About Me
I am an active researcher in the field of blood stem cell biology. My work primarily focuses on the expansion of human hematopoietic stem cells and understanding retrovirus behaviors. During my Master's studies (2012–2015), I worked on the antiviral restriction factor IFITM protein family in the context of HCMV infection at the Institut Pasteur of Shanghai under the supervision of Prof. Zhikang Qian. I completed my Ph.D. (2015–2019) in the laboratory of Prof. Serge Benichou at the University of Paris, specializing in microbiology. My research focused on HIV-1 cell-to-cell transfer and viral dissemination in myeloid cells. In 2019, I joined University College London (UCL) in the UK to study how virus evade innate immunity response with a little help from viral accessory proteins. My work led to the discovery that SARS-CoV-2 Orf6 and HIV-1 Vpr antagonize interferon responses by suppressing STAT nuclear transport. Additionally, I have been serving as a grant reviewer for the National Science Centre (NCN, Poland) since 2021.
Research Interests
My research is centered around stem cell biology and virology. I explore how hematopoietic stem cells can be manipulated for better therapeutic outcomes and study retroviruses for better understanding of their pathogenesis.
Projects
HIV-1 cell-to-cell transfer and viral dissemination in myeloid cells
Most enveloped viruses encode viral fusion proteins to penetrate host cells via membrane fusion. Interestingly, many enveloped viruses, such as HIV-1 and SARS-CoV-2, can also use these viral fusion proteins to induce cell-cell fusion, both in vitro and in vivo, leading to the formation of syncytia or multinucleated giant cells (MGCs). Virus cell-to-cell spread through inducing cell-cell fusion may overcome entry and post-entry blocks in target cells and allow evasion of neutralizing antibodies.
Learn MoreHIV-1 Vpr antagonises Interferon by suppressing STAT nuclear transport.
Viruses have evolved various strategies to evade the host's innate immune response, one of which is incorporating viral proteins into virions to antagonize these immune responses and support efficient viral replication. HCMV incorporates several viral proteins, such as pUL83 (pp65) and the UL26 tegument protein, to target various stages of the IFN signaling pathway, effectively dampening the host's antiviral response(Abate et al., 2004; Ciesla et al., 2024; Munger et al., 2006). Similarly, the Ebola virus incorporates viral proteins like VP35 and VP24 to strategically inhibit the host's IFN response(Messaoudi et al., 2015; Xu et al., 2014). With respect to HIV-1, Vpr is the only accessory protein that is incorporated into virions. I found that HIV-1 Vpr can directly antagonise IFN by targeting the STAT proteins activated by IFN signaling.
Learn MoreKey Publications
- Virus-Induced Cell Fusion and Syncytia Formation - Read More
- Cell-to-cell spreading of HIV-1 in myeloid target cells escapes SAMHD1 restriction - Read More
- Mechanisms for cell-to-cell transmission of HIV-1 - Read More
- T cell-macrophage fusion triggers multinucleated giant cell formation for HIV-1 spreading - Read More
Talks & Conferences
- Retroviruses 2023, Cold Spring Harbor, New York, May 2023
HIV-1 Vpr antagonises interferon by suppressing STAT nuclear transport. - Evolving Concepts in HIV and Emerging Viral Infections, Miami Winter Symposium 2019
HIV-1 cell-to-cell fusion mediates productive infection of macrophages and dendritic cells by both macrophage- and non-macrophage-tropic viruses.
News and Updates
- May 2024 - I moved to the Department of Biology at the University of York to develop novel molecules for ex vivo hematopoietic stem cell expansion in the laboratories of Professor David Kent and Professor Ian Hitchcock.
- CSHL Retroviruses 2023 - May 2023 - Poster presentation at the International Retrovirus Conference 2023.
Contact
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