Maureen M. Goodenow, Ph.D.

Chief, Molecular HIV Host Interactions Section
Director, NIH Office of AIDS Research

Major Areas of Research

  • Interactions between HIV-1 and host, in particular children, adolescents, and young adults, at the molecular level

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Program Description

The major research focus of the Molecular HIV Host Interactions Section is to investigate interactions between HIV-1 and host, in particular children, adolescents, and young adults, at the molecular level, which includes the following: 

  • HIV-mediated chronic systematic immune activation, perturbation, and efficiency in B cells, T cells, and macrophages

  • Influence of recreational substance use, e.g., marijuana, tobacco products, and alcohol, on HIV-modulated gene expression and functional pathways 

  • HIV-1 cell tropism, potency, reservoir, reactivation, and molecular evolution of the HIV-1 genome over the course of infection with/without antiretroviral therapy 


Dr. Goodenow received her undergraduate degree in biology from Fordham University and her Ph.D. in molecular genetics from the Albert Einstein College of Medicine. Following a postdoctoral fellowship in molecular oncology at the Sloan Kettering Institute, Dr. Goodenow was a visiting scientist at the Pasteur Institute in Paris, where she began her study of HIV. 

Dr. Goodenow was a professor of pathology, immunology, and laboratory medicine at the University of Florida, Gainesville, where she held the Stephany W. Holloway University Endowed Chair for AIDS Research. She also was the Director of the Center for Research in Pediatric Immune Deficiency Diseases. 

She served as the acting director of the Office for Research and Science in the U.S. Department of State, Office of the U.S. Global AIDS Coordinator, and Office of Global Health Diplomacy. Dr. Goodenow was the 2012 recipient of the prestigious Jefferson Science Fellowship at the State Department, where she served as senior science advisor in the Office of Economic Policy’s Bureau of East Asian and Pacific Affairs. 

Dr. Goodenow was appointed associate director for AIDS Research at NIH and director of the NIH Office of AIDS Research in 2016, coordinating the HIV/AIDS research agenda across NIH. She also is chief of the Molecular HIV Host Interactions Section. 

Dr. Goodenow is the recipient of the Gertrude and Herman Silver 24th Annual Lecture Award and the Wistar Institute’s Jonathan Lax Memorial Award. 

She continues to invest in the next generation of scientists and has trained more than 50 doctoral and postdoctoral fellows. A respected, peer-reviewed author, Dr. Goodenow has published more than 100 articles and book chapters, in addition to serving as a reviewer for more than 10 journals. 

Research Group

Li Yin, staff scientist 

Kai-Fen Chang, biologist 

Samiksha Borkar, technician

Selected Publications

Appelberg KS, Wallet MA, Taylor JP, Cash MN, Sleasman JW, Goodenow MM. HIV-1 infection primes macrophages through STAT signaling to promote enhanced inflammation and viral replication. AIDS Res Hum Retroviruses. 2017 Jul;33(7):690-702. 

Yin L, Yao J, Chang K, Gardner BP, Yu F, Giuliano AR, Goodenow MM. HPV population profiling in healthy men by next-generation deep sequencing coupled with HPV-QUEST. Viruses. 2016 Jan 25;8(2). pii: E28.  

Appelberg KS, Goodenow MM. Editorial: Passive aggressive avoidance of SAMHD1 restriction by HIV-1. J Leukoc Biol. 2015 Jul;98(1):1-3.  

Wallet MA, Buford TW, Joseph AM, Sankuratri M, Leeuwenburgh C, Pahor M, Manini T, Sleasman JW, Goodenow MM. Increased inflammation but similar physical composition and function in older-aged, HIV-1 infected subjects. BMC Immunol. 2015 Jul 24;16:43. 

Williams JC, Klein TW, Goldberger BA, Sleasman JW, Mackman N, Goodenow MM. Δ(9)-Tetrahydrocannabinol (THC) enhances lipopolysaccharide-stimulated tissue factor in human monocytes and monocyte-derived microvesicles. J Inflamm (Lond). 2015 Jun 12;12:39.  

Williams JC, Appelberg S, Goldberger BA, Klein TW, Sleasman JW, Goodenow MM. Δ(9)-Tetrahydrocannabinol treatment during human monocyte differentiation reduces macrophage susceptibility to HIV-1 infection. J Neuroimmune Pharmacol. 2014 Jun 9(3):369-79. 

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