Intertwined: SAMHD1 cellular functions, restriction, and viral evasion strategies

Majer, Catharina; Schüssler, Jan Moritz; König, Renate

doi:10.1007/s00430-019-00593-x

Cited by 21 publications

(30 citation statements)

References 185 publications

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“…However, some studies have reported that T592 phosphorylation does not affect the dNTPase activity of the enzyme suggesting that another mechanism independent of dNTPase activity is involved in SAMHD1-mediated viral restriction [156,158]. For review, see [159]. Whatever the mechanism involved, T592 phosphorylation of SAMHD1 severely affects HIV-1 restriction [156,160].…”

Section: Restriction Factors Belonging To the Interferon Stimulatementioning

confidence: 99%

Interplay between Intrinsic and Innate Immunity during HIV Infection

Bergantz

Subra

Deprez

et al. 2019

Cells

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Restriction factors are antiviral components of intrinsic immunity which constitute a first line of defense by blocking different steps of the human immunodeficiency virus (HIV) replication cycle. In immune cells, HIV infection is also sensed by several pattern recognition receptors (PRRs), leading to type I interferon (IFN-I) and inflammatory cytokines production that upregulate antiviral interferon-stimulated genes (ISGs). Several studies suggest a link between these two types of immunity. Indeed, restriction factors, that are generally interferon-inducible, are able to modulate immune responses. This review highlights recent knowledge of the interplay between restriction factors and immunity inducing antiviral defenses. Counteraction of this intrinsic and innate immunity by HIV viral proteins will also be discussed.

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Section: Restriction Factors Belonging To the Interferon Stimulatementioning

confidence: 99%

Interplay between Intrinsic and Innate Immunity during HIV Infection

Bergantz

Subra

Deprez

et al. 2019

Cells

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“…Current evidence suggests SAMHD1 is an effective antiviral restriction factor suitably targeting numerous other medically relevant viruses (62). However, it is to note that the study on CHIKV and ZIKV reported that SAMHD1 might be proviral as it promotes their replication.…”

Section: Potential Host Responses To Covid-19mentioning

confidence: 99%

“…Among such genes, SAMDH1 is probably the one. Notably, SAMDH1 has been related to Aicardi-Goutieres syndrome—a congenital disease that includes neurodegeneration as one of its main symptoms ( 62 ). As mentioned above, SAMDH1 appears to control the NF-κB pathway.…”

Section: Ace2 Localization In the Human Brainmentioning

confidence: 99%

SAMHD1 as the Potential Link Between SARS-CoV-2 Infection and Neurological Complications

Khan

Sergi

2020

Front. Neurol.

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The recent pandemic of coronavirus infectious illness 2019 (COVID19) triggered by SARS-CoV-2 has rapidly spread around the globe, generating in severe events an acute, highly lethal pneumonia and death. In the past two hitherto similar CoVs, the severe acute respiratory syndrome CoV (SARS-CoV-1) and Middle East respiratory syndrome CoV (MERS-CoV) also gained universal attention as they produced clinical symptoms similar to those of SARS-CoV-2 utilizing angiotensin-converting enzyme 2 (ACE2) receptor and dipeptidyl peptidase 4 (DPP4) to go into the cells. COVID-19 may also present with overtly neurological symptoms. The proper understanding of the expression and dissemination of ACE2 in central and peripheral nerve systems is crucial to understand better the neurological morbidity caused by COVID-19. Using the STRING bioinformatic tool and references through text mining tools associated to Coronaviruses, we identified SAMHD1 as the probable link to neurological symptoms. Paralleled to the response to influenza A virus and, specifically, respiratory syncytial virus, SARS-CoV-2 evokes a response that needs robust induction of a subclass of cytokines, including the Type I and, obviously, Type III interferons as well as a few chemokines. We correlate ACE2 to the pathogenesis and neurologic complications of COVID-19 and found that SAMHD1 links to NF-κB pathway. No correlation was found with other molecules associated with Coronavirus infection, including ADAR, BST2, IRF3, IFITM3, ISG15, MX1, MX2, RNASEL, RSAD2, and VPRBP. We suggest that SAMHD1 is the molecule that may be behind the mechanisms of the neurological complications associated with COVID-19.

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“…In contrast to exogenous retroviruses, however, the mechanism of restriction seems to be different for retrotransposons and, for most members of the family, to be deaminase independent [40]. SAMHD1 is a dNTP hydrolase known to regulate intracellular dNTP levels in a cell cycle-dependent manner and to restrict the replication of many viruses in non-dividing cells by limiting the number of available dNTPs needed to replicate viral genomes (recently summarized in [41]). The mechanism how SAMHD1 restricts retrotransposons seems also to differ from its activity against exogenous viruses, with different potential models of restriction being proposed [42][43][44][45].…”

Section: Controlling Mobile Elementsmentioning

confidence: 99%

Recognize Yourself—Innate Sensing of Non-LTR Retrotransposons

Lagisquet

Zuber

Gramberg

2021

Viruses

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Although mobile genetic elements, or transposons, have played an important role in genome evolution, excess activity of mobile elements can have detrimental consequences. Already, the enhanced expression of transposons-derived nucleic acids can trigger autoimmune reactions that may result in severe autoinflammatory disorders. Thus, cells contain several layers of protective measures to restrict transposons and to sense the enhanced activity of these “intragenomic pathogens”. This review focuses on our current understanding of immunogenic patterns derived from the most active elements in humans, the retrotransposons long interspersed element (LINE)-1 and Alu. We describe the role of known pattern recognition receptors in nucleic acid sensing of LINE-1 and Alu and the possible consequences for autoimmune diseases.

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Intertwined: SAMHD1 cellular functions, restriction, and viral evasion strategies

Cited by 21 publications

References 185 publications

Interplay between Intrinsic and Innate Immunity during HIV Infection

Interplay between Intrinsic and Innate Immunity during HIV Infection

SAMHD1 as the Potential Link Between SARS-CoV-2 Infection and Neurological Complications

Recognize Yourself—Innate Sensing of Non-LTR Retrotransposons

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