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Article: HIV-1 Vpr-induced DNA damage activates NF-κB through ATM-NEMO independent of cell cycle arrest.

Sandoval, Carina / Nisson, Karly / Fregoso, Oliver I

bioRxiv : the preprint server for biology

2024

Abstract: Lentiviral accessory genes enhance replication through diverse mechanisms. HIV-1 accessory protein Vpr modulates the host DNA damage response (DDR) at multiple steps through DNA damage, cell cycle arrest, the degradation of host proteins, and both the ... ...

Abstract	Lentiviral accessory genes enhance replication through diverse mechanisms. HIV-1 accessory protein Vpr modulates the host DNA damage response (DDR) at multiple steps through DNA damage, cell cycle arrest, the degradation of host proteins, and both the activation and repression of DDR signaling. Vpr also alters host and viral transcription; however, the connection between Vpr-mediated DDR modulation and transcriptional activation remains unclear. Here, we determined the cellular consequences of Vpr-induced DNA damage using Vpr mutants that allow us to separate the ability of Vpr to induce DNA damage from cell cycle arrest and other DDR phenotypes including host protein degradation and repression of DDR. RNA-sequencing of cells expressing Vpr or Vpr mutants identified that Vpr alters cellular transcription through mechanisms both dependent and independent of cell cycle arrest. In tissue-cultured U2OS cells and primary human monocyte-derived macrophages (MDMs), Vpr-induced DNA damage activates the ATM-NEMO pathway and alters cellular transcription via NF-κB/RelA signaling. HIV-1 infection of primary MDMs validated Vpr-dependent NF-κB transcriptional activation during infection. Both virion delivered and
Language	English
Publishing date	2024-01-25
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.23.541990
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Article: NSC95397 is a Novel HIV Latency Reversing Agent.

Nichols Doyle, Randilea / Yang, Vivian / Damoiseaux, Robert / Fregoso, Oliver I

bioRxiv : the preprint server for biology

2023

Abstract: The latent viral reservoir represents one of the major barriers of curing HIV. Focus on the "kick and kill" approach, in which virus expression is reactivated then cells producing virus are selectively depleted, has led to the discovery of many latency ... ...

Abstract	The latent viral reservoir represents one of the major barriers of curing HIV. Focus on the "kick and kill" approach, in which virus expression is reactivated then cells producing virus are selectively depleted, has led to the discovery of many latency reversing agents (LRAs) that can reactivate latently integrated virus and further our understanding of the mechanisms driving HIV latency and latency reversal. Thus far, individual compounds have yet to be robust enough to work as a therapy, highlighting the importance of identifying new compounds that can act in novel pathways and synergize with known LRAs. In this study, we identified a promising LRA, NSC95397, from a screen of ~4250 compounds in J-Lat cell lines. We validated that NSC95397 reactivates latent viral transcription and protein expression from cells with unique integration events. Cotreating cells with NSC95397 and known LRAs demonstrated that NSC95397 has the potential to synergize with different drugs, such prostratin, a PKC agonist, and SAHA, an HDAC inhibitor. By looking at multiple common markers of open chromatin, we show that NSC95397 does not increase open chromatin globally. Bulk RNA sequencing revealed that NSC95397 does not greatly change cellular transcription. Instead, NSC95397 downregulates many pathways key to metabolism, cell growth, and DNA repair - highlighting the potential of these pathways in regulating HIV latency. Overall, we identified NSC95397 as a novel LRA that does not alter global transcription, that shows potential for synergy with known LRAs, and that may act through novel pathways not previously recognized for their ability to modulate HIV latency.
Language	English
Publishing date	2023-05-25
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.24.542213
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Article ; Online: Mind Your Cs and Gs.

Fregoso, Oliver I

Cell host & microbe

2017 Volume 22, Issue 5, Page(s) 575–576

Abstract: How can an innate immune sensor shape viral evolution? In recent work, Takata et al. (2017) determined that the antiviral protein ZAP recognizes CG dinucleotide composition to differentiate self from non-self. This pressure may have driven CG ... ...

