Around 400 million cases of dengue are reported annually, with a growing geographic region at risk for exposure. Dengue, a viral infection caused by the dengue virus (DENV), is transmitted to humans through a bite by an infected mosquito. Currently, there are no specific treatments for dengue and infection has been linked to an increased future risk of leukemia. While previous research has shown that dengue infection can lead to DNA damage in blood cells more research is needed into the extent of dengue virus infection and impacts to host DNA metabolic processes.
New research from the laboratory of Nimrat Chatterjee, PhD, published in the Proceedings of the National Academy of Sciences (PNAS), showcases how infection with the understudied dengue subtype DENV-4 results in significant DNA damage while simultaneously suppressing DNA repair. Ultimately, the insults to DNA leave “biological scars”. The researchers believe that these biological scars incrementally create disease-vulnerability windows that put patients at an increased risk for carcinogenesis and other postdengue symptoms.
The study brought together investigators from the University of Vermont, M.I.T., University of Washington, Harvard Medical School, Duke University School of Medicine, and NYU Grossman School of Medicine, highlighting a multidisciplinary collaboration spanning genome stability and virology.
The study also highlights trainee-driven research, with Erica Lamkin, Jessica Reich, and CMB graduate Josh Victor as co-first authors, alongside UVM’s Barry Goldwater Scholars Madison Guyette and Naveen Kothandaraman. Lamkin is now pursuing MD/PhD training.
Read the study: DENV-4 infection suppresses transcription of DNA repair genes, PNAS, 2026
