EDITORIAL-DETAILS (JNND)
Rajnish S Dave
Associate Scientist
Temple University School of Medicine
United States
Tel: (215) 707-3150
Biography
Dr Dave was born and grew up in Mumbai, India. He received his Ph.D. degree from University of Mumbai in 1998. Dr. Dave for his postdoctoral training in molecular virology at Columbia University and subsequently continued his training in neuroAIDS and molecular virology at Thomas Jefferson University. Dr Dave joined the Center for neuroAIDS Research in the Department of Neuroscience in 2008 where his research is focused on elucidating role of miRNAs in HIV-induced brain diseases in opiate-abusers.
Research Interest
His research interest is focused on investigating the role of small non-coding RNAs, in HIV-1 neuropathogenesis. Small non-coding RNAs, such as microRNAs (miRNAs) and small interfering RNAs (siRNAs) possess the ability to regulate gene expression through post-transcriptional gene silencing mechanisms. Both miRNAs and siRNAs have an integral role in disease etiology and host-virus interactions. Alterations in miRNA expression often correlate with onset of cancers, viral infections or mental disorders. Several human viruses also express miRNAs. HIV-1 infection of the Central Nervous System (CNS) often leads to HIV-1-associated dementia (HAD) and HIV-1-associated minor cognitive motor disorder (HMCMD). HIV-1 infection is associated with macrophage infiltration, formation of microglial nodules and multinucleated giant cells, astrocyte activation and neuronal loss. Perivascular macrophages and microglia present in the hippocampus and basal ganglia are predominantly infected. However, the role of miRNAs and siRNAs in HIV-1 infection of CNS remains unclear. Currently, we are investigating alterations in miRNA expression profiles and how they might affect the course of disease progression in HIV-1-infected opiate abusers. This cohort is of interest as it often exhibits an accelerated form of HIV-1 associated dementia and enhanced neurological dysfunction. His observations indicate involvement of inflammation and oxidative stress in response to morphine in CNS with a potential role for cellular miRNAs to regulate these processes.
