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1. Africa-specific human genetic variation near CHD1L associates with HIV-1 load

Author

McLaren, Paul J., Porreca, Immacolata, Iaconis, Gennaro, Mok, Hoi Ping, Mukhopadhyay, Subhankar, Karakoc, Emre, Cristinelli, Sara, Pomilla, Cristina, Bartha, István, Thorball, Christian W., Tough, Riley H., Angelino, Paolo, Kiar, Cher S., Carstensen, Tommy, Fatumo, Segun, Porter, Tarryn, Jarvis, Isobel, Skarnes, William C., Bassett, Andrew, DeGorter, Marianne K., Sathya Moorthy, Mohana Prasad, Tuff, Jeffrey F., Kim, Eun-Young, Walter, Miriam, Simons, Lacy M., Bashirova, Arman, Buchbinder, Susan, Carrington, Mary, Cossarizza, Andrea, De Luca, Andrea, Goedert, James J., Goldstein, David B., Haas, David W., Herbeck, Joshua T., Johnson, Eric O., Kaleebu, Pontiano, Kilembe, William, Kirk, Gregory D., Kootstra, Neeltje A., Kral, Alex H., Lambotte, Olivier, Luo, Ma, Mallal, Simon, Martinez-Picado, Javier, Meyer, Laurence, Miro, José M., Moodley, Pravi, Motala, Ayesha A., Mullins, James I., Nam, Kireem, Obel, Niels, Pirie, Fraser, Plummer, Francis A., Poli, Guido, Price, Matthew A., Rauch, Andri, Theodorou, Ioannis, Trkola, Alexandra, Walker, Bruce D., Winkler, Cheryl A., Zagury, Jean-François, Montgomery, Stephen B., Ciuffi, Angela, Hultquist, Judd F., Wolinsky, Steven M., Dougan, Gordon, Lever, Andrew M. L., Gurdasani, Deepti, Groom, Harriet, Sandhu, Manjinder S., and Fellay, Jacques

Published
2023
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3. Entry of Polarized Effector Cells into Quiescence Forces HIV Latency

Author

Dobrowolski, Curtis, Valadkhan, Saba, Graham, Amy C, Shukla, Meenakshi, Ciuffi, Angela, Telenti, Amalio, and Karn, Jonathan

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, HIV/AIDS, Sexually Transmitted Infections, Infectious Diseases, Genetics, 2.1 Biological and endogenous factors, Infection, CD4-Positive T-Lymphocytes, Cells, Cultured, Cytokines, Flow Cytometry, HIV, HIV Infections, Humans, Models, Biological, T-Lymphocyte Subsets, Virus Activation, Virus Latency, HIV latency, HIV reservoir, P-TEFb, cell quiescence, human immunodeficiency virus, Microbiology, Biochemistry and cell biology, Medical microbiology
Abstract

The latent HIV reservoir is generated following HIV infection of activated effector CD4 T cells, which then transition to a memory phenotype. Here, we describe an ex vivo method, called QUECEL (quiescent effector cell latency), that mimics this process efficiently and allows production of large numbers of latently infected CD4+ T cells. Naïve CD4+ T cells were polarized into the four major T cell subsets (Th1, Th2, Th17, and Treg) and subsequently infected with a single-round reporter virus which expressed GFP/CD8a. The infected cells were purified and coerced into quiescence using a defined cocktail of cytokines, including tumor growth factor beta, interleukin-10 (IL-10), and IL-8, producing a homogeneous population of latently infected cells. Flow cytometry and transcriptome sequencing (RNA-Seq) demonstrated that the cells maintained the correct polarization phenotypes and had withdrawn from the cell cycle. Key pathways and gene sets enriched during transition from quiescence to reactivation include E2F targets, G2M checkpoint, estrogen response late gene expression, and c-myc targets. Reactivation of HIV by latency-reversing agents (LRAs) closely mimics RNA induction profiles seen in cells from well-suppressed HIV patient samples using the envelope detection of in vitro transcription sequencing (EDITS) assay. Since homogeneous populations of latently infected cells can be recovered, the QUECEL model has an excellent signal-to-noise ratio and has been extremely consistent and reproducible in numerous experiments performed during the last 4 years. The ease, efficiency, and accuracy of the mimicking of physiological conditions make the QUECEL model a robust and reproducible tool to study the molecular mechanisms underlying HIV latency.IMPORTANCE Current primary cell models for HIV latency correlate poorly with the reactivation behavior of patient cells. We have developed a new model, called QUECEL, which generates a large and homogenous population of latently infected CD4+ memory cells. By purifying HIV-infected cells and inducing cell quiescence with a defined cocktail of cytokines, we have eliminated the largest problems with previous primary cell models of HIV latency: variable infection levels, ill-defined polarization states, and inefficient shutdown of cellular transcription. Latency reversal in the QUECEL model by a wide range of agents correlates strongly with RNA induction in patient samples. This scalable and highly reproducible model of HIV latency will permit detailed analysis of cellular mechanisms controlling HIV latency and reactivation.

