Dr. Rosen is a prolific physician-scientist with approximately 200 original peer-reviewed manuscripts investigating the cellular and molecular underpinnings of liver diseases. He is an elected member of ASCI and AAP and the recipient of numerous awards, including the Senator Hatfield Award for Research. He became the first hepatologist awarded the prestigious Research Award for Clinical Science by the American Society of Transplantation. Among his early seminal contributions, he identified epidemiologic factors that shape the variable natural history of hepatitis C virus infection (HCV) and developed mathematical models to predict outcome in liver re-transplantation that influenced policies and decision-making.

“Hugo is an astute clinician who has reengineered himself to become one of the nation’s leading immunologists,” according to Lasker Award winner and Distinguished National Institutes of Health Investigator Emeritus, Dr. Harvey Alter. Dr. Rosen’s research has provided highly novel and significant insights into the roles of multicellular immunity in liver disease, particularly to HCV, and more recently, in non-alcoholic fatty liver disease. It would be challenging to find another research lab in the world working on HCV in the past 20 years that has been more comprehensive in characterizing the diverse roles of multiple cell types (T cells, dendritic cells, macrophages, NK cells, liver sinusoidal endothelial cells, and trophoblasts) in mediating viral protection/recovery, persistence, and treatment-induced cure. Exemplary advances that have shaped the field include:
· HCV-specific CD4+ T cells prevent viral escape in acute human infection and their absence leads to persistence;
· race-related differences in HCV-specific immunity
· identification of multiple co-inhibitory receptors (and their ligands) that mediate T cell exhaustion and chronicity that could be targeted;
· the first recognition that Kupffer cell-derived galectin-9 induces apoptosis of HCV-specific CD8+ T cells and expansion of regulatory T cells, confirmed to be important in other liver diseases;
· the liver allograft primes novel CTLs that are HCV-specific provided the first insight into how recipient T cells can mediate viral-specific immunity across HLA mismatch
· FXR signaling reverses innate immune dysfunction in NAFLD;
· HCV triggers responses in human trophoblasts and recruitment of maternal NK cells as an explanation for protection against vertical transmission
· transmitter/founder HCV induces genotype- and cell type-specific differences in innate immune signaling
· dietary cholesterol differentially impacts populations of hepatic macrophages mediating NASH progression
Remarkable in their originality, scope and impact, these studies have advanced scientific thought by identifying many aspects of the division of labor played by different immune cells in liver diseases. Funded continuously for over 20 years, his research program enjoys training the next generation of translational scientists, including PhD and MD/PhD candidates, post-doctoral fellows, and faculty.