Samira Asgari
@samiraasgari.bsky.social
There is a crack in everything, that’s how the light gets in.
Scientist, Computational biologist. Asst. Prof. Icahn School of Medicine at Mount Sinai 🧬. Alum. Harvard Medical School 🇺🇸, EPFL🇨🇭, University of Tehran 🇮🇷
Scientist, Computational biologist. Asst. Prof. Icahn School of Medicine at Mount Sinai 🧬. Alum. Harvard Medical School 🇺🇸, EPFL🇨🇭, University of Tehran 🇮🇷
Biomedical sciences need more comprehensive disease risk models that assess all potential risk factors together. Our work contributes to this effort, showing the power of integrating social determinants of health into risk models for more equitable and accurate prediction.
October 2, 2025 at 3:50 PM
Biomedical sciences need more comprehensive disease risk models that assess all potential risk factors together. Our work contributes to this effort, showing the power of integrating social determinants of health into risk models for more equitable and accurate prediction.
What we found:
- Including social, behavioral & environmental context in disease risk models consistently improved prediction.
- Their contribution often outweighed polygenic risk.
- Genetic and non-genetic risks act largely additively (little interaction effect at the level we examined).
- Including social, behavioral & environmental context in disease risk models consistently improved prediction.
- Their contribution often outweighed polygenic risk.
- Genetic and non-genetic risks act largely additively (little interaction effect at the level we examined).
October 2, 2025 at 3:50 PM
What we found:
- Including social, behavioral & environmental context in disease risk models consistently improved prediction.
- Their contribution often outweighed polygenic risk.
- Genetic and non-genetic risks act largely additively (little interaction effect at the level we examined).
- Including social, behavioral & environmental context in disease risk models consistently improved prediction.
- Their contribution often outweighed polygenic risk.
- Genetic and non-genetic risks act largely additively (little interaction effect at the level we examined).
Then, using data from >170,000 All of Us biobank participants, we asked how adding these profiles changes disease risk prediction and modifies the impact of genetic risk.
October 2, 2025 at 3:50 PM
Then, using data from >170,000 All of Us biobank participants, we asked how adding these profiles changes disease risk prediction and modifies the impact of genetic risk.
First, we developed a scalable framework that distills hundreds of lifestyle, environmental, and social measures into clear, independent profiles that can be used to assess disease risk on their own or alongside genetic scores.
October 2, 2025 at 3:50 PM
First, we developed a scalable framework that distills hundreds of lifestyle, environmental, and social measures into clear, independent profiles that can be used to assess disease risk on their own or alongside genetic scores.
While these are initial findings from a small cohort, they suggest that diversity in lifetime viral exposures may be an underappreciated factor influencing individual variability in responses to infections, vaccines, and inflammatory triggers.
September 17, 2025 at 2:48 PM
While these are initial findings from a small cohort, they suggest that diversity in lifetime viral exposures may be an underappreciated factor influencing individual variability in responses to infections, vaccines, and inflammatory triggers.
Additionally, we observed a measurable imprint on future innate cytokine production after past infection with viruses such as HSV-1 and HSV-2.
September 17, 2025 at 2:48 PM
Additionally, we observed a measurable imprint on future innate cytokine production after past infection with viruses such as HSV-1 and HSV-2.
What we found:
Strong protein-level immunodominance to viral surface proteins.
Striking individual variability at the epitope level (even within the same proteins)
Strong protein-level immunodominance to viral surface proteins.
Striking individual variability at the epitope level (even within the same proteins)
September 17, 2025 at 2:48 PM
What we found:
Strong protein-level immunodominance to viral surface proteins.
Striking individual variability at the epitope level (even within the same proteins)
Strong protein-level immunodominance to viral surface proteins.
Striking individual variability at the epitope level (even within the same proteins)
To link past viral infections with future innate immune responses, we combined VirScan (which measures antibody responses to past viral infections), with Olink proteomics after ex vivo TLR stimulation of blood samples.
September 17, 2025 at 2:48 PM
To link past viral infections with future innate immune responses, we combined VirScan (which measures antibody responses to past viral infections), with Olink proteomics after ex vivo TLR stimulation of blood samples.
While sepsis is our starting point, our broader goal is to apply this whole-human, multi-omic lens to other infectious and immune-mediated diseases.
August 12, 2025 at 6:35 PM
While sepsis is our starting point, our broader goal is to apply this whole-human, multi-omic lens to other infectious and immune-mediated diseases.
Our immune response is shaped by inherited variants, somatic mutations, cell- and tissue-specific functions, environmental exposures, and social and behavioral factors. This award will allow us to study how these layers interact.
August 12, 2025 at 6:35 PM
Our immune response is shaped by inherited variants, somatic mutations, cell- and tissue-specific functions, environmental exposures, and social and behavioral factors. This award will allow us to study how these layers interact.