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Elijah Paintsil, FAAP, MD

Professor Adjunct in Pediatrics; Affiliated Faculty, Yale Institute for Global Health; Professor of Pediatrics (Infectious Diseases), Pediatrics; Professor, Epidemiology of Microbial Diseases; Professor of Pharmacology, Molecular Medicine, Pharmacology, and Physiology; Professor of Management, School of Management

Contact Information

Elijah Paintsil, FAAP, MD

Mailing Address

  • Pediatric Infectious Diseases

    PO Box 208064

    New Haven, CT 06520-8064

    United States

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Research Summary

Research focus is on

  1. Effect of antiretroviral therapy (ART) on mitochondrial function
  2. Mechanisms of non-infectious comorbidities in people living with HIV such as metabolic syndrome

Specialized Terms: HIV translational research; Mitochondrial function; Cellular pharmacology of HIV-RT inhibitors in relation to clinical toxicities

Extensive Research Description

Our research focuses on understanding the determinants of individual differences in response to antiretroviral therapy (ART) (e.g., virologic suppression, resistance evolution, and clinical toxicities). This research interest was fostered by an NIH career development award (K08) from 2008 to 2013. During this period, we studied various host determinants such as individual differences in the intracellular concentrations of antiretroviral drugs, cellular kinases involved in the phosphorylation of nucleoside analogs, and ATP-binding Cassette (ABC) transport proteins, and effect of treatment on mitochondrial function. These findings challenged the existing paradigm that only nucleoside reverse transcriptase inhibitors (NRTIs) caused mitochondrial dysfunction through inhibition of mitochondrial DNA polymerase gamma (Pol-ɣ) – the “Pol-ɣ hypothesis.” The studies identified other Pol-ɣ-independent pathways that can lead to mitochondrial dysfunction such as depletion of nucleotide pool and mitochondria DNA mutations. This led to the development of the novel hypothesis that ART causes mitochondrial dysfunction through both pol-γ-dependent and pol-γ-independent mechanisms, which results in a decrease in cellular dNTP and rNTP pools and genomic instability resulting in clinical toxicity and aging-related disorders in HIV-infected.

Coauthors

Research Interests

Brazil; Ghana; Hepatitis C; HIV; Pediatrics; Pharmacology; Molecular Epidemiology; HIV Reverse Transcriptase; Infectious Disease Medicine

Selected Publications

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