Viruses Seen by Our Cells: The Role of Viral RNA Sensors

Said, Elias A.; Tremblay, Nicolas; Al-Balushi, Mohammed S.; Al-Jabri, Ali A.; Lamarre, Daniel

doi:10.1155/2018/9480497

Cited by 48 publications

(74 citation statements)

References 154 publications

(161 reference statements)

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“…Different early stages of HIV-1 infection, such as virus attachment and accumulation of reverse-transcription products in cells, can induce multiple signaling events, which can lead to many changes in cellular functions (33,34). Using NVP treatment of HIV-1-infected cells and heat-inactivated HIV-1 as controls, we demonstrated that viral replication is not required for the up-regulation of m 6 A levels of cellular RNA.…”

Section: Discussionmentioning

confidence: 90%

HIV-1 envelope proteins up-regulate N6-methyladenosine levels of cellular RNA independently of viral replication

Tirumuru

2019

Journal of Biological Chemistry

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Edited by Charles E. Samuel N 6 -methyladenosine (m 6 A) modification of HIV-1 RNA regulates viral replication and protein expression. The m 6 A modification is regulated by two groups of cellular proteins named writers and erasers that add or remove m 6 A, respectively. HIV-1 infection of CD4 ؉ T-cells increases m 6 A levels of cellular mRNA, but the underlying mechanism is unknown. Here, we show that HIV-1 infection of CD4 ؉ primary T-cells or Jurkat cells significantly increases m 6 A levels of cellular RNA independently of viral replication. Compared with HIV-1-infected CD4 ؉ T-cells, similar m 6 A up-regulation was detected in total RNA from HIV-1-infected cells treated with a reverse-transcriptase inhibitor or with heat-inactivated HIV-1. Compared with mock controls, significantly increased m 6 A levels were detected in total RNA from Jurkat cells infected by single-cycle HIV-1 pseudotyped with an HIV-1 envelope (Env) glycoprotein, but not with vesicular stomatitis virus glycoprotein G (VSV-G).Overexpression of HIV-1 Env in HEK293T cells did not affect m 6 A levels of cellular RNA, suggesting that de novo synthesis of Env is not required for m 6 A up-regulation. Interestingly, treatment of Jurkat cells with recombinant gp120 of HIV-1 Env significantly increased m 6 A levels of cellular RNA, which was reduced by a gp120-neutralizing antibody. Preincubation of Jurkat cells with a CD4 receptor-neutralizing antibody blocked HIV-1-induced up-regulation of m 6 A levels in cellular RNA. Moreover, HIV-1 infection or gp120 treatment did not alter the protein expression of m 6 A writers and erasers in cells. Our findings suggest that HIV-1 gp120 binding to the CD4 receptor is required for m 6 A up-regulation in cells. . 2 The abbreviations used are: m 6 A, N 6 -methyladenosine; MOI, multiplicity of infection; hpi, hours post-infection; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; NVP, nevirapine; Env, HIV-1 envelope proteins; METTL, methyltransferase-like protein; FTO, fat mass and obesity-associated protein; AlkBH5, AlkB family member 5; MB, methylene blue; sncRNA, small noncoding RNA; sCD4, soluble CD4; NARP, National Institutes of Health AIDS Reagent Program; SSC, saline-sodium citrate.

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Section: Discussionmentioning

confidence: 90%

HIV-1 envelope proteins up-regulate N6-methyladenosine levels of cellular RNA independently of viral replication

Tirumuru

2019

Journal of Biological Chemistry

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“…To facilitate comparison between the respiratory viruses described here, known and arguably important innate immune evasion strategies are listed, and for each strategy it is discussed how each virus group exploits its own mechanism. Innate immune evasion obviously links to the innate immune responses that are known to be elicited by respiratory and other (RNA) viruses, and while this will be elaborated to a limited extent below, they have also been reviewed comprehensively in recent reviews by others [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Innate Immune Evasion by Human Respiratory RNA Viruses

2019

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The impact of respiratory virus infections on the health of children and adults can be very significant. Yet, in contrast to most other childhood infections as well as other viral and bacterial diseases, prophylactic vaccines or effective antiviral treatments against viral respiratory infections are either still not available, or provide only limited protection. Given the widespread prevalence, a general lack of natural sterilizing immunity, and/or high morbidity and lethality rates of diseases caused by influenza, respiratory syncytial virus, coronaviruses, and rhinoviruses, this difficult situation is a genuine societal challenge. A thorough understanding of the virushost interactions during these respiratory infections will most probably be pivotal to ultimately meet these challenges. This review attempts to provide a comparative overview of the knowledge about an important part of the interaction between respiratory viruses and their host: the arms race between host innate immunity and viral innate immune eva-

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“…PAMPs consisting of viral RNA, DNA and proteins are recognized by pattern recognition receptors (PRRs) expressed and sensed by DCs. PRRs include Toll-like receptors, RIG-like receptors, NOD-like receptors and cGAS [ 81 , 82 , 83 ]. Due to the involvement of PRR, DC produces pro-inflammatory cytokines (e.g., TNF-α and IL-12) and antiviral type I IFN.…”

Section: The Tme and Ov Infectionmentioning

confidence: 99%

Efficient Delivery and Replication of Oncolytic Virus for Successful Treatment of Head and Neck Cancer

Hamada

Yura

2020

IJMS

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Head and neck cancer has been treated by a combination of surgery, radiation, and chemotherapy. In recent years, the development of immune checkpoint inhibitors (ICIs) has made immunotherapy a new treatment method. Oncolytic virus (OV) therapy selectively infects tumor cells with a low-pathogenic virus, lyses tumor cells by the cytopathic effects of the virus, and induces anti-tumor immunity to destroy tumors by the action of immune cells. In OV therapy for head and neck squamous cell carcinoma (HNSCC), viruses, such as herpes simplex virus type 1 (HSV-1), vaccinia virus, adenovirus, reovirus, measles virus, and vesicular stomatitis virus (VSV), are mainly used. As the combined use of mutant HSV-1 and ICI was successful for the treatment of melanoma, studies are underway to combine OV therapy with radiation, chemotherapy, and other types of immunotherapy. In such therapy, it is important for the virus to selectively replicate in tumor cells, and to express the viral gene and the introduced foreign gene in the tumor cells. In OV therapy for HNSCC, it may be useful to combine systemic and local treatments that improve the delivery and replication of the inoculated oncolytic virus in the tumor cells.

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Viruses Seen by Our Cells: The Role of Viral RNA Sensors

Cited by 48 publications

References 154 publications

HIV-1 envelope proteins up-regulate N6-methyladenosine levels of cellular RNA independently of viral replication

HIV-1 envelope proteins up-regulate N6-methyladenosine levels of cellular RNA independently of viral replication

Innate Immune Evasion by Human Respiratory RNA Viruses

Efficient Delivery and Replication of Oncolytic Virus for Successful Treatment of Head and Neck Cancer

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