Interferon -Inducible Protein 27 Computational Network Construction and Comparison between the Frontal Cortex of HIV Encephalitis (HIVE) and HIVE-Control Patients
نویسندگان
چکیده
Interferon -inducible protein 27 (IFI27) computational network construction and analysis of frontal cortex of HIV encephalitis (HIVE) is very useful to identify novel markers and potential targets for prognosis and therapy. Based on integrated gene regulatory network infer (GRNInfer) method by linear programming and a decomposition procedure with analysis of the significant function cluster using Kappa statistics and fuzzy heuristic clustering from DAVID, we identified and constructed significant molecular IFI27 networks from 12 frontal cortex of HIVE-control patients and 16 HIVE in the same GEO Dataset GDS1726. Our integrative results reflected an IFI27 membrane module only in the upstream of the frontal cortex of HIVE-control patients (BTN3A2, RASGRP3, ROR1 inhibition), and the frontal cortex of HIVE (DGKG, LY96 activation; RASGRP3 inhibition); IFI27 organelle only in the upstream of HIVE-control patients (CREB5, OAS1, PDCD4 activation), and HIVE (PDCD4 activation; ZC3HAV1, ZNF652 inhibition); IFI27 sequence variant only in the upstream of HIVE-control patients (ISG15_2, OAS1, TNFRSF11B activation; BTN3A2, LCAT, ROR1 inhibition), and HIVE (CFB, DGKG, LCAT, LY96 activation; ISG15_2, TNFRSF11B, ZC3HAV1 inhibition).
منابع مشابه
Amelioration of neurotoxic effects of HIV envelope protein gp120 by fibroblast growth factor: a strategy for neuroprotection.
Approximately two thirds of patients with human immunodeficiency virus encephalitis (HIVE) show cognitive impairment and neurodegeneration, while one third are cognitively unimpaired and their neuronal populations are preserved. Thus, it is possible that these individuals might have the capacity to produce neurotrophic factors capable of protecting neurons against the deleterious effects of HIV...
متن کاملGene expression patterns associated with neurological disease in human HIV infection
The pathogenesis and nosology of HIV-associated neurological disease (HAND) remain incompletely understood. Here, to provide new insight into the molecular events leading to neurocognitive impairments (NCI) in HIV infection, we analyzed pathway dysregulations in gene expression profiles of HIV-infected patients with or without NCI and HIV encephalitis (HIVE) and control subjects. The Gene Set E...
متن کاملNeurobiology of Disease Interferon- Causes Neuronal Dysfunction in Encephalitis
Interferon(IFN ) is a pleomorphic cytokine produced by nucleated cells in response to viral infection. In patients, treatment with IFN has side effects including cognitive impairment resembling subcortical dementia, which is a hallmark of human immunodeficiency virus (HIV)-associated dementia (HAD). IFN is increased in the CSF of HAD patients compared with HIV patients without dementia. In this...
متن کاملAspartoacylase Deficiency in the White Matter of Human Immunodeficiency Virus Encephalitis: Novel Mechanism in Axonal Damage
Aspartoacylase/aminoacylase II (ASPA/ACY II) is mainly synthesized in oligodendrocytes to contribute in myelin synthesis. Although axonal damage is seen in the brain with human immunodeficiency virus encephalitis (HIVE), ASPA contribution in the pathology is not known. Immunostaining study showed that ASPA protein is reduced in the white matter of patients with HIVE compared to the control. Wes...
متن کاملHIV-1 Tat Co-Operates with IFN-γ and TNF-α to Increase CXCL10 in Human Astrocytes
HIV-associated neurological disorders (HAND) are estimated to affect 60% of the HIV infected population. HIV-encephalitis (HIVE), the pathological correlate of the most severe form of HAND is often characterized by glial activation, cytokine/chemokine dysregulation, and neuronal damage and loss. However, the severity of HIVE correlates better with glial activation rather than viral load. One of...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره شماره
صفحات -
تاریخ انتشار 2010