A complete application in a minute
Tailored resume and cover letter, ready to send.
The Holmes Lab at the University at Buffalo is seeking a postdoctoral researcher to study innate immunity and pathogenesis in arthritogenic alphavirus infections. The role focuses on tissue tropism, infection permissiveness, and virus dissemination using in vivo and in vitro approaches.
Research explores two phases of alphavirus transport, with work on PDGFRα+ skeletal muscle mesenchymal cells and VEGF signaling.
The Holmes Lab is looking for a postdoctoral researcher to join our lab to carry out research projects related to innate immunity and pathogenesis in arthritogenic alphavirus infections. Our research focuses on defining the tissue tropism of emerging arthritogenic alphaviruses and determining how cells that are permissive to infection influence virus dissemination and disease progression.
Our most recent published work demonstrated that, in contrast to established paradigms, there are two phases of alphavirus transport through the lymphatics at early times of infection, one that precedes viral replication, and a second that requires replication in the skin which enables transit to the bloodstream (Holmes AC et al., doi: 10.1016/j.celrep.2024.113876). We found that skin-infiltrating Ly6Chi monocytes promote infection of several non-hematopoietic cell types in the skin. Unexpectedly, in contrast to the skin, lymph node-associated monocytes are refractory to virus infection. Our work highlighted that there is an underappreciated role for cell‑free, fluid‑phase lymphatic trafficking during early alphavirus dissemination and that there may be tissue‑specific signals that govern monocyte permissiveness to alphavirus infection. Our aim is to identify and define the mechanisms that drive monocyte heterogeneity in arthritogenic alphavirus infections.
In a forthcoming manuscript (Holmes AC et al., submitted, PLoS Pathogens), we have identified a subset of platelet‑derived growth factor alpha‑positive (PDGFRα+) skeletal muscle mesenchymal cells that are infected via the major arthritogenic alphavirus entry receptor, matrix remodeling‑associated protein 8 (MXRA8). Infection of this PDGFRα+ cell subset increases local vascular permeability to mediate virus spread directly to the bloodstream in a manner that is dependent on vascular endothelial growth factor (VEGF) signaling. Our aim is to define the molecular events that underlie the VEGF signaling cascade during arthritogenic alphavirus infections and determine how virus disseminates across the vasculature.
We are a new lab supported by funding from the Howard Hughes Medical Institute (HHMI) and are looking to grow! The lab is committed to the success of all members and provides mentorship and opportunities for research and career development. We are located at the Jacobs School of Medicine and Biomedical Sciences in downtown Buffalo, NY.
Oalthy mix of work, personal and academic pursuit – all in an effort to support your work‑lifeutstanding Benefits Package
Working at UB comes with benefits that exceed salary alone. There are personal rewards including comprehensive health and retirement plan options. We also focus on creating and sustaining a he effectiveness. We support your growth and development through our career coaching and training department and we qualify as a public service loan forgiveness organization. Learn more about the great benefits the University at Buffalo has to offer. Visit our website to learn more about the University at Buffalo.
The Research Foundation of SUNY is an EOE and welcomes all to apply including veterans and individuals with a disability.