Postgraduate
Virology
The George Washington University
1996
See all Profiles
Faculty
Faculty
Sergei Nekhai, Ph.D.
Professor
Department/Office
- Medicine
School/College
- College of Medicine
Additional Positions
-
ProfessorMicrobiology
Biography
Sergei Nekhai, Ph.D., is a professor of medicine and microbiology. He has a master’s degree in physics and engineering from St. Petersburg Polytechnic University, Russia and Ph.D. degree in Biophysics from Petersburg Nuclear Physics Institute. He had a postdoctoral training at George Washington University and Children’s National Medical Center in 1994-1997 in Virology and Immunology.
Nekhai joined Howard University’s Center for Sickle Cell Disease in 2000 where he conducts basic and translation studies on Sickle Cell Disease, HIV-1 and Ebola virus infections. He is also involved in translational studies on pulmonary hypertension in sickle cell disease and community service for sickle cell patients. He investigates iron metabolism in Africans and African Americans. He served as co-Director for Howard University Center for Sickle Cell Disease from 2011-2017, and as Deputy Director since 2017. He leads Research Centers in Minority Institution (RCMI) Proteomics Program at Howard University. He serves as Director for Basic Science for Washington DC Center for AIDS Research.
Nekhai’s current and past funding includes National Institute of Health grants including RO1, U19, P50 and G12 for which he has served as a PI, co-PI or PD. He supervised and trained primarily African American minority junior Faculty, Ph.D. students and MD fellows, undergraduate and high school students. He has over 150 publications in basic virology and hematology journals. Dr. Nekhai serves on National Institute of Health grant review panels. He chairs Howard University Radiation Safety Committee and Appointment, Promotion and Tenure Committee for Howard University College of Medicine.
Education & Expertise
Education
Postgraduate
Immunology
Children’s National Research Center
1996
Doctor of Philosophy (Ph.D.)
Physics and Mathematics (Biophysics)
St. Petersburg Nuclear Physics Institute
1994
Master of Science (M.Sc.)
Physics and Engineering (Biophysics)
Leningrad Polytechnic Institute
1986
Research
Research
Funding
Title: Sickle cell disease and sickle cell trait protection against HIV-1 infection in
Africans and African Americans
Major Goals: to define molecular mechanism of HIV-1 restriction in Sickle Cell Disease
Project Number: 1 R01 HL 125005 - 09
Name of PD/PI: Nekhai, S.
Source of Support: NHLBI
Primary Place of Performance: Howard University, Washington DC
Project/Proposal Start and End Date: 05/2014-02/2025
Total Award Amount (including Indirect Costs): $2,029,527
Title: Howard University Research Center for Minority Health and Health Disparities
Major Goals: to enhance Howard’s capacity for basic biomedical and clinical approaches
to health disparities research.
Project Number: 5 U54 MD 007597 - 33
Name of PD/PI: Southerland, W. M.
Source of Support: NIMHD
Primary Place of Performance: Howard University, Washington DC
Project/Proposal Start and End Date: (MM/YYYY) (if available): 09/1997-01/2024
Total Award Amount (including Indirect Costs): $16,918,485
Person Months (Calendar/Academic/Summer) per budget period.
Title: District of Columbia Center for AIDS Research (DC CFAR)
Major Goals: To expand our multi-institutional effort to support research that contributes
to ending the HIV epidemic in Washington, DC and beyond in partnership with
government and community.
Project Number: P30AI117970
Name of PD/PI: Greenberg, Alan E.
Source of Support: NIH
Primary Place of Performance: Howard University, Washington DC
Project/Proposal Start and End Date: (MM/YYYY) (if available): 06/2020 – 05/2025
Total Award Amount (including Indirect Costs): $83,493
Person Months (Calendar/Academic/Summer) per budget period.
Accomplishments
Accomplishments
“Glimmers of Hope” Excellence in Research in Sickle Cell Disease, Roland B. Scott Symposium, 2021
Researcher of the Year Award, Department of Medicine, Howard University, 2014
Outstanding Faculty Researcher Award, Howard University College of Medicine, 2014
Publications and Presentations
Publications and Presentations
Ferroptosis as an emerging target in sickle cell disease
Ferroptosis as an emerging target in sickle cell disease
This review highlights the importance of balancing the complex interactions among various factors and exploitation of the knowledge in developing novel therapeutics for this devastating disease.
CK1 and PP1 regulate Rift Valley fever virus
CK1 and PP1 regulate Rift Valley fever virus genome replication through L protein phosphorylation
This study shows that RVFV L protein is serine phosphorylated and identified Casein Kinase 1 alpha (CK1α) and protein phosphatase 1 alpha (PP1α) as L protein binding partners. Inhibition of CK1 and PP1 through small molecule inhibitor treatment, D4476 and 1E7-03, respectively, caused a change in the phosphorylated status of the L protein.
Antiviral response and HIV-1 inhibition in sickle cell disease
Antiviral response and HIV-1 inhibition in sickle cell disease
Sickle cell hemoglobin (HbS) treatment of THP-1-derived and primary monocyte-derived macrophages induced production of IFN-β, upregulated antiviral gene expression, and suppressed HIV-1 infection. Infection with mouse-adapted EcoHIV was suppressed in the SCD mice that also exhibited elevated levels of antiviral restriction factors. Our findings suggest that hemolysis and release of HbS leads to the induction of IFN-β production, induction of cellular antiviral state by the expression of iron and IFN-driven factors, and suppression of HIV-1 infection.
Shear-reversible clusters of HIV-1 in solution
Shear-reversible clusters of HIV-1 in solution: stabilized by antibodies, dispersed by mucin
The phenomenon of reversible clustering is expected to further nuance HIV immune stealth because virus surfaces can escape interaction with antibodies (Abs) by hiding temporarily within clusters. It is well known that mucin reduces HIV virulence, and the current perspective is that mucin aggregates HIV-1 to reduce infections. Our findings, however, suggest that mucin is dispersing HIV clusters. The study proposes a new paradigm for how HIV-1 may broadly evade Ab recognition with reversible clustering and why mucin effectively neutralizes HIV-1.
Gene expression changes in sickle cell reticulocytes and their clinical associations
Gene expression changes in sickle cell reticulocytes and their clinical associations
Transcriptional changes in compensatory erythropoiesis in sickle cell anemia (SCA) and their disease modulation are unclear. We detected 1226 differentially expressed genes in hemoglobin SS reticulocytes compared to non-anemic hemoglobin AA controls. Assessing developmental expression changes in hemoglobin AA erythroblasts for these genes suggests heightened terminal differentiation in early erythroblasts in SCA that diminishes toward the polychromatic to orthochromatic stage transition.
Induction of Hepcidin Expression in the Renal Cortex of Sickle Cell Disease Mice
Induction of Hepcidin Expression in the Renal Cortex of Sickle Cell Disease Mice
In this study, we observed a significant accumulation of iron in the renal cortex of a mouse model of SCD, and assessed the expression of the proteins involved in maintaining renal iron homeostasis. Despite the intracellular iron accumulation, the levels of the transferrin receptor in the kidneys were increased, but the levels of the iron exporter ferroportin were not altered in SCD mice.
Clonal haematopoiesis and risk of chronic liver disease
Clonal haematopoiesis and risk of chronic liver disease
Here we examined the association between clonal haematopoiesis of indeterminate potential (CHIP) and chronic liver disease in 214,563 individuals from 4 independent cohorts with whole-exome sequencing data (Framingham Heart Study, Atherosclerosis Risk in Communities Study, UK Biobank and Mass General Brigham Biobank).