Abstract	How can an innate immune sensor shape viral evolution? In recent work, Takata et al. (2017) determined that the antiviral protein ZAP recognizes CG dinucleotide composition to differentiate self from non-self. This pressure may have driven CG dinucleotide suppression in HIV-1 and other RNA viruses to evade host antiviral defenses.
MeSH term(s)	Antiviral Agents ; HIV-1 ; Humans ; Immunity, Innate/immunology ; RNA Viruses/genetics ; Virus Replication/drug effects
Chemical Substances	Antiviral Agents
Language	English
Publishing date	2017-11-09
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2017.10.012
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Article: Viral Modulation of the DNA Damage Response and Innate Immunity: Two Sides of the Same Coin

Lopez, Andrew / Nichols Doyle, Randilea / Sandoval, Carina / Nisson, Karly / Yang, Vivian / Fregoso, Oliver I.

Journal of molecular biology. 2021 Oct. 18,

2021

Abstract: The DDR consists of multiple pathways that sense, signal, and respond to anomalous DNA. To promote efficient replication, viruses have evolved to engage and even modulate the DDR. In this review, we will discuss a select set of diverse viruses and the ... ...

Abstract	The DDR consists of multiple pathways that sense, signal, and respond to anomalous DNA. To promote efficient replication, viruses have evolved to engage and even modulate the DDR. In this review, we will discuss a select set of diverse viruses and the range of mechanisms they evolved to interact with the DDR and some of the subsequent cellular consequences. There is a dichotomy in that the DDR can be both beneficial for viruses yet antiviral. We will also review the connection between the DDR and innate immunity. Previously believed to be disparate cellular functions, more recent research is emerging that links these processes. Furthermore, we will discuss some discrepancies in the literature that we propose can be remedied by utilizing more consistent DDR-focused assays. By doing so, we hope to obtain a much clearer understanding of how broadly these mechanisms and phenotypes are conserved among all viruses. This is crucial for human health since understanding how viruses manipulate the DDR presents an important and tractable target for antiviral therapies.
Keywords	DNA ; DNA damage ; human health ; innate immunity ; molecular biology
Language	English
Dates of publication	2021-1018
Publishing place	Elsevier Ltd
Document type	Article
Note	Pre-press version
ZDB-ID	80229-3
ISSN	1089-8638 ; 0022-2836
ISSN (online)	1089-8638
ISSN	0022-2836
DOI	10.1016/j.jmb.2021.167327
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Activation of the DNA Damage Response Is a Conserved Function of HIV-1 and HIV-2 Vpr That Is Independent of SLX4 Recruitment.

Fregoso, Oliver I / Emerman, Michael

mBio

2016 Volume 7, Issue 5

Abstract: Unlabelled: There has been extraordinary progress in understanding the roles of lentiviral accessory proteins in antagonizing host antiviral defense proteins. However, the precise primary function of the accessory gene Vpr remains elusive. Here we ... ...

Abstract	Unlabelled: There has been extraordinary progress in understanding the roles of lentiviral accessory proteins in antagonizing host antiviral defense proteins. However, the precise primary function of the accessory gene Vpr remains elusive. Here we suggest that engagement with the DNA damage response is an important function of primate lentiviral Vpr proteins because of its conserved function among diverse lentiviral lineages. In contrast, we show that, for HIV-1, HIV-2, and related Vpr isolates and orthologs, there is a lack of correlation between DNA damage response activation and interaction with the host SLX4 protein complex of structure specific endonucleases; some Vpr proteins are able to interact with SLX4, but the majority are not. Using the clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 method to knock out SLX4, we formally showed that HIV-1 and HIV-2 Vpr orthologs can still activate the DNA damage response and cell cycle arrest in the absence of SLX4. Together, our data suggest that activation of the DNA damage response, but not SLX4 interaction, is conserved and therefore indicative of an important function of Vpr. Our data also indicate that Vpr activates the DNA damage response through an SLX4-independent mechanism that remains uncharacterized. Importance: HIV-1 and HIV-2 belong to a family of viruses called lentiviruses that infect at least 40 primate species, including humans. Lentiviruses have been circulating in primates for at least 5 million years. In order to better fight HIV, we must understand the viral and host factors necessary for infection, adaptation, and transmission of these viruses. Using the natural variation of HIV-1, HIV-2, and related lentiviruses, we have investigated the role of the DNA damage response in the viral life cycle. We have found that the ability of lentiviruses to activate the DNA damage response is largely conserved. However, we also found that the SLX4 host factor is not required for this activation, as was previously proposed. This indicates that the DNA damage response is an important player in the viral life cycle, and yet the mechanism(s) by which HIV-1, HIV-2, and other primate lentiviruses engage the DNA damage response is still unknown.
MeSH term(s)	Cell Cycle Checkpoints ; Cell Line ; DNA Damage ; Gene Knockout Techniques ; HIV-1/physiology ; HIV-2/physiology ; Host-Pathogen Interactions ; Humans ; Recombinases/genetics ; Recombinases/metabolism ; vpr Gene Products, Human Immunodeficiency Virus/metabolism
Chemical Substances	Recombinases ; vpr Gene Products, Human Immunodeficiency Virus ; vpr protein, Human immunodeficiency virus 1 ; vpr protein, Human immunodeficiency virus 2 ; SLX4 protein, human (EC 3.1.-)
Language	English
Publishing date	2016-09-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mBio.01433-16
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Article ; Online: Viral Modulation of the DNA Damage Response and Innate Immunity: Two Sides of the Same Coin.