Published
2019

4. Author Correction: Africa-specific human genetic variation near CHD1L associates with HIV-1 load

Author

McLaren, Paul J., Porreca, Immacolata, Iaconis, Gennaro, Mok, Hoi Ping, Mukhopadhyay, Subhankar, Karakoc, Emre, Cristinelli, Sara, Pomilla, Cristina, Bartha, István, Thorball, Christian W., Tough, Riley H., Angelino, Paolo, Kiar, Cher S., Carstensen, Tommy, Fatumo, Segun, Porter, Tarryn, Jarvis, Isobel, Skarnes, William C., Bassett, Andrew, DeGorter, Marianne K., Sathya Moorthy, Mohana Prasad, Tuff, Jeffrey F., Kim, Eun-Young, Walter, Miriam, Simons, Lacy M., Bashirova, Arman, Buchbinder, Susan, Carrington, Mary, Cossarizza, Andrea, De Luca, Andrea, Goedert, James J., Goldstein, David B., Haas, David W., Herbeck, Joshua T., Johnson, Eric O., Kaleebu, Pontiano, Kilembe, William, Kirk, Gregory D., Kootstra, Neeltje A., Kral, Alex H., Lambotte, Olivier, Luo, Ma, Mallal, Simon, Martinez-Picado, Javier, Meyer, Laurence, Miro, José M., Moodley, Pravi, Motala, Ayesha A., Mullins, James I., Nam, Kireem, Obel, Niels, Pirie, Fraser, Plummer, Francis A., Poli, Guido, Price, Matthew A., Rauch, Andri, Theodorou, Ioannis, Trkola, Alexandra, Walker, Bruce D., Winkler, Cheryl A., Zagury, Jean-François, Montgomery, Stephen B., Ciuffi, Angela, Hultquist, Judd F., Wolinsky, Steven M., Dougan, Gordon, Lever, Andrew M. L., Gurdasani, Deepti, Groom, Harriet, Sandhu, Manjinder S., and Fellay, Jacques

Published
2023
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5. Role of the pol gene enhancer in HIV-1 transcription and replication in myeloid infected cells

Author

Journées Francophones de Virologie 2024 (XXVI: 10-12 avril 2024: Bruxelles, Belgium), Marray, Tristan, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Dutilleul, Antoine, Nestola, Lorena, Stiernon, Lara, Cristinelli, Sara SC, Verhasselt, Bruno, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, Rohr, Olivier, Van Lint, Carine, Journées Francophones de Virologie 2024 (XXVI: 10-12 avril 2024: Bruxelles, Belgium), Marray, Tristan, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Dutilleul, Antoine, Nestola, Lorena, Stiernon, Lara, Cristinelli, Sara SC, Verhasselt, Bruno, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, Rohr, Olivier, and Van Lint, Carine

Abstract

info:eu-repo/semantics/published

Published
2024

6. Role of the pol gene enhancer in HIV-1 transcription and replication in myeloid infected cells

Author

Interuniversity PhD Day, Stiernon, Lara, Marray, Tristan, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Dutilleul, Antoine, Nestola, Lorena, Cristinelli, Sara SC, Monceaux, Valerie, Verhasselt, Bruno, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, Rohr, Olivier, Van Lint, Carine, Interuniversity PhD Day, Stiernon, Lara, Marray, Tristan, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Dutilleul, Antoine, Nestola, Lorena, Cristinelli, Sara SC, Monceaux, Valerie, Verhasselt, Bruno, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, Rohr, Olivier, and Van Lint, Carine

