HIV associated dementia and HIV encephalitis II: Genes on chromosome 22 expressed in individually microdissected Globus pallidus neurons (Preliminary analysis)



Paul Shapshak1, 2*, Robert Duncan3, Pandajarasamme Kangueane4, 5, Charurut Somboonwit1, 6, John Sinnott1, 6, Deborah Commins7, 8, Elyse Singer8, 9, Andrew Levine8, 9



1Division of Infectious Disease and International Medicine, Tampa General Hospital, USF Health, Tampa, FL 33601; 2Department of Psychiatry & Behavioral Medicine, University of South Florida, College of Medicine, Tampa, FL 33613; 3Department of Epidemiology, University of Miami Miller School of Medicine, Miami, FL 33136; 4Biomedical Informatics, Pondicherry 607 402, India; 5AIMST University, Malaysia 08100; 6Clinical Research Unit, Hillsborough Health Department, Tampa, FL 33602; 7Department of Pathology, USC School of Medicine, Los Angeles, CA 90089; 8National Neurological AIDS Bank, UCLA School of Medicine, Westwood, CA 90095; 9Department of Neurology, UCLA School of Medicine, Westwood, CA 90095


Email; *Corresponding author








Article Type




Received May 10, 2011; Accepted May 13, 2011; Published May 26, 2011



We analyzed RNA gene expression in neurons from 16 cases in four categories, HIV associated dementia with HIV encephalitis (HAD/HIVE), HAD alone, HIVE alone, and HIV-1-positive (HIV+)with neither HAD nor HIVE. We produced the neurons by laser capture microdissection (LCM) from cryopreserved Globus pallidus. Of 55,000 gene fragments analyzed, expression of 197 genes was identified with significance (p = 0.005).We examined each gene for its position in the human genome and found a non-stochastic occurrence for only seven genes, on chromosome 22. Six of the seven genes were identified, CSNK1E (casein kinase 1 epsilon), DGCR8 (Di George syndrome critical region 8), GGA1 (Golgi associated gamma adaptin ear containing ARF binding protein 1), MAPK11 (mitogen activated protein kinase 11), SMCR7L (Smith-Magenis syndrome chromosome region candidate 7-like), andTBC1D22A (TBC1 domain family member 22A). Six genes (CSNK1E, DGCR8, GGA1, MAPK11, SMCR7L, and one unidentified gene) had similar expression profiles across HAD/HIVE, HAD, and HIVE vs. HIV+ whereas one gene (TBC1D22A) had a differing gene expression profile across these patient categories. There are several mental disease-related genes including miRNAs on chromosome 22 and two of the genes (DGCR8 and SMCR7L) identified here are mental disease-related. We speculate that dysregulation of gene expression may occur through mechanisms involving chromatin damage and remodeling. We conclude that the pathogenesis of NeuroAIDS involves dysregulation of expression of mental disease-related genes on chromosome 22 as well as additional genes on other chromosomes. The involvement of these genes as well as miRNA requires additional investigation since numerous genes appear to be involved.



Chromosome 22, gene expression, network, pathway, miRNA, HAD, HIVE, LCM, Globus pallidus, neuron, brain.



Shapshak et al. Bioinformation 6(5): 183-186 (2011)

Edited by

Peter N Pushparaj






Biomedical Informatics



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