Lopez, Andrew / Nichols Doyle, Randilea / Sandoval, Carina / Nisson, Karly / Yang, Vivian / Fregoso, Oliver I

Journal of molecular biology

2021 Volume 434, Issue 6, Page(s) 167327

Abstract	The DDR consists of multiple pathways that sense, signal, and respond to anomalous DNA. To promote efficient replication, viruses have evolved to engage and even modulate the DDR. In this review, we will discuss a select set of diverse viruses and the range of mechanisms they evolved to interact with the DDR and some of the subsequent cellular consequences. There is a dichotomy in that the DDR can be both beneficial for viruses yet antiviral. We will also review the connection between the DDR and innate immunity. Previously believed to be disparate cellular functions, more recent research is emerging that links these processes. Furthermore, we will discuss some discrepancies in the literature that we propose can be remedied by utilizing more consistent DDR-focused assays. By doing so, we hope to obtain a much clearer understanding of how broadly these mechanisms and phenotypes are conserved among all viruses. This is crucial for human health since understanding how viruses manipulate the DDR presents an important and tractable target for antiviral therapies.
MeSH term(s)	Antiviral Agents/pharmacology ; DNA Damage ; DNA Repair ; Humans ; Immunity, Innate/genetics ; Virus Replication ; Viruses/drug effects ; Viruses/immunology
Chemical Substances	Antiviral Agents
Language	English
Publishing date	2021-10-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80229-3
ISSN	1089-8638 ; 0022-2836
ISSN (online)	1089-8638
ISSN	0022-2836
DOI	10.1016/j.jmb.2021.167327
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Zs.A 867: Show issues

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Article ; Online: Distinct evolutionary trajectories of SARS-CoV-2-interacting proteins in bats and primates identify important host determinants of COVID-19.

Cariou, Marie / Picard, Léa / Guéguen, Laurent / Jacquet, Stéphanie / Cimarelli, Andrea / Fregoso, Oliver I / Molaro, Antoine / Navratil, Vincent / Etienne, Lucie

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 35, Page(s) e2206610119

Abstract: The coronavirus disease 19 (COVID-19) pandemic is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a coronavirus that spilled over from the bat reservoir. Despite numerous clinical trials and vaccines, the burden remains immense, ... ...