Abstract

info:eu-repo/semantics/nonPublished

Published
2024

7. Integration

Author

Ciuffi, Angela, Bushman, Frederic D., Hope, Thomas J., editor, Richman, Douglas D., editor, and Stevenson, Mario, editor

Published
2018
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16. Role of the pol gene enhancer in HIV-1 transcription and replication in myeloid infected cells

Author

Marray, Tristan, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Dutilleul, Antoine, Nestola, Lorena, Stiernon, Lara, Cristinelli, Sara SC, Monceaux, Valerie, Verhasselt, Bruno, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, Rohr, Olivier, Van Lint, Carine, Marray, Tristan, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Dutilleul, Antoine, Nestola, Lorena, Stiernon, Lara, Cristinelli, Sara SC, Monceaux, Valerie, Verhasselt, Bruno, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, Rohr, Olivier, and Van Lint, Carine

Abstract

info:eu-repo/semantics/nonPublished

Published
2023

17. Role of the lineage-determining transcription factor PU.1 in the transcriptional activity of the Human Immunodeficiency Virus Type 1 (HIV-1) intragenic enhancer

Author

Van Lint, Carine, Droogmans, Louis, Marini, Anna Maria, Vanhollebeke, Benoît, Ciuffi, Angela, Decottignies, Anabelle, Hernalsteens, Olivier, Van Lint, Carine, Droogmans, Louis, Marini, Anna Maria, Vanhollebeke, Benoît, Ciuffi, Angela, Decottignies, Anabelle, and Hernalsteens, Olivier

Abstract

Human Immunodeficiency Virus type 1 (HIV-1) infection can be managed but not cured by the current combinatory antiretroviral therapy (cART). The replication rate of HIV-1, which is directly correlated to the rate of disease progression to Acquired Immunodeficiency Syndrome (AIDS), is controlled primarily at the transcription level of viral genes, which is not targeted by cART. The arrest of the cART is associated with a rapid viremia rebound due to the persistence of long-term reservoirs of virally infected cells, which cannot be eliminated by cART corresponding to cell types or tissue compartments where virally infected cells are maintained. These reservoirs are heterogeneous and principally composed of CD4+ T cells and myeloid cells, the latter understudied and poorly represented in cure-based efforts. Importantly, each reservoir harbors a unique regulation of HIV-1 gene expression. Even though most transcriptional studies on HIV-1 have only focused on the viral promoter 5’long terminal repeat (5’LTR), our laboratory has previously reported an intragenic cis-regulatory region (IRR), which the complete functional unit forming the HIV-1 IRR is composed, from 5’ to 3’, of three subdomains: the 5103 fragment, the hypersensitive site 7 (HS7), and the 5105 fragment. In this context, further deciphering the specific molecular mechanisms underlying HIV-1 gene expression in all host cell types (including myeloid cells) and from each transcriptional regulatory element (including the IRR) is crucial for a deeper understanding of HIV-1 biology and pathogenesis.In the first part of my PhD thesis, we determined the in vivo epigenetic landscape of the IRR in latent and reactivated conditions and in both T-lymphoid and myeloid-infected cells, representing the two major cellular contexts of HIV-1 infection. We demonstrated that the IRR harbored the characteristic features of an enhancer in these two physiological contexts. Second, we explored the contribution of the intragenic lin, Doctorat en Sciences, info:eu-repo/semantics/nonPublished

Published
2023

18. Transcriptomic Profiling Reveals Intense Host-Pathogen Dispute Compromising Homeostasis during Acute Rift Valley Fever Virus Infection

Author

Bermúdez-Méndez, Erick, Angelino, Paolo, van Keulen, Lucien, van de Water, Sandra, Rockx, Barry, Pijlman, Gorben P., Ciuffi, Angela, Kortekaas, Jeroen, Wichgers Schreur, Paul J., Bermúdez-Méndez, Erick, Angelino, Paolo, van Keulen, Lucien, van de Water, Sandra, Rockx, Barry, Pijlman, Gorben P., Ciuffi, Angela, Kortekaas, Jeroen, and Wichgers Schreur, Paul J.

