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Biomedical subjects

Ronald Ellis

Publications and source records attributed to Ronald Ellis.

6 recordsLinked to original sources
PubMed2007

HIV and antiretroviral therapy in the brain: neuronal injury and repair.

Approximately 40 million people worldwide are infected with human immunodeficiency virus (HIV). Despite HIV's known propensity to infect the CNS and cause neurological disease, HIV neurocognitive disorders remain under-recognized. Although combination antiretroviral therapy has improved the health of millions of those living with HIV, the penetration into the CNS of many such therapies is limited, and patients' quality of life continues to be diminished by milder, residual neurocognitive impairment. Synaptodendritic neuronal injury is emerging as an important mediator of such deficits in HIV. By carefully selecting specific antiretrovirals and supplementing them with neuroprotective agents, physicians might be able to facilitate innate CNS repair, promoting enhanced synaptodendritic plasticity, neural function and clinical neurological status.

Animals↗
PubMed2006

Relationship of CSF leukocytosis to compartmentalized changes in MCP-1/CCL2 in the CSF of HIV-infected patients undergoing interruption of antiretroviral therapy.

Although monocyte chemoattractant protein (MCP-1)/CCL2 is believed to mediate trafficking of HIV-activated leukocytes into the CNS, its role has not been studied directly in humans. To evaluate MCP-1's effects on CNS leukocyte infiltration, we measured CSF leukocytes and MCP-1 levels in serial plasma and cerebrospinal fluid (CSF) samples from subjects who experienced large increases in viral load after interrupting antiretrovirals. Following large increases in CSF MCP-1, CSF leukocytosis (15-166 cells/microL) developed in 4 of 6 subjects. Both initial MCP-1 levels and subsequent changes were 3-fold larger in CSF than plasma. The magnitude and timing of changes suggested that MCP-1 triggers the development of CSF pleocytosis.

Adult↗
PubMed2005

Dynamics of monocyte chemoattractant protein type one (MCP-1) and HIV viral load in human cerebrospinal fluid and plasma.

BACKGROUND: Increased expression of monocyte chemoattractant protein type 1 (MCP-1) is associated with HIV CNS disease. This study evaluated the temporal relationships between MCP-1 expression and HIV replication in the CNS. METHODS: MCP-1 and HIV viral load (VL) were measured in serially obtained samples of plasma and cerebrospinal fluid (CSF) in subjects either interrupting (TI) or starting (TS) antiretroviral therapy. RESULTS: Following TI, plasma VL rebounded first, followed by increases in CSF MCP-1, which immediately preceded or coincided with a rebound of CSF VL. CONCLUSION