Abstract	The coronavirus disease 19 (COVID-19) pandemic is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a coronavirus that spilled over from the bat reservoir. Despite numerous clinical trials and vaccines, the burden remains immense, and the host determinants of SARS-CoV-2 susceptibility and COVID-19 severity remain largely unknown. Signatures of positive selection detected by comparative functional genetic analyses in primate and bat genomes can uncover important and specific adaptations that occurred at virus-host interfaces. We performed high-throughput evolutionary analyses of 334 SARS-CoV-2-interacting proteins to identify SARS-CoV adaptive loci and uncover functional differences between modern humans, primates, and bats. Using DGINN (Detection of Genetic INNovation), we identified 38 bat and 81 primate proteins with marks of positive selection. Seventeen genes, including the ACE2 receptor, present adaptive marks in both mammalian orders, suggesting common virus-host interfaces and past epidemics of coronaviruses shaping their genomes. Yet, 84 genes presented distinct adaptations in bats and primates. Notably, residues involved in ubiquitination and phosphorylation of the inflammatory RIPK1 have rapidly evolved in bats but not primates, suggesting different inflammation regulation versus humans. Furthermore, we discovered residues with typical virus-host arms race marks in primates, such as in the entry factor TMPRSS2 or the autophagy adaptor FYCO1, pointing to host-specific in vivo interfaces that may be drug targets. Finally, we found that FYCO1 sites under adaptation in primates are those associated with severe COVID-19, supporting their importance in pathogenesis and replication. Overall, we identified adaptations involved in SARS-CoV-2 infection in bats and primates, enlightening modern genetic determinants of virus susceptibility and severity.
MeSH term(s)	Animals ; COVID-19/genetics ; Chiroptera/virology ; Evolution, Molecular ; Genetic Predisposition to Disease ; Host Adaptation/genetics ; Humans ; Pandemics ; Primates/genetics ; Primates/virology ; SARS-CoV-2/genetics ; Selection, Genetic ; Spike Glycoprotein, Coronavirus/genetics
Chemical Substances	Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2
Language	English
Publishing date	2022-08-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2206610119
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Zs.A 1148: Show issues

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Article ; Online: HIV Vpr Modulates the Host DNA Damage Response at Two Independent Steps to Damage DNA and Repress Double-Strand DNA Break Repair.

Li, Donna / Lopez, Andrew / Sandoval, Carina / Nichols Doyle, Randilea / Fregoso, Oliver I

mBio

2020 Volume 11, Issue 4

Abstract: The DNA damage response (DDR) is a signaling cascade that is vital to ensuring the fidelity of the host genome in the presence of genotoxic stress. Growing evidence has emphasized the importance of both activation and repression of the host DDR by ... ...

Abstract	The DNA damage response (DDR) is a signaling cascade that is vital to ensuring the fidelity of the host genome in the presence of genotoxic stress. Growing evidence has emphasized the importance of both activation and repression of the host DDR by diverse DNA and RNA viruses. Previous work has shown that HIV-1 is also capable of engaging the host DDR, primarily through the conserved accessory protein Vpr. However, the extent of this engagement has remained unclear. Here, we show that HIV-1 and HIV-2 Vpr directly induce DNA damage and stall DNA replication, leading to the activation of several markers of double- and single-strand DNA breaks. Despite causing damage and activating the DDR, we found that Vpr represses the repair of double-strand breaks (DSB) by inhibiting homologous recombination (HR) and nonhomologous end joining (NHEJ). Mutational analyses of Vpr revealed that DNA damage and DDR activation are independent from repression of HR and Vpr-mediated cell cycle arrest. Moreover, we show that repression of HR does not require cell cycle arrest but instead may precede this long-standing enigmatic Vpr phenotype. Together, our data uncover that Vpr globally modulates the host DDR at at least two independent steps, offering novel insight into the primary functions of lentiviral Vpr and the roles of the DNA damage response in lentiviral replication.
MeSH term(s)	Cell Line, Tumor ; DNA ; DNA Breaks, Double-Stranded ; DNA Repair ; HEK293 Cells ; HIV Infections/virology ; HIV-1/genetics ; HIV-1/pathogenicity ; HIV-2/genetics ; HIV-2/pathogenicity ; Host-Pathogen Interactions/genetics ; Humans ; Osteosarcoma ; Virus Replication ; vpr Gene Products, Human Immunodeficiency Virus/genetics
Chemical Substances	vpr Gene Products, Human Immunodeficiency Virus ; DNA (9007-49-2)
Language	English
Publishing date	2020-08-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mBio.00940-20
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Distinct evolutionary trajectories of SARS-CoV-2 interacting proteins in bats and primates identify important host determinants of COVID-19

Cariou, Marie / Picard, Lea / Gueguen, Laurent / Jacquet, Stephanie / Cimarelli, Andrea / Fregoso, Oliver I / Molaro, Antoine / Navratil, Vincent / Etienne, Lucie

bioRxiv

Abstract: The COVID-19 pandemic is caused by SARS-CoV-2, a novel coronavirus that spilled from the bat reservoir. Despite numerous clinical trials and vaccines, the burden remains immense, and the host determinants of SARS-CoV-2 susceptibility and COVID-19 ... ...

