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    Team: Retrovirus, Infection and Latency

    Team Leaders


    THE TEAM IN BRIEF... Human pathogenic retroviruses arise from two genera, the deltaretrovirus genus with HTLV-1, and the lentivirus genus with HIV-1 and HIV-2. HTLV-1 is responsible of T-cell leukemia and lymphoma, and of a demyelinating disease called HTLV-I associated myelopathy/Tropical spastic paraparesis (HAM/TSP) and HIV is responsible of AIDS.




    HTLV-1 and HIV share important common points: they are RNA viruses and, as an obligate step in their life cycle, they reverse transcribe their RNA genome into a cDNA copy that reaches the host chromatin and integrates into the host genome. The basic cycle of both viruses, from the attachment to the production of viral particles, is governed by the activity of the products of the Gag, Env and Pol genes and by regulating proteins, Tat and Rev in the case of HIV, Tax and Rex in the case of HTLV. Besides these essential proteins, both viruses express a set of so-called auxiliary proteins. In the case of HIV, the auxiliary proteins are experts in manipulating the cellular environment to allow optimal viral replication. In the case of HTLV-1, those proteins have been implicated in the regulation of viral transcription and latency as well as in the modulation of T-cell proliferation.
    On the cell side, CD4+ T lymphocytes are major cellular targets of both HIV and HTLV, but here the similarities stop. First, the outcomes of the infections are very different: while T cells infected by HTLV actively divide and become immortalized and for a fraction of them, transformed, T cells infected by HIV quickly die following the massive production of viral particles, which are ready to infect new cells. Second, while HTLV is believed to only infect dividing cells, mainly activated CD4+ T lymphocytes, HIV distinguishes himself by its capacity to also infect quiescent cells of the myeloid lineage such as macrophages. These myeloid cells survive HIV viral infection and constitute viral reservoirs of latent viruses.

    Altogether, comparing the molecular strategies developed by HTLV-1 and HIV to replicate in cells appears as a promising strategy to understand how viruses deal with the cellular environment. With this in mind, the general objective of our team is to explore the interplay between HTLV-1 and HIV and the cycling status of the host cell.


     Some publications 


    Martella C, Tollenaere I A, Waast L, Lacombe B, Groussaud D, Margottin-Goguet F, Ramirez BC, Pique C. HTLV-1  transactivator Tax exploits the XPB subunit of TFIIH during viral transcription. J. Virol2020 DOI: 10.1128/JVI.02171-19

    Chougui G, Margottin-Goguet F. HUSH, a Link Between Intrinsic Immunity and HIV Latency. Front Microbiol. 2019 Feb 12;10:224. doi: 10.3389/fmicb.2019.00224. eCollection 2019. Review.

    Avettand-Fenoel V, T Bayan, E Gardiennet, F Boufassa, P Lopez, C Lecuroux, N Noel, P Trémeaux, B Autran, L Meyer, A Saez-Cirion, O Lambotte, C Rouzioux, for the CODEX ANRS Cohort Study Group. Dynamics in HIV DNA levels over time in HIV Controllers.  Journal of International AIDS Society 2019, 22:e25221 

     Tremeaux P, Lenfant T, Boufassa F, Essat E, Mélard A, Gousset M, Delelis O, Viard JP, Bary M, Goujard C, Rouzioux C, Meyer L, Avettand-Fenoel V for the ANRS-SEROCO and PRIMO cohorts. Increasing contribution of integrated forms to total HIV DNA in blood during HIV disease progression from primary infection. EBioMed 2019, 10.1016/j.ebiom.2019.02.016.

    Chougui G, Munir-Matloob S, Matkovic R, Martin MM, Morel M, Lahouassa H, Leduc M, Ramirez BC, Etienne L, Margottin-Goguet F. HIV-2/SIV viral protein X counteracts HUSH repressor complex. Nat Microbiol. 2018 Aug;3(8):891-897. doi: 10.1038/s41564-018-0179-6. Epub 2018 Jun 11.

    Marcais, A., Waast, L., Bruneau, J., Hanssens, K., Asnafi, V., Gaulard, P., Suarez, F., Dubreuil, P., Gessain, A., Hermine, O., Pique, C. Adult T cell leukemia aggressivenness correlates with loss of both 5-hydroxymethylcytosine and TET2 expression Oncotarget 2017. 8(32):52256-68

    Groussaud, D., Khair, M., Tollenaere, A. I., Waast, L., Kuo, M. S., Mangeney, M., Martella, C., Fardini, Y., Coste, S., Souidi, M., Benit, L., Pique, C*., Issad, *T. (2017) Hijacking of the O-GlcNAcZYME complex by the HTLV-1 Tax oncoprotein facilitates viral transcription PLoS Pathog 2017. 13(7):e1006518. * co-last authors

    Lahouassa H, Daddacha W, Hofmann H, Ayinde D, Logue EC, Dragin L, Bloch N, Maudet C, Bertrand M, Gramberg T, Pancino G, Priet S, Canard B, Laguette N, Benkirane M, Transy C, Landau NR, Kim B, Margottin-Goguet F. SAMHD1 restricts the replication of human immunodeficiency virus type 1 by depleting the intracellular pool of deoxynucleoside triphosphatesNat Immunol. 2012 Feb 12;13(3):223-8. 



    We are very glad the team has expanded since January 2019 upon the arrival of the group of Véronique Avettand-Fenoel. Her research is dedicated to HIV reservoirs in clinical and pathophysiological conditions.