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Senior Investigator

Avindra Nath, M.D.

Section of Infections of the Nervous System


Building 10-CRC Room 7C103
10 Center Drive
Bethesda MD 20814
Office: 301-496-1561
Lab: 301-496-1561
Fax: 301-496-1561
natha@mail.nih.gov

Dr. Nath received his MD degree from Christian Medical College in India in 1981 and completed a residency in Neurology from University of Texas Health Science Center in Houston, followed by a fellowship in Multiple Sclerosis and Neurovirology at the same institution and then a fellowship in Neuro-AIDS at NINDS. He held faculty positions at the University of Manitoba (1990-97) and the University of Kentucky (1997-02). In 2002, he joined Johns Hopkins University as Professor of Neurology and Director of the Division of Neuroimmunology and Neurological Infections. He joined NIH in 2011 as the Clinical Director of NINDS, the Director of the Translational Neuroscience Center and Chief of the Section of Infections of the Nervous System. His research focuses on understanding the pathophysiology of retroviral infections of the nervous system and the development of new diagnostic and therapeutic approaches for these diseases.



Neuropathogenesis of HIV infection: While important strides have been made in developing anti-retroviral therapies, no impact has been made to control HIV reservoirs in the brain. Our laboratory is focused on characterizing the virus in the brain by studying the mechanisms by which the virus enters different cell types in the brain and it ability to persist in glial cells for extended periods of time. Our laboratory has shown that the HIV-Tat protein is produced in the brain despite adequate antiretroviral therapy, hence we are trying understand its role in HIV pathogenesis and in developing means to block its effects.

Role of endogenous retroviruses in neurological diseases: Retroviral sequences remains dormant in the human genome and occupy nearly 7-8% of the genomic sequence. We have shown that one of these viruses termed HERV-K is activated in ALS, and transgenic animals that express the envelop protein of HERV-K develop ALS like symptoms. Hence we are now using a wide variety of in vitro, and in vivo studies to determine the mechanism by which its expression is regulated and causes neurotoxicity to motor neurons.

Management of Neuroimmune and neuroinfectious diseases: Undiagnosed neuroinflammatory diseases carry a huge burden with devastating consequences. In collaboration with other clinicians in NINDS and other institutes, we are investigating these patients and developing new diagnostic methods and modes of treatment for these diseases.

Staff Image
  • Caroline Anderson, B.S.
    Technician
    301-827-4080

  • Lauren Bowen, M.D.
    Clinical Fellow
    301-435-7531

  • Nicholas Geiger, B.S.
    Post baccalaureate IRTA Fellow

  • Lisa Henderson, Ph.D.
    Postdoctoral Fellow
    301-402-3836

  • Barbara Jaruga, Ph.D.
    Laboratory Manager
    301-496-7621

  • Myounghwa Lee, Ph.D.
    Research Fellow
    301-451-3821

  • Wenxue Li, Ph.D.
    Staff Scientist
    301-480-8208

  • Guanhan Li, Ph.D.
    Research Fellow
    301-402-0840

  • Marta Montojo, Ph.D.
    Research Fellow
    301-402-8316

  • Alina Popescu, Ph.D.
    Research Scientist
    301-480-8630

  • Peter Selim Siyahhan Julnes, B.S.
    Post baccalaureate IRTA Fellow
    301-480-8215

  • Bryan Smith, M.D.
    Staff Clinician
    301-451-4585

  • Sally Steinbach, RN, BSN, CCRP
    Protocol Nurse Coordinator II
    301-594-5194

  • Richa Tyagi, M.S.
    Biologist
    301-827-4077

  • Yadi Xu, B.S.
    Post baccalaureate IRTA Fellow

  • 1) Tory P. Johnson, Richa Tyagi, Paul R. Lee, Myoung-Hwa Lee, Kory R. Johnson, Jeffrey Kowalak, Abdel Elkahloun, Marie Medynets, Alina Hategan, Joseph Kubofcik, James Sejvar, Jeffrey Ratto, Sudhir Bunga, Issa Makumbi, Jane R. Aceng, Thomas B. Nutman, Scott F. Dowell and Avindra Nath (2017)
  • Nodding syndrome may be an autoimmune reaction to the parasitic worm Onchocerca volvulus
  • Science Translational Medicine 15 Feb 2017, Vol. 9, Issue 377, DOI: 10.1126/scitranslmed.aaf6953
  • 2) Li GH, Anderson C, Jaeger L, Do T, Major EO, Nath A (2015)
  • Cell-to-cell contact facilitates HIV transmission from lymphocytes to astrocytes via CXCR4
  • AIDS, 24;29(7):755-66
  • 3) Nath A. (2015)
  • Eradication of Human Immunodeficiency Virus from Brain Reservoirs
  • J. Neurovirology, 21, 227-234
  • 4) Uzasci L, Bianchet MA, Cotter R, Nath A (2014)
  • Identification of nitrated immunoglobulin variable regions in the HIV-Infected human brain: Implications in HIV Infection and Immune response
  • J Proteome Research 2014 Mar 7, 13(3), 1614-23
  • 5) Alfahad T, Nath A. (2013)
  • Retroviruses and Amyotropic lateral sclerosis
  • Antiviral Research, 99, 180-187
  • 6) Johnson TP, Patel, K, Johnson K, Maric D, Calabresi, P, Hasbun R, Nath A* (2013)
  • Induction of IL-17 and non-classical T-cell activation by HIV-Tat protein
  • Proc Natl Acad Sci, 110(33), 15388-93
  • 7) Wang T, Choi E, Monaco MC, Campanac E, Medynets M, Do T, Rao P, Johnson KR, Elkahloun AG, Von Geldern G, Johnson T, Subramaniam S, Hoffman D, Major E, Nath A. (2013)
  • Derivation of Neural Stem Cells from Human Adult Peripheral CD34+ Cells for an Autologous Model of Neuroinflammation
  • PLoS One, 8(11), e81720
  • 8) Wang T, Lee M-H, Choi E, Pardo CA, Lee SB, Yang IH, Calabresi PA, Nath A. (2012)
  • Granzyme B-induced neurotoxicity is mediated via activation of PAR-1 receptor and Kv1.3 channel
  • PLoS ONE , 7(8), e43950
  • 9) Rumbaugh J, Bachani M, Li W, Butler T, Smith K, Bianchet M, Wang T, Prendergast M, Sacktor N, Nath A. (2012)
  • HIV Immune Complexes Prevent Excitotoxicity by Interaction with NMDA Receptors
  • Neurobiology of Disease, 49C, 169-76
  • 10) Li G, Li W, Mumper R, Nath A. (2012)
  • Molecular mechanisms in the dramatic enhancement of HIV-Tat transduction by cationic liposomes
  • FASEB J, 26(7), 2824-34
  • 11) Douville R, Liu J, Rothstein J, Nath A*. (2011)
  • Identification of active loci of a Human Endogenous Retrovirus in neurons of patients with Amyotrophic Lateral Sclerosis
  • Ann Neurol, 69(1), 141(51)
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