Abstract	The COVID-19 pandemic is caused by SARS-CoV-2, a novel coronavirus that spilled from the bat reservoir. Despite numerous clinical trials and vaccines, the burden remains immense, and the host determinants of SARS-CoV-2 susceptibility and COVID-19 severity remain largely unknown. Signatures of positive selection detected by comparative functional-genetic analyses in primate and bat genomes can uncover important and specific adaptations that occurred at virus-host interfaces. Here, we performed high-throughput evolutionary analyses of 334 SARS-CoV-2 interacting proteins to identify SARS-CoV adaptive loci and uncover functional differences between modern humans, primates and bats. Using DGINN (Detection of Genetic INNovation), we identified 38 bat and 81 primate proteins with marks of positive selection. Seventeen genes, including the ACE2 receptor, present adaptive marks in both mammalian orders, suggesting common virus-host interfaces and past epidemics of coronaviruses shaping their genomes. Yet, 84 genes presented distinct adaptations in bats and primates. Notably, residues involved in ubiquitination and phosphorylation of the inflammatory RIPK1 have rapidly evolved in bats but not primates, suggesting different inflammation regulation versus humans. Furthermore, we discovered residues with typical virus-host arms-race marks in primates, such as in the entry factor TMPRSS2 or the autophagy adaptor FYCO1, pointing to host-specific in vivo important interfaces that may be drug targets. Finally, we found that FYCO1 sites under adaptation in primates are those associated with severe COVID-19, supporting their importance in pathogenesis and replication. Overall, we identified functional adaptations involved in SARS-CoV-2 infection in bats and primates, critically enlightening modern genetic determinants of virus susceptibility and severity.
Keywords	covid19
Language	English
Publishing date	2022-04-07
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2022.04.07.487460
Database	COVID19

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Article ; Online: Distinct evolutionary trajectories of SARS-CoV-2 interacting proteins in bats and primates identify important host determinants of COVID-19

Cariou, Marie / Picard, Léa / Guéguen, Laurent / Jacquet, Stéphanie / Cimarelli, Andrea / Fregoso, Oliver I / Molaro, Antoine / Navratil, Vincent / Etienne, Lucie

bioRxiv

Abstract	The COVID-19 pandemic is caused by SARS-CoV-2, a novel coronavirus that spilled from the bat reservoir. Despite numerous clinical trials and vaccines, the burden remains immense, and the host determinants of SARS-CoV-2 susceptibility and COVID-19 severity remain largely unknown. Signatures of positive selection detected by comparative functional-genetic analyses in primate and bat genomes can uncover important and specific adaptations that occurred at virus-host interfaces. Here, we performed high-throughput evolutionary analyses of 334 SARS-CoV-2 interacting proteins to identify SARS-CoV adaptive loci and uncover functional differences between modern humans, primates and bats. Using DGINN (Detection of Genetic INNovation), we identified 38 bat and 81 primate proteins with marks of positive selection. Seventeen genes, including the ACE2 receptor, present adaptive marks in both mammalian orders, suggesting common virus-host interfaces and past epidemics of coronaviruses shaping their genomes. Yet, 84 genes presented distinct adaptations in bats and primates. Notably, residues involved in ubiquitination and phosphorylation of the inflammatory RIPK1 have rapidly evolved in bats but not primates, suggesting different inflammation regulation versus humans. Furthermore, we discovered residues with typical virus-host arms-race marks in primates, such as in the entry factor TMPRSS2 or the autophagy adaptor FYCO1, pointing to host-specific in vivo important interfaces that may be drug targets. Finally, we found that FYCO1 sites under adaptation in primates are those associated with severe COVID-19, supporting their importance in pathogenesis and replication. Overall, we identified functional adaptations involved in SARS-CoV-2 infection in bats and primates, critically enlightening modern genetic determinants of virus susceptibility and severity.
Keywords	covid19
Language	English
Publishing date	2022-04-07
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2022.04.07.487460
Database	COVID19

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