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Mohamed Abdel-Mohsen, Ph.D.

Mohamed Abdel-Mohsen, Ph.D.

Laboratory

The Abdel-Mohsen Laboratory

Contact

215-898-6008
mmohsen@wistar.org

Assistant Professor, Vaccine & Immunotherapy Center

About the Scientist

Abdel-Mohsen’s research focuses on investigating the role of host glycosylation machinery in viral persistence and immunopathogenesis.

Abdel-Mohsen joined The Wistar Institute as Assistant Professor in 2017 after completing his Ph.D. and postdoctoral training at the University of California, San Francisco (UCSF) and the Blood Systems Research Institute (BSRI), where he was subsequently appointed as a research scientist. Previously, he was a virologist for the World Health Organization Regional Reference Laboratory for poliovirus in his home country of Egypt. He received the UCSF-Gladstone CFAR Early-Career Award of Excellence in Basic Science in 2015.

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The Abdel-Mohsen Laboratory

The Abdel-Mohsen laboratory investigates the role of host-virus interactions in persistence and immunopathogenesis of HIV infection by combining virological, glycobiological, and immune-based basic and translational research. The multidisciplinary studies aim to develop novel approaches to enhance immune function and control/eradicate HIV.

The focus of the work in the lab is based on a combination of approaches including investigating the role of glycan-lectin interactions and altered cell-surface glycosylation in mediating cellular processes central to immune regulation and human diseases; designing multi-omics approaches to study host immune response to HIV infection; and developing and implementing robust and sensitive molecular biology-based assays to measure cellular and tissue HIV reservoirs.

Staff

Postdoctoral Fellow

Florent Colomb, Ph.D.
Leila Giron, Ph.D.

Research Assistant

Alitzel Greet Anzurez Reyes

Research

All living cells assemble a diverse repertoire of glycan structures on their surface via their glycosylation machinery. With recent advances in the glycobiology field, host glycosylation and glycan-lectin signaling have been shown to play critical roles in immune responses and in cell-cell and cell-pathogen interactions. Glycan structure alterations have been identified as biomarkers for cancer and multiple cellular processes. Activated, HIV-infected cells have altered cell-surface glycosylation patterns with respect to resting, uninfected cells. While the association between hyposialylation and chronic HIV infection was suggested over two decades ago, the relevance of host glycosylation to HIV persistence has never been characterized. However, recent development in glycobiological technologies provides an opportunity to revisit this critical issue. In a recent publication, we demonstrated that the human carbohydrate-binding protein galectin-9 regulates HIV transcription and potently reactivates latent HIV in vitro, as well as ex vivo using CD4+ T cells from the blood of HIV+ individuals on suppressive antiretroviral therapy, in an N-glycan-dependent manner. This suggests that host glycan-lectin interactions likely mediate signals that define, in part, the transcriptional state of HIV and that host glycosylation machinery may be exploited to develop novel HIV therapeutic strategies. Furthermore, we used cutting-edge glycomics technologies to demonstrate that host glycan-lectin interactions and altered host glycosylation are associated with deficits in immune function that in turn contribute to HIV persistence. The cell-surface sugar-coating may hold the key to new therapeutics that can be harnessed to cure HIV and possibly a range of other infectious diseases.

Selected Publications

Abdel-Mohsen, M., Kuri-Cervantes, L., Montaner, L.J., et al. “CD32 is expressed on cells with transcriptionally active HIV but does not enrich for HIV DNA in resting T cells.” Sci Transl Med. 2018 Apri 18;10 (437) pii: eaar6759. doi: 10.1126/scitranslmed.aar6759.

Vadrevu, S.K., Trbojevic-Akmacic, I., Abdel-Mohsen, M., et al. "Frontline Science: Plasma and immunoglobulin G galactosylation associate with HIV persistence during antiretroviral therapy." J Leukoc Biol. 2018 Apr 6. doi: 10.1002/JLB.3HI1217-500R.

Krarup, A.R., Abdel-Mohsen, M., Denton P.W., et al. "The TLR9 agonist MGN1703 triggers a potent type I interferon response in the sigmoid colon." Mucosal Immunol. 2018 Mar;11(2):449-461. doi: 10.1038/mi.2017.59. Epub 2017 Aug 2.

Abdel-Mohsen, M., Chavez, L., Pillai, S.K., et al. "Human Galectin-9 Is a Potent Mediator of HIV Transcription and Reactivation." PLoS Pathog. 2016 Jun 2;12(6):e1005677. doi: 10.1371/journal.ppat.1005677. eCollection 2016 Jun.

Abdel-Mohsen, M., Wang, C., Pillai, S.K., et al. "Select host restriction factors are associated with HIV persistence during antiretroviral therapy." AIDS. 2015 Feb 20;29(4):411-20. doi: 10.1097/QAD.0000000000000572.

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