J Pediatr Infect Dis 2009; 04(04): 367-373
DOI: 10.3233/JPI-2009-0207
Original Article
Georg Thieme Verlag KG Stuttgart – New York

Different profiles of apoptosis and activation in children with progressive or static HIV-related encephalopathy

Almudena Blanco
a  Department of Laboratorio Inmuno-Biología Molecular, Hospital General Universitario Gregorio Marañón, Madrid, Spain
,
Roberta Nardacci
b  National Institute for Infectious Diseases IRCCS “L. Spallanzani”, Rome, Italy
,
Franca Del Nonno
b  National Institute for Infectious Diseases IRCCS “L. Spallanzani”, Rome, Italy
,
Francesco Callea
c  Department of Pathology, Children’s Hospital Bambino Gesù, Rome, Italy
,
Paola Francalanci
d  Department of Biology, University of Rome “Tor Vergata”, Rome, Italy
,
Mauro Piacentini
b  National Institute for Infectious Diseases IRCCS “L. Spallanzani”, Rome, Italy
d  Department of Biology, University of Rome “Tor Vergata”, Rome, Italy
,
Ma Ángeles Muñoz Fernández
b  National Institute for Infectious Diseases IRCCS “L. Spallanzani”, Rome, Italy
e  CIBER de Bioquímica, Biomateriales y Nanomedicina, Instituto Salud Carlos III, Zaragoza, Spain
› Author Affiliations

Subject Editor:
Further Information

Publication History

24 September 2008

27 May 2009

Publication Date:
28 July 2015 (online)

Abstract

To analyze neurodegeneration in brain cortex samples from human immunodeficiency virus (HIV)-vertically-infected children diagnosed with progressive or static HIV-encephalopathy. We performed a descriptive retrospective and cross-sectional study on 15 HIV-infected children. Eight children were diagnosed with progressive-encephalopathy (EP) and seven with static-EP. Autopsy samples of the frontal cortex from the 15 children were studied. Apoptotic analysis was performed by an assay, which detects apoptotic cells by labeling the fragmentation of DNA by TdT – mediated dUTP nick end labeling (TUNEL) assay. The presence of phosphorylated p53 (p53Ser46P) indicates the beginning of the cell death process. Glial fibrillary acidic protein a marker for glial cells, and p53Ser46P were detected by immunohistochemical assays. All samples from the 15 HIV-infected children showed positive results using TUNEL and showed an increase in p53Ser46P. However, the number of apoptotic cells was higher in samples from children with progressive-EP and was comprised of a higher number of dying neurons than dying glial cells. In contrast, glial cells were more affected in children with static-EP. We observed gliosis (abnormal proliferation of astrocytes in damaged areas of the brain) in all samples, but in the static-EP samples, gliosis was observed in areas close to blood vessels, and it was more pronounced than in progressive-EP samples. Our results suggest that depending whether the diagnosis is progressive-EP or static-EP, neural affliction activates programmed cell death in brain tissue of HIV-infected children. Moreover, there are differences in the type of cellular population affected as well as in the level of glial cell activation.