PubMed Health⌕ Search

PubMed · 2099987

[Decrease in notifications of AIDS dementia complex in 1989-1990 in Italy: possible role of the early treatment with zidovudine].

Abstract

We evaluated the incidence of AIDS dementia complex (ADC) in groups of patients who acquired infection through different risk behaviours, and attempted to evaluate the possible role of zidovudine (AZT) treatment in preventing or delaying the onset of ADC. The Italian National AIDS Registry was used to study patients with AIDS for whom ADC was reported as an index disease. Relative risk of presenting ADC between different patient categories has been determined. Logistic regression was used to analyse temporal trends in the proportion of AIDS cases presenting with ADC. Of the 6466 cases reported between August '87 and August '90, ADC was seen in 640 (9.9%). I. V. drug addicts had twice the risk (estimated odds ratio: 1.9; 95% confidence interval: 1.5-2.6, p less than 0.001), compared to homo/bisexuals, of presenting with ADC. There is significant evidence (p less than 0.0001) that after a progressive increase in the period '87-'89, it began a definite decrease in the monthly proportion of ADC cases, starting August '89. AZT was introduced in Italy in July 1987 for patients with AIDS or advanced ARC. The incidence of AIDS dementia complex at the moment of AIDS diagnosis in our population of patients, began to decline 24 months after the introduction of systematic AZT treatment in Italy. This could have been due to inhibition of HIV replication in the Central Nervous System among patients who initiated AZT-treatment before developing full-blown AIDS.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A Chiesi, M G Agresti, L G Dally, M Zaccarelli, C Tomino, M Floridia, S Vella. [Decrease in notifications of AIDS dementia complex in 1989-1990 in Italy: possible role of the early treatment with zidovudine].. https://pubmed.ncbi.nlm.nih.gov/2099987/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Neuronal apoptotic signaling pathways probed and intervened by synthetically and modularly modified (SMM) chemokines.

As the main coreceptors for human immunodeficiency virus type 1 (HIV-1) entry, CXCR4 and CCR5 play important roles in HIV-associated dementia (HAD). HIV-1 glycoprotein gp120 contributes to HAD by causing neuronal damage and death, either directly by triggering apoptotic pathways or indirectly by stimulating glial cells to release neurotoxins. Here, to understand the mechanism of CXCR4 or CCR5 signaling in neuronal apoptosis associated with HAD, we have applied synthetically and modularly modified (SMM)-chemokine analogs derived from natural stromal cell-derived factor-1alpha or viral macrophage inflammatory protein-II as chemical probes of the mechanism(s) whereby these SMM-chemokines prevent or promote neuronal apoptosis. We show that inherently neurotoxic natural ligands of CXCR4, such as stromal cell-derived factor-1alpha or viral macrophage inflammatory protein-II, can be modified to protect neurons from apoptosis induced by CXCR4-preferring gp120(IIIB), and that the inhibition of CCR5 by antagonist SMM-chemokines, unlike neuroprotective CCR5 natural ligands, leads to neurotoxicity by activating a p38 mitogen-activated protein kinase (MAPK)-dependent pathway. Furthermore, we discover distinct signaling pathways activated by different chemokine ligands that are either natural agonists or synthetic antagonists, thus demonstrating a chemical biology strategy of using chemically engineered inhibitors of chemokine receptors to study the signaling mechanism of neuronal apoptosis and survival.

AIDS Dementia Complex↗

Evidence for BAG3 modulation of HIV-1 gene transcription.

A family of co-chaperone proteins that share the Bcl-2-associated athanogene (BAG) domain are involved in a number of cellular processes, including proliferation and apoptosis. Among these proteins, BAG3 has received increased attention due to its high levels in several disease models and ability to associate with Hsp70 and a number of other molecular partners. BAG3 expression is stimulated during cell response to stressful conditions, such as exposure to high temperature, heavy metals, and certain drugs. Here, we demonstrate that BAG3 expression is elevated upon HIV-1 infection of human lymphocytes and fetal microglial cells. Furthermore, BAG3 protein was detectable in the cytoplasm of reactive astrocytes in HIV-1-associated encephalopathy biopsies, suggesting that induction of BAG3 is part of the host cell response to viral infection. To assess the impact of BAG3 upregulation on HIV-1 gene expression, we performed transcription assays and demonstrated that BAG3 can suppress transcription of the HIV-1 long terminal repeat (LTR) in microglial cells. This activity was mapped to the kappaB motif of the HIV-1 LTR. Results from in vitro and in vivo binding assays revealed that BAG3 suppresses interaction of the p65 subunit of NF-kappaB with the kappaB DNA motif of the LTR. Results from binding and transcriptional assay identified the C-terminus of BAG3 as a potential domain involved in the observed inhibitory effect of BAG3 on p65 activity. These observations reveal a previously unrecognized cell response, that is, an increase in BAG3, elicited by HIV-1 infection, and may provide a new avenue for the suppression of HIV-1 gene expression.

AIDS Dementia Complex↗