Silence
is a Behaviour
Quantitative Virology Research Group
RESEARCH PROJECTS
2023-2027: Role of HIV antisense transcripts in the establishment of latency: genome-wide map antisense RNAs to understand how they regulate HIV transcription (Principal Investigator: H.C. Chen, Łukasiewicz Research Network - PORT, Wrocław, Poland)
Project is funded by National Science Centre Poland (NCN) SONATA BIS 12 (ID: 563746; Reg. No: DEC-2022/46/E/NZ6/00022; 3,724,878 PLN).
2020-2022: Understanding the intrinsic mechanism of elite controller patients to restrict HIV infection (Supervisor: M. Benkirane, Institut de Génétique Humaine, Montpellier, France)
We attempt to understand why the intrinsic property of elite controller CD4+ T cells does not favor for the selection of HIV integration sites, transcription and reactivation. Furthermore, we conducted an A.I. approach to massively analyze RNA-seq data to seek for possible molecular determinants responsible for elite control. (Chen et al., manuscript under preparation).
2019-2022: Genetically defective HIV proviruses are prone to be present in host genomic repeat regions (Supervisor: M. Benkirane, Institut de Génétique Humaine, Montpellier, France)
We developed a new technology LAMP-seq to associate the nearly full-length HIV genomic sequences with host genomic sequences surrounding integration sites. We show that the genetic integrity of the proviruses present in host genomic repeat regions is less intact than those outside the host genomic repeat regions. (Chen et al., manuscript under preparation).
2019-2022: The impact of γc-cytokines on the selection of HIV integration sites, expression and reactivation (Supervisor: M. Benkirane, Institut de Génétique Humaine, Montpellier, France)
We proof that HIV displays different transcriptional profiles in primary CD4+ T cells activated by different γc-cytokines. HIV proviruses are prone to be reactivated by the same γc-cytokines used for primary CD4+ T cells activation upon infection (Chen et al., manuscript under preparation).
2017-2020: The chromatin landscape at the HIV-1 provirus integration site determines viral expression (Personal Research Collaboration with the lab of Dr. Debyser, KU Leuven, Leuven, Flanders, Belgium)
We proof that LEDGINs, which are small molecule inhibitors of HIV integrase-LEDGF/p75 interaction enable to retarget HIV out of gene-dense and actively transcribed regions and consequently reduce viral RNA expression and increase the proportion of silent provirus (Vansant*, G., H.-C. Chen* et al., 2020).
2015-2018: The selection of HIV integration sites in the 3D genome (Supervisor: G. Filion, Centre de Regulació Genòmica, Barcelona, Spain)
We show the bias of HIV integration in the 3D genomic architecture: viruses tend to integrate in spatial proximity of super-enhancers in primary CD4+ T cells and in T cell cultures in vitro (Lucic*, B., H.-C. Chen* et al., 2019).
2013-2016: Position effects influence HIV latency reversal (Supervisor: G. Filion, Centre de Regulació Genòmica, Barcelona, Spain)
We successfully proof that HIV transcription is influenced by the local genomic context: viruses which integrate close to endogenous enhancers display the higher transcriptional level than those integrating far from enhancers (Chen et al., 2017).
2008-2011: Identification and characterization of a novel Salmonella gene product STM0029 (Supervisor: L.H. Wieler & K. Tedin, Humboldt-Universität zu Berlin, Berlin, Germany)
We reveal the importance of a novel Salmonella gene product STM0029 which contributes to the resistance to host antimicrobial peptide killing (DOI: 10.18452/16658).
2004-2006: Characterization of a putative function of the two-component system ScnRK in Streptococcus mutans (Supervisor: J.S. Chia, National Taiwan University, Taipei, Taiwan)
We identify the function of S. mutans two-component system ScnRK involved in the resistance of hydrogen peroxide and murine macrophage killing (Chen et al., 2008).