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Neuropathogenesis of HIV infection : HIV reservoirs get established in the brain early during infection and current antiretroviral therapy does not impact the size of the reservoir. The brain also accumulates defective viral sequences, the role of which is poorly understood but is reminiscent of the endogenous retroviruses in the human genome. Our laboratory is focused on characterizing the virus in the brain and studying the mechanisms by which the virus persists for extended periods of time. We have shown that the HIV-Tat protein is produced in the brain despite adequate antiretroviral therapy, hence we are developing means to block its effects. We have established a well characterized cohort of HIV-infected individuals to determine the various forms of neurological manifestations and underlying disease pathophysiology. This cohort is also being used for early phase clinical trials to impact the viral reservoirs in the brain.
Role of endogenous retroviruses in neurological diseases : Retroviral sequences remain 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 (HML-2) is activated in patients with amyotrophic lateral sclerosis (ALS), and transgenic animals that express the envelope 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 physiological role of HERV-K in early stages of development and the mechanisms by which its expression is regulated and causes neurotoxicity to motor neurons. We are also developing new antiviral compounds and molecular techniques for blocking HERV-K.
Undiagnosed Neuroimmune and neuroinfectious diseases : Undiagnosed neuroinflammatory diseases carry a huge burden with devastating consequences. In collaboration with other researchers in NINDS and other institutes, we are investigating these patients and developing new diagnostic methods and modes of treatment for these diseases. An example of which is our observation that patients with Nodding syndrome have autoantibodies to a newly discovered protein in the brain, liemodin-1, caused by a molecular mimicry with a protein in a parasite, onchocerca. We have also discovered that under certain circumstances, RNA viruses such as Dengue can persist in the brain and present as a neurodegenerative disease.
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ARQUIVOS DE NEURO-PSIQUIATRIAno. 1 (2024): 1-6
Sarah R Rivas,Mynor J Mendez Valdez, Jay S Chandar, Jelisah F Desgraves,Victor M Lu, Leo Ampie, Eric B Singh,Deepa Seetharam,Christian K Ramsoomair, Anna Hudson, Shreya M Ingle,Vaidya Govindarajan,
Cancersno. 9 (2024): 1754
Brian Walitt,Komudi Singh, Samuel R. LaMunion,Mark Hallett, Steve Jacobson,Kong Chen,Yoshimi Enose-Akahata,Richard Apps,Jennifer J. Barb,Patrick Bedard,Robert J. Brychta,Ashura Williams Buckley,
Catherine DeMarino,Maria Cowen, Anastasia Williams,Pooja Khatkar,Fardokht A Abulwerdi,Lisa Henderson, Julia Denniss,Michelle L Pleet, Delores R Luttrell,Iosif Vaisman,Lance A Liotta,Joseph Steiner,
William Hayward,Ethan R Buch,Gina Norato,Fumiaki Iwane, Dabedatta Dash, Roberto F Salamanca-Girón,Elizabeth Bartrum,Brian Walitt,Avindra Nath,Leonardo G Cohen
Neurologyno. 3 (2024): e208073-e208073
Deepa Seetharam, Jay Chandar, Jelisah Desgraves,Vaidya Govindarajan,Mynor J. Mendez Valdez,Christian Ramsoomair, Jesus Castro, Sarah Rivas,Kory Johnson,Yong Zhang,Avindra Nath,John D. Heiss,
Neurosurgeryno. Supplement_1 (2024): 116-116
JAMA NEUROLOGYno. 3 (2024): 231-232
crossref(2024)
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