Dendritic cell maturation, but not type I interferon exposure, restricts infection by HTLV-1, and viral transmission to T-cells

Rizkallah, Gergès; Alais, Sandrine; Futsch, Nicolas; Tanaka, Yuetsu; Journo, Chloé; Mahieux, Renaud; Dutartre, Hélène

doi:10.1371/journal.ppat.1006353

Cited by 38 publications

(65 citation statements)

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“…Tax stimule également l'activité transcriptionnelle de CREB, en induisant la phosphorylation de la sérine 133 de la protéine [4]. En terme de modifications post-transcriptionnelles, CREB est également la cible d'une glycosylation particulière, la O-GlcNac glycosylation (ou O-Glc-NAcylation) [5].…”

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“…Au vu de la diversité des cellules dendritiques dans l'organisme [4], de leur rôle dans l'établissement de la réponse immunitaire, et des différentes voies d'entrées d'HTLV-1 [1], nous avons examiné si tous les sous-types de cellules dendritiques étaient similairement sensibles à l'infection par l'HTLV-1, et si ces sous-types contribuaient de manière équivalente à la dissémination du virus dans l'organisme. Ces travaux ont fait l'objet d'une publication récente dans la revue PLOS Pathogens [5]. Les cellules dendritiques matures présentent des vésicules plus acides que les cellules dendritiques immatures [8].…”

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HTLV-1 et cellules dendritiques

2018

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HTLV-1 et cellules dendritiques

2018

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“…HTLV-1 is a complex retrovirus that mainly infects CD4+ T cells, although it has the potential to infect a wide variety of other cells: CD8+ T cells, B lymphocytes, myeloid cells, endothelial cells, fibroblasts, neutrophils, monocytes, myeloid and plasmacytoid dendritic cells [7][8][9][10]. Cell-free HTLV-1 virions have poor infectivity, and the spreading of this virus depends mainly on two cell-to-cell between HTLV-1 virological parameters or clinical status and the expression of TRIM5α and TRIM22.…”

Section: Htlv-1 Infection Cycle and Host Restriction Factors (Figure 1)mentioning

confidence: 99%

“…To date, no host RFs have been fully characterized regarding the integration (4), transcription and splicing (5) or RNA export (6) steps. However, viral mRNA can be targeted at the post-transcriptional level by the ZAP protein and at the translational level by the NMD process (7). Finally, BST2 can tether nascent virions at the budding step (8) before the release and maturation of the viral particle (9).…”

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confidence: 99%

An Antiviral Process Targeting HTLV-1: The Complex Relationship between HTLV-1 and Nonsense-mediated mRNA Decay

Prochasson¹,

Jalinot²,

Mocquet³

2020

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Before the adaptive immune response is established, retroviruses can be targeted by several cellular host factors at different stages of the viral replication cycle. This intrinsic immunity relies on a large diversity of antiviral processes. In the case of HTLV-1 infection, these active innate host defence mechanisms are debated. Among these mechanisms, we focused on a RNA decay pathway called nonsense-mediated mRNA decay (NMD), which can target multiple viral RNAs, including HTLV-1 unspliced RNA, as it has been recently demonstrated. NMD is a cotranslational process that depends on the RNA helicase UPF1 and regulates the expression of multiple types of host mRNAs. RNA sensitivity to NMD depends on mRNA organization and the ribonucleoprotein (mRNP) composition.HTLV-1 has evolved several means to evade the NMD threat, leading to NMD inhibition. In the early steps of infection, NMD inhibition favours the production of HTLV-1 infectious particles, which may contribute to the survival of the most fit clones despite genome instability; however, its direct longterm impact remains to be investigated.

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“…Interestingly, in the context of HIV-1, another retrovirus that spreads from DCs to T cells in newly infected individuals, mature DCs have been shown to be more efficient than immature DCs in viral transmission to T cells [16]. Since interaction of HTLV-1 with mature DCs has not been described yet, we examined in a recent work whether immature or mature MDDCs have the same susceptibility to HTLV-1 infection and replication and whether they have the same ability to transfer HTLV-1 to T cells [17].…”

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How Does Susceptibility to HTLV-1 Infection Varies With the Maturation State of Dendritic Cells?

et al. 2017

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Keywords: dendritic cells • dendritic cell maturation • HTLV-1 infection • viral infectionHuman T-lymphotropic virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma and HTLV-1-associated myelopathy. In patients, the provirus is detected in CD4 + T cells. HTLV-1 also infects blood or monocyte-derived dendritic cells (DCs) in vitro. Since DCs are more susceptible to HTLV-1 infection than autologous T cells, it has been suggested that they might be intermediaries for the viral spread to lymphocytes. DCs can switch from an immature to a mature state after contact with pathogens. In other viral infection, mature DCs are more efficient than immature DCs in viral transmission to T cells. In this editorial, we highlight a work demonstrating that mature DCs are unable to transmit HTLV-1 to T cells and discuss the mechanism of such restriction.HTLV-1 was identified as the first human oncogenic retrovirus [1,2]. It is the etiological agent of adult T-cell leukemia (ATL), an oligoclonal malignancy of infected CD4 + T lymphocytes, and of tropical spastic paraparesis, a chronic progressive inflammatory disease. Five to ten million individuals are HTLV-1 carriers worldwide [3], a probably underestimated number. HTLV-1 inter-individual transmission relies on mother-to-child transmission through prolonged breastfeeding, on sexual transmission and on transmission with contaminated blood products [4].In chronically infected individuals, HTLV-1 proviral DNA is mainly found in CD4 + T cells, but several reports have demonstrated that others immune cell types are infected by HTLV-1 in vivo [5][6][7]. These cell types include DCs, which are specialized antigen-presenting cells and essential mediators in shaping innate and adaptive immunity [8]. In vitro studies conducted by our lab and others confirmed that HTLV-1 productively infects myeloid blood DCs [7] and monocyte-derived DCs (MDDCs) [9][10][11]. Of note, exposure of target cells to cell-free viruses only leads to very low levels of productive infection [9], consistent with the observation that efficient infection of target cells requires close cell-to-cell contacts with infected donor cells [12]. Viral entry in T cells requires expression of the HTLV-1 receptor complex, in other words, neuropilin-1 and heparan sulfate proteoglycans, used for binding [13], and the glucose transporter Glut-1, required for fusion [14], while viral binding to DCs was also shown to require DC-SIGN [11].Importantly, we demonstrated that primary MDDCs are more susceptible to productive HTLV-1 infection than their autologous T cells [9]. Given that productively infected MDDCs are able to transfer HTLV-1 to T cells [7,9,11], it is thus proposed that DCs might be important intermediaries for HTLV-1 spread to T cells in newly infected individuals.Upon stimulation, DCs can switch from an immature to a mature state characterized by morphological, phenotypic and functional changes [15]. Interestingly, in the context of HIV-1, another retrovirus that spreads from DCs to T cells in ne...

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Dendritic cell maturation, but not type I interferon exposure, restricts infection by HTLV-1, and viral transmission to T-cells

Cited by 38 publications

References 60 publications

HTLV-1 et cellules dendritiques

HTLV-1 et cellules dendritiques

An Antiviral Process Targeting HTLV-1: The Complex Relationship between HTLV-1 and Nonsense-mediated mRNA Decay

How Does Susceptibility to HTLV-1 Infection Varies With the Maturation State of Dendritic Cells?

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