Menelaos Symeonides, Ph.D.

Assistant Professor

Training and Education

Dr. Symeonides received his Ph.D. in Cell and Molecular Biology from the University of Vermont in 2015, studying cell-to-cell transmission of HIV with Dr. Markus Thali. For his postdoctoral research, he stayed in the Thali group at UVM and continued working on HIV, while expanding into endogenous retroviruses and placental biology, and also joined Dr. Benjamin Lee’s group at UVM, studying human immune responses to rotavirus vaccination and natural infection. Dr. Symeonides was promoted to Faculty Scientist in the Department of Microbiology and Molecular Genetics in October 2021. 

Research Interests

My research focuses on the cell biology of viral infections.

Human Immunodeficiency Virus (HIV)
A hallmark of HIV infection is chronic inflammation, possibly due to sensing of HIV-infected T cells and subsequent cytokine production by plasmacytoid dendritic cells (pDCs) and natural killer (NK) cells. Our preliminary work indicates that HIV-induced T cell syncytia (multinucleated cells resulting from cell-cell fusion) may be the primary inducers of cytokine production by pDCs and NK cells. We are currently testing this hypothesis as part of an NIH-funded R21 project in the Thali lab using novel cell isolation tools and functional in vitro pDC/NK cell assays. In parallel, we are studying the motility of syncytia in 3D collagen cultures using long-term light sheet fluorescence microscopy and computational analysis of large 3D cell tracking datasets.

HIV-1-infected T cells migrating through a 3D collagen hydrogel

Placental Biology
The syncytiotrophoblast is the outermost fetal layer of the placenta, which forms due to the fusogenic action of endogenous retroviral glycoproteins, the syncytins. We (the Thali lab) are studying how cell-cell fusion is tightly regulated to ensure proper formation of the syncytiotrophoblast.

Rotavirus (RV)
RV is a major cause of diarrheal disease in children and infants in low and middle-income countries, particularly because they do not mount a sufficiently protective immune response to available RV vaccines. In the Lee group, we are investigating this problem by measuring adaptive immune responses to RV vaccination and natural RV infection in infants and children, with my particular focus being on memory B cells.


  1. Whitaker EE, Matheson NJ, Perlee S, Munson PB, Symeonides M*, Thali M*. EWI-2 Inhibits Cell-Cell Fusion at the HIV-1 Virological Presynapse. Viruses. 2019 Nov 20;11(12). doi:10.3390/v11121082. PubMed PMID: 31757023             *co-senior authors
  2. Ikeda T, Symeonides M, Albin JS, Li M, Thali M, Harris RS. HIV-1 adaptation studies reveal a novel Env-mediated homeostasis mechanism for evading lethal hypermutation by APOBEC3G. PLoS Pathog. 2018 Apr;14(4):e1007010. doi: 10.1371/journal.ppat.1007010. eCollection 2018 Apr. PubMed PMID: 29677220
  3. Symeonides M, Murooka TT, Bellfy LN, Roy NH, Mempel TR, Thali M. HIV-1-Induced Small T Cell Syncytia Can Transfer Virus Particles to Target Cells through Transient Contacts. Viruses. 2015 Dec 12;7(12):6590-603. doi: 10.3390/v7122959. PubMed PMID: 26703714
  4. Symeonides M, Lambelé M, Roy NH, Thali M. Evidence showing that tetraspanins inhibit HIV-1-induced cell-cell fusion at a post-hemifusion stage. Viruses. 2014 Mar 7;6(3):1078-90. doi: 10.3390/v6031078. PubMed PMID: 24608085
Mel Symeonides smiling

Contact Information

Office: 318/208 Stafford Hall

Phone: 802-656-1161