Bumsuk Hahm
University of Missouri-Columbia, MO·Microbiology & Immunology
Every virus infection is a tug-of-war over the host cell's own chemistry. Work in this lab centers on a family of fat-derived signaling molecules called sphingolipids, and especially on sphingosine 1-phosphate (S1P), a lipid messenger that cells use to tune growth, movement and immune signaling.
- Fields
Microbiology & Immunology
Pharmacology
Biochemistry
- Topics
influenza virus
sphingosine 1-phosphate
sphingosine kinase 2
- Grants
- 2 known grants, through May 2027
What they work on
- Determine how influenza virus lowers S1P lyase (SPL), the enzyme that degrades the lipid messenger S1P, and raises sphingosine kinase 2 (SK2), which makes it, and how these shifts speed viral replication in infected cells.
- Work out the mechanisms behind the opposing activities of these enzymes, testing whether SPL restrains influenza by boosting IKK-epsilon-driven type I interferon alarm signaling while SK2 favors the virus.
- Establish what S1P-metabolizing enzymes do during influenza infection in live mice, using genetic and inhibitor approaches to link enzyme levels to viral load, disease severity and survival.
- Test whether SK2 activation in CD4+ helper T cells limits virus-specific T-cell expansion during persistent LCMV clone 13 infection in mice, and examine T cells from patients with chronic viral infections for the same pattern.
- Define the molecular steps by which SK2 suppresses virus-specific CD4+ T-cell responses and holds back immune-mediated kidney pathology, using SK2-deficient mice infected with LCMV.
- Evaluate oral SK2 inhibitor treatment in mice with persistent LCMV infection, measuring how fast virus is cleared and which features of host immunity are restored.
More about the research
Two enzymes control how much S1P is around: sphingosine kinase 2 (SK2), which makes it, and S1P lyase (SPL), which breaks it down. Both projects ask how viruses exploit or disarm these enzymes, one in a fast, acute infection (influenza) and one in a long-lasting infection that wears down the immune system. Together they test a single idea: that lipid-metabolizing enzymes sit at a control point that decides whether the host clears a virus or the virus wins.
Why it matters
Influenza still causes widespread illness and death each year, and chronic viral infections remain hard to clear. By identifying host enzymes that viruses depend on or disable, this work points to drug targets in the host rather than the virus, which may be harder for viruses to evade. An SK2-blocking drug taken by mouth could, if the findings hold, offer a route to limiting flu replication or to reawakening exhausted T cells in long-term infections, while also clarifying how immune responses turn damaging to organs such as the kidney.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Rabindra Mandal
CUNY Hunter College, NY·Microbiology & Immunology
Determine how the makeup of the gut bacterial community affects intestinal levels of sphingosine 1-phosphate (S1P), a lipid signaling molecule, and how those levels track with parasite burden in mice infected with Plasmodium yoelii 17XNL.
Mandy J Mcgeachy
Cornell University, NY·Microbiology & Immunology
Determine how the interaction between PIP5K1a, an enzyme making the nuclear lipid PIP2, and ARS2, an mRNA cap-binding protein, is regulated as Th17 cells differentiate, using primary human T cells and CD28-humanized CD28A210P mice.
Stefanka Spassieva
University of Kentucky, KY·Neuroscience
Test whether high brain levels of sphingoid bases and their phosphates in CerS1-deficient mice change gene activity in neurons and glia over time, disrupting neuronal maturation and differentiation.
The school
University of Missouri-Columbia: 21 labs on PI Pages, $509M a year on research, 260 research doctorates a year.
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