Abstract

Rift Valley fever virus (RVFV) (family Phenuiviridae) can cause severe disease, and outbreaks of this mosquito-borne pathogen pose a significant threat to public and animal health. Yet many molecular aspects of RVFV pathogenesis remain incompletely understood. Natural RVFV infections are acute, characterized by a rapid onset of peak viremia during the first days post-infection, followed by a rapid decline. Although in vitro studies identified a major role of interferon (IFN) responses in counteracting the infection, a comprehensive overview of the specific host factors that play a role in RVFV pathogenesis in vivo is still lacking. Here, the host in vivo transcriptional profiles in the liver and spleen tissues of lambs exposed to RVFV are studied using RNA sequencing (RNA-seq) technology. We validate that IFN-mediated pathways are robustly activated in response to infection. We also link the observed hepatocellular necrosis with severely compromised organ function, which is reflected as a marked downregulation of multiple metabolic enzymes essential for homeostasis. Furthermore, we associate the elevated basal expression of LRP1 in the liver with RVFV tissue tropism. Collectively, the results of this study deepen the knowledge of the in vivo host response during RVFV infection and reveal new insights into the gene regulation networks underlying pathogenesis in a natural host

Published
2023

19. Transcriptomic profiling of lambs during acute Rift Valley fever virus infection

Author

Bermúdez-Méndez, Erick, Angelino, Paolo, van Keulen, Lucien, van de Water, Sandra, Rockx, Barry, Pijlman, Gorben P., Ciuffi, Angela, Kortekaas, Jeroen, Wichgers Schreur, Paul J., Bermúdez-Méndez, Erick, Angelino, Paolo, van Keulen, Lucien, van de Water, Sandra, Rockx, Barry, Pijlman, Gorben P., Ciuffi, Angela, Kortekaas, Jeroen, and Wichgers Schreur, Paul J.

Abstract

We used RNA-seq technology to study the host in vivo transcriptional profiles in liver and spleen tissues of lambs exposed to Rift Valley fever virus., We used RNA-seq technology to study the host in vivo transcriptional profiles in liver and spleen tissues of lambs exposed to Rift Valley fever virus.

Published
2023

20. Dual and Opposite Effects of hRAD51 Chemical Modulation on HIV-1 Integration

Author

Thierry, Sylvain, Benleulmi, Mohamed Salah, Sinzelle, Ludivine, Thierry, Eloise, Calmels, Christina, Chaignepain, Stephane, Waffo-Teguo, Pierre, Merillon, Jean-Michel, Budke, Brian, Pasquet, Jean-Max, Litvak, Simon, Ciuffi, Angela, Sung, Patrick, Connell, Philip, Hauber, Ilona, Hauber, Joachim, Andreola, Marie-Line, Delelis, Olivier, and Parissi, Vincent

Published
2015
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22. Determinants of HIV-1 broadly neutralizing antibody induction

Author

Rusert, Peter, Kouyos, Roger D, Kadelka, Claus, Ebner, Hanna, Schanz, Merle, Huber, Michael, Braun, Dominique L, Hozé, Nathanael, Scherrer, Alexandra, Magnus, Carsten, Weber, Jacqueline, Uhr, Therese, Cippa, Valentina, Thorball, Christian W, Kuster, Herbert, Cavassini, Matthias, Bernasconi, Enos, Hoffmann, Matthias, Calmy, Alexandra, Battegay, Manuel, Rauch, Andri, Yerly, Sabine, Aubert, Vincent, Klimkait, Thomas, Böni, Jürg, Fellay, Jacques, Regoes, Roland R, Günthard, Huldrych F, Trkola, Alexandra, Bucher, Heiner C, Ciuffi, Angela, Dollenmaier, Günther, Egger, Matthias, Elzi, Luigia, Fehr, Jan, Furrer, Hansjakob, Fux, Christoph A, Haerry, David, Hasse, Barbara, Hirsch, Hans H, Hösli, Irene, Kahlert, Christian, Kaiser, Laurent, Keiser, Olivia, Kovari, Helen, Ledergerber, Bruno, Martinetti, Gladys, de Tejada, Begoña Martinez, Marzolini, Catia, Metzner, Karin J, Müller, Nicolas, Nicca, Dunja, Pantaleo, Giuseppe, Paioni, Paolo, Rudin, Christoph, Schmid, Patrick, Speck, Roberto, Stöckle, Marcel, Tarr, Philip, Vernazza, Pietro, Wandeler, Gilles, and Weber, Rainer

