathogenetic viruses and bacteria that have a proven or may have a potential role in the development of this lymphoma type. The possible role of B-cell receptor signaling in the microenvironment is also discussed. The causative role of the Epstein–Barr virus (EBV), human herpesvirus-8 (HHV-8), Hepatitis C virus (HCV), human immunodeficiency virus (HIV), Hepatitis B virus (HBV), and other viruses are explored. Bacterial infections, such as Helicobacter pylori, Campylobacter jejuni, Chlamydia psittaci, Borrelia burgdorferi, and other bacteria, are also reviewed.

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Section: Viral Infectionsmentioning

confidence: 99%

Section: Viral Infectionsmentioning

confidence: 99%

Section: Viral Infectionsmentioning

confidence: 99%

Section: Viral Infectionsmentioning

confidence: 99%

See 2 more Smart Citations

The Possible Role of Pathogens and Chronic Immune Stimulation in the Development of Diffuse Large B-Cell Lymphoma

Gergely,

Udvardy,

Illes

2024

Biomedicines

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SARS-CoV-2 predation of Golgi-bound PI4P primes the massive activation of the DNA Damage Response kinase ATM in the cytoplasm

Rebendenne,

Soulet,

Valadaõ

et al. 2024

Preprint

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Like all viruses, SARS-CoV-2, the causative agent of COVID-19, relies on host cell resources to replicate. Our study reveals that, among these resources, SARS-CoV-2 hijacks the oxysterol-binding protein 1 (OSBP1) transporter to exploit the Golgi-bound phosphatidylinositol-4-phosphate (PI4P) pool. This leads to a depletion of Golgi-resident PI4P, triggering the activation of the ATM DNA Damage Response (DDR) kinase in the cytoplasm. As such, ATM, typically anchored to PI4P at the Golgi in an inactive state, undergoes auto-phosphorylation and cytoplasmic release upon SARS-CoV-2-induced PI4P depletion. Conversely, pharmacological inhibition of ATM auto-phosphorylation, which stabilizes its interaction with PI4P, significantly impairs SARS-CoV-2 replication. The requirement for PI4P and impact of ATM inhibition might be conserved across coronaviruses, as similar effects were observed with HCoV-229E. Finally, SARS-CoV-2-induced, cytoplasmic ATM pre-activation primes cells for an accelerated response to DNA damage, which might contribute to the severe outcomes of COVID-19 observed in cancer patients undergoing chemo- or radiotherapy. Therefore, this study uncovers a DNA damage-independent mode of ATM activation and highlights the potential of ATM inhibitors as therapeutic agents against COVID-19.

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Abortive Infection of Animal Cells: What Goes Wrong

Embry,

Gammon

2024

Annual Review of Virology

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Even if a virus successfully binds to a cell, defects in any of the downstream steps of the viral life cycle can preclude the production of infectious virus particles. Such abortive infections are likely common in nature and can provide fundamental insights into the cell and host tropism of viral pathogens. Research over the past 60 years has revealed an incredible diversity of abortive infections by DNA and RNA viruses in various animal cell types. Here we discuss the general causes of abortive infections and provide specific examples from the literature to illustrate the range of abortive infections that have been reported. We also discuss how abortive infections can have critical roles in shaping host immune responses and in the development of virus-induced cancers. Finally, we describe how abortive infections can be applied to basic and clinical research, underscoring the importance of understanding these fascinating aspects of virus biology.

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Interplay between the DNA damage response and the life cycle of DNA tumor viruses

Cited by 4 publications

References 197 publications

The Possible Role of Pathogens and Chronic Immune Stimulation in the Development of Diffuse Large B-Cell Lymphoma

The Possible Role of Pathogens and Chronic Immune Stimulation in the Development of Diffuse Large B-Cell Lymphoma

SARS-CoV-2 predation of Golgi-bound PI4P primes the massive activation of the DNA Damage Response kinase ATM in the cytoplasm

Abortive Infection of Animal Cells: What Goes Wrong

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