Lack of association of HIV-1 biological or molecular properties with neurotropism for brain cells.

Despite HAART, a significant number of HIV-1-infected patients develop neurological complications. However, the presence of specific neurotropic HIV-1 strains, the extent of viral replication in the brain, and the type of cells infected remain controversial issues. To address this controversy we have analyzed different V3 loop sequences of viral isolates from four vertically HIV-1-infected children who developed HIV-1-related encephalopathy.

HIV-1 infection of neurons might account for progressive HIV-1-associated encephalopathy in children.

Direct and productive infection of neurons in vivo is still a matter of debate, although in vitro experiments have demonstrated that immature neuronal cells can be productively infected by various human immunodeficiency virus (HIV) strains. To address this controversy we have analyzed, using light microscopy and in situ hybridization (ISH), HIV-1 infected cells in brain tissue from four pediatric cases of HIV-1-associated encephalopathy (EP). HIV-1 RNA-expressing cells--therefore, actively infected cells--were detected by ISH in different amounts in all brain specimens from the four children.

A new possible mechanism of human immunodeficiency virus type 1 infection of neural cells.

To study the mechanism by which HIV-1 infects neurons we have used human neuroblastoma cell lines (NB). NB (SK-N-SH and SK-N-MC) were found to be susceptible to productive infection by X4 or R5 HIV-1, as detected by viral load and Ag-p24. To identify the putative receptor, we tested the cell surface expression of previously described receptors such as CD4, nucleolin, galactosylceramide, and CCR1, CCR5, and CXCR4 by cytometry and RT-PCR.

Low blood CD8+ T-lymphocytes and high circulating monocytes are predictors of HIV-1-associated progressive encephalopathy in children.

Objective: Human immunodeficiency virus type 1 (HIV-1)-associated progressive encephalopathy (PE) is a common and devastating complication of HIV-1 infection in children, whose risk factors have not yet been clearly defined. Regardless of the age of presentation, PE shortens life expectancy. Paradoxically, as survival of patients has been prolonged as a result of the use of antiretroviral therapy, the prevalence of PE has increased.

Reconstructing the course of HIV-1-associated progressive encephalopathy in children.

The factors that trigger the clinical onset of HIV-1-associated progressive encephalopathy (PE) in children remain unknown. HIV-1 invades the central nervous system (CNS) from the very beginning of infection, but the timeframe for PE development is variable. It has recently been suggested that increased traffic into the brain of HIV-1-infected or activated monocytes arising directly from the bone marrow may be the first step to clinical onset of adult HIV encephalopathy.

In situ hybridization and immunolabelling study of the early replication of simian immunodeficiency virus (SIVmacJ5) in vivo.

The distribution of virus-infected cells in cynomolgus macaques was determined at 4, 7, 14 and 28 days following intravenous challenge with 1000 TCID(50) of the wild-type simian immunodeficiency virus SIVmacJ5 (stock J5C). At each time-point, pairs of macaques were killed humanely and the presence of SIV was determined and quantified in blood, spleen, peripheral and mesenteric lymph nodes, thymus, lung and ileum by virus co-cultivation with C8166 cells, by quantitative DNA PCR or by in situ hybridization (ISH). At day 4 post-infection (p.