Subjects
Observations, Care and treatment, Development and progression, Host-virus relationships, HIV infections -- Development and progression -- Care and treatment, Antibodies -- Observations, Immune response -- Observations
Abstract

Author(s): Peter Rusert [1]; Roger D Kouyos [1, 2]; Claus Kadelka [1, 2]; Hanna Ebner [1]; Merle Schanz [1]; Michael Huber [1]; Dominique L Braun [1, 2]; Nathanael Hozé [3]; [...], Broadly neutralizing antibodies (bnAbs) are a focal component of HIV-1 vaccine design, yet basic aspects of their induction remain poorly understood. Here we report on viral, host and disease factors that steer bnAb evolution using the results of a systematic survey in 4,484 HIV-1-infected individuals that identified 239 bnAb inducers. We show that three parameters that reflect the exposure to antigen--viral load, length of untreated infection and viral diversity--independently drive bnAb evolution. Notably, black participants showed significantly (P = 0.0086-0.038) higher rates of bnAb induction than white participants. Neutralization fingerprint analysis, which was used to delineate plasma specificity, identified strong virus subtype dependencies, with higher frequencies of CD4-binding-site bnAbs in infection with subtype B viruses (P = 0.02) and higher frequencies of V2-glycan-specific bnAbs in infection with non-subtype B viruses (P = 1 x 10[sup.-5]). Thus, key host, disease and viral determinants, including subtype-specific envelope features that determine bnAb specificity, remain to be unraveled and harnessed for bnAb-based vaccine design.

Published
2016
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27. Role of the pol gene enhancer in HIV-1 transcription and replication in myeloid infected cells.

Author

AIDS 2022, the 24th International AIDS Conference (Montréal, Canada), Van Lint, Carine, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Dutilleul, Antoine, Cristinelli, Sara SC, Marray, Tristan, Nestola, Lorena, Monceaux, Valerie, David, Annie, Verhasselt, Bruno, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, Rohr, Olivier, AIDS 2022, the 24th International AIDS Conference (Montréal, Canada), Van Lint, Carine, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Dutilleul, Antoine, Cristinelli, Sara SC, Marray, Tristan, Nestola, Lorena, Monceaux, Valerie, David, Annie, Verhasselt, Bruno, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, and Rohr, Olivier

Abstract

info:eu-repo/semantics/published

Published
2022

28. Role of the cellular factor CTCF in the regulation of bovine leukemia virus latency and three-dimensional chromatin organization

Author

Bellefroid, Maxime, Rodari, Anthony, Galais, Mathilde, Krijger, Peter H L, Tjalsma, Sjoerd J D, Nestola, Lorena, Plant, Estelle, Vos, Erica S M, Cristinelli, Sara, Van Driessche, Benoit, Vanhulle, Caroline, Ait-Ammar, Amina, Burny, Arsène, Ciuffi, Angela, de Laat, Wouter, Van Lint, Carine, Bellefroid, Maxime, Rodari, Anthony, Galais, Mathilde, Krijger, Peter H L, Tjalsma, Sjoerd J D, Nestola, Lorena, Plant, Estelle, Vos, Erica S M, Cristinelli, Sara, Van Driessche, Benoit, Vanhulle, Caroline, Ait-Ammar, Amina, Burny, Arsène, Ciuffi, Angela, de Laat, Wouter, and Van Lint, Carine

Abstract

Bovine leukemia virus (BLV)-induced tumoral development is a multifactorial phenomenon that remains incompletely understood. Here, we highlight the critical role of the cellular CCCTC-binding factor (CTCF) both in the regulation of BLV transcriptional activities and in the deregulation of the three-dimensional (3D) chromatin architecture surrounding the BLV integration site. We demonstrated the in vivo recruitment of CTCF to three conserved CTCF binding motifs along the provirus. Next, we showed that CTCF localized to regions of transitions in the histone modifications profile along the BLV genome and that it is implicated in the repression of the 5'Long Terminal Repeat (LTR) promoter activity, thereby contributing to viral latency, while favoring the 3'LTR promoter activity. Finally, we demonstrated that BLV integration deregulated the host cellular 3D chromatin organization through the formation of viral/host chromatin loops. Altogether, our results highlight CTCF as a new critical effector of BLV transcriptional regulation and BLV-induced physiopathology.

Published
2022

29. Implication of the cellular factor CTCF in the regulation of Bovine Leukemia Virus latency and tridimensional chromatin organization

Author

2022 Télévie Seminar (Amphithéâtre de l’Europe – ULiège), Plant, Estelle, Bellefroid, Maxime, Rodari, Anthony, Galais, Mathilde, Krijger, Peter, Nestola, Lorena, Vos, Erica, Van Driessche, Benoît, Vanhulle, Caroline, Ait-Ammar, Amina, Ciuffi, Angela, De Laat, Wouter, Van Lint, Carine, 2022 Télévie Seminar (Amphithéâtre de l’Europe – ULiège), Plant, Estelle, Bellefroid, Maxime, Rodari, Anthony, Galais, Mathilde, Krijger, Peter, Nestola, Lorena, Vos, Erica, Van Driessche, Benoît, Vanhulle, Caroline, Ait-Ammar, Amina, Ciuffi, Angela, De Laat, Wouter, and Van Lint, Carine

Abstract

info:eu-repo/semantics/published

Published
2022

30. Role of the pol gene enhancer in HIV-1 transcription and replication in myeloid infected cells

Author

AC41 Host-Virus interactions Annual international symposium "HIV reservoirs in all its forms: Detection, characterisation and targeting" (14th and 15th November 2022: Institut Pasteur Paris), Dutilleul, Antoine, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Marray, Tristan, Cristinelli, Sara SC, Nestola, Lorena, Monceaux, Valerie, David, Annie, Verhasselt, Bruno, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, Rohr, Olivier, Van Lint, Carine, AC41 Host-Virus interactions Annual international symposium "HIV reservoirs in all its forms: Detection, characterisation and targeting" (14th and 15th November 2022: Institut Pasteur Paris), Dutilleul, Antoine, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Marray, Tristan, Cristinelli, Sara SC, Nestola, Lorena, Monceaux, Valerie, David, Annie, Verhasselt, Bruno, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, Rohr, Olivier, and Van Lint, Carine

Abstract

info:eu-repo/semantics/nonPublished

Published
2022

31. Implication of the cellular factor CTCF in the regulation of Bovine Leukemia Virus latency and tridimensional chromatin organization

Author

Epigenetics and Epigenomics in Health and Disease (17-19 November 2022: Brussels), Plant, Estelle, Bellefroid, Maxime, Rodari, Anthony, Galais, Mathilde, Krijger, Peter, Nestola, Lorena, Vos, Erica, Van Driessche, Benoît, Vanhulle, Caroline, Ait-Ammar, Amina, Ciuffi, Angela, De Laat, Wouter, Van Lint, Carine, Epigenetics and Epigenomics in Health and Disease (17-19 November 2022: Brussels), Plant, Estelle, Bellefroid, Maxime, Rodari, Anthony, Galais, Mathilde, Krijger, Peter, Nestola, Lorena, Vos, Erica, Van Driessche, Benoît, Vanhulle, Caroline, Ait-Ammar, Amina, Ciuffi, Angela, De Laat, Wouter, and Van Lint, Carine

Abstract

info:eu-repo/semantics/published

Published
2022

32. Role of the pol gene enhancer in HIV-1 transcription and replication in myeloid infected cells

Author

Van Lint, Carine, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Dutilleul, Antoine, Cristinelli, Sara SC, Marray, Tristan TM, Nestola, Lorena, Monceaux, Valerie, David, Annie, Verhasselt, Bruno, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, Rohr, Olivier, Van Lint, Carine, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Dutilleul, Antoine, Cristinelli, Sara SC, Marray, Tristan TM, Nestola, Lorena, Monceaux, Valerie, David, Annie, Verhasselt, Bruno, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, and Rohr, Olivier

Abstract

info:eu-repo/semantics/published

Published
2022

33. Role of the cellular factor CTCF in the regulation of bovine leukemia virus latency and three-dimensional chromatin organization

Author

CMM Groep Burgering, Genetica, Cancer, Hubrecht Institute with UMC, Bellefroid, Maxime, Rodari, Anthony, Galais, Mathilde, Krijger, Peter H.L., Tjalsma, Sjoerd J.D., Nestola, Lorena, Plant, Estelle, Vos, Erica S.M., Cristinelli, Sara, Van Driessche, Benoit, Vanhulle, Caroline, Ait-Ammar, Amina, Burny, Arsène, Ciuffi, Angela, De Laat, Wouter, Van Lint, Carine, CMM Groep Burgering, Genetica, Cancer, Hubrecht Institute with UMC, Bellefroid, Maxime, Rodari, Anthony, Galais, Mathilde, Krijger, Peter H.L., Tjalsma, Sjoerd J.D., Nestola, Lorena, Plant, Estelle, Vos, Erica S.M., Cristinelli, Sara, Van Driessche, Benoit, Vanhulle, Caroline, Ait-Ammar, Amina, Burny, Arsène, Ciuffi, Angela, De Laat, Wouter, and Van Lint, Carine

Published
2022

37. Role of the cellular factor CTCF in the regulation of bovine leukemia virus latency and three-dimensional chromatin organization

Author

Bellefroid, Maxime, primary, Rodari, Anthony, additional, Galais, Mathilde, additional, Krijger, Peter H L, additional, Tjalsma, Sjoerd J D, additional, Nestola, Lorena, additional, Plant, Estelle, additional, Vos, Erica S M, additional, Cristinelli, Sara, additional, Van Driessche, Benoit, additional, Vanhulle, Caroline, additional, Ait-Ammar, Amina, additional, Burny, Arsène, additional, Ciuffi, Angela, additional, de Laat, Wouter, additional, and Van Lint, Carine, additional

Published
2022
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38. VIH: prévention, traitement et perspectives

Author

Kampouri, Eleftheria, Papadimitriou-Olivgeris, Matthaios, Calmy, Alexandra, Ciuffi, Angela, and Cavassini, Matthias

Subjects
ddc:616, HIV Infections/drug therapy/prevention & control, Humans, General Medicine, Heterocyclic Compounds, 3-Ring, Anti-Retroviral Agents/therapeutic use, HIV Integrase Inhibitors/therapeutic use
Abstract

Cet article aborde les aspects préventifs, thérapeutiques et les perspectives de « guérison » du VIH. La PrEP se positionne comme un pilier essentiel pour contrôler l'épidémie. La bithérapie antirétrovirale visant à diminuer les toxicités médicamenteuses n'est pas qu'un sujet de recherche, mais aussi une réalité. Les molécules de longue durée d'action injectables sont prometteuses et très attendues par les patients fatigués de leurs prises quotidiennes. Sur le plan des effets secondaires, la prise pondérale avec les inhibiteurs d'intégrase et la sécurité du dolutégravir chez les femmes enceintes ont fait couler beaucoup d'encre. Enfin, la suppression virologique soutenue après transplantation allogénique de cellules souches hématopoïétiques mutées sur le corécepteur CCR5 provoque de nouvelles vagues d'optimisme face à une cure par thérapie génique.

Published
2020
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39. Africa-specific human genetic variation near CHD1Lassociates with HIV-1 load

Author

McLaren, Paul J., Porreca, Immacolata, Iaconis, Gennaro, Mok, Hoi Ping, Mukhopadhyay, Subhankar, Karakoc, Emre, Cristinelli, Sara, Pomilla, Cristina, Bartha, István, Thorball, Christian W., Tough, Riley H., Angelino, Paolo, Kiar, Cher S., Carstensen, Tommy, Fatumo, Segun, Porter, Tarryn, Jarvis, Isobel, Skarnes, William C., Bassett, Andrew, DeGorter, Marianne K., Sathya Moorthy, Mohana Prasad, Tuff, Jeffrey F., Kim, Eun-Young, Walter, Miriam, Simons, Lacy M., Bashirova, Arman, Buchbinder, Susan, Carrington, Mary, Cossarizza, Andrea, De Luca, Andrea, Goedert, James J., Goldstein, David B., Haas, David W., Herbeck, Joshua T., Johnson, Eric O., Kaleebu, Pontiano, Kilembe, William, Kirk, Gregory D., Kootstra, Neeltje A., Kral, Alex H., Lambotte, Olivier, Luo, Ma, Mallal, Simon, Martinez-Picado, Javier, Meyer, Laurence, Miro, José M., Moodley, Pravi, Motala, Ayesha A., Mullins, James I., Nam, Kireem, Obel, Niels, Pirie, Fraser, Plummer, Francis A., Poli, Guido, Price, Matthew A., Rauch, Andri, Theodorou, Ioannis, Trkola, Alexandra, Walker, Bruce D., Winkler, Cheryl A., Zagury, Jean-François, Montgomery, Stephen B., Ciuffi, Angela, Hultquist, Judd F., Wolinsky, Steven M., Dougan, Gordon, Lever, Andrew M. L., Gurdasani, Deepti, Groom, Harriet, Sandhu, Manjinder S., and Fellay, Jacques

Abstract

HIV-1 remains a global health crisis1, highlighting the need to identify new targets for therapies. Here, given the disproportionate HIV-1 burden and marked human genome diversity in Africa2, we assessed the genetic determinants of control of set-point viral load in 3,879 people of African ancestries living with HIV-1 participating in the international collaboration for the genomics of HIV3. We identify a previously undescribed association signal on chromosome 1 where the peak variant associates with an approximately 0.3 log10-transformed copies per ml lower set-point viral load per minor allele copy and is specific to populations of African descent. The top associated variant is intergenic and lies between a long intergenic non-coding RNA (LINC00624) and the coding gene CHD1L, which encodes a helicase that is involved in DNA repair4. Infection assays in iPS cell-derived macrophages and other immortalized cell lines showed increased HIV-1 replication in CHD1L-knockdown and CHD1L-knockout cells. We provide evidence from population genetic studies that Africa-specific genetic variation near CHD1Lassociates with HIV replication in vivo. Although experimental studies suggest that CHD1L is able to limit HIV infection in some cell types in vitro, further investigation is required to understand the mechanisms underlying our observations, including any potential indirect effects of CHD1L on HIV spread in vivo that our cell-based assays cannot recapitulate.

Published
2023
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42. Implication of the cellular factor CTCF in the regulation of Bovine Leukemia Virus latency and tridimensional chromatin organization

Author

Rodari, Anthony, primary, Bellefroid, Maxime, additional, Galais, Mathilde, additional, Krijger, Peter H.L., additional, Nestola, Lorena, additional, Plant, Estelle, additional, Vos, Erica S.M., additional, Van Driessche, Benoit, additional, Vanhulle, Caroline, additional, Ammar, Amina Ait, additional, Ciuffi, Angela, additional, de Laat, Wouter, additional, and Van Lint, Carine, additional

Published
2021
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44. Intragenic PU-boxes control HIV-1 transcription and replication in myeloid infected cells

Author

Virtual Keystone Symposia :HIV Pathogenesis and Cure EK43, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Cristinelli, Sara SC, Delacourt, Nadège, Dutilleul, Antoine, Bendoumou, Maryam, Monceaux, Valerie, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, Rohr, Olivier, Van Lint, Carine, Virtual Keystone Symposia :HIV Pathogenesis and Cure EK43, Hernalsteens, Olivier, Verdikt, Roxane, Vanhulle, Caroline, Cristinelli, Sara SC, Delacourt, Nadège, Dutilleul, Antoine, Bendoumou, Maryam, Monceaux, Valerie, Galons, Hervé, Ciuffi, Angela, Sáez-Cirión, Asier, Rohr, Olivier, and Van Lint, Carine

Abstract

info:eu-repo/semantics/published

Published
2021

45. Bioinformatics and HIV Latency

Author

Ciuffi, Angela, Mohammadi, Pejman, Golumbeanu, Monica, di Iulio, Julia, Telenti, Amalio, Ciuffi, Angela, Mohammadi, Pejman, Golumbeanu, Monica, di Iulio, Julia, and Telenti, Amalio

Abstract

Despite effective treatment, HIV is not completely eliminated from the infected organism because of the existence of viral reservoirs. A major reservoir consists of infected resting CD4+ T cells, mostly of memory type, that persist over time due to the stable proviral insertion and a longcellular lifespan. Resting cells do not produce viral particles and are protected from viral-induced cytotoxicity or immune killing. However, these latently infected cells can be reactivated by stochastic events or by external stimuli. The present review focuses on novel genome-wide technologies applied to the study of integration, transcriptome, and proteome characteristics and their recent contribution to the understanding of HIV latency.

Published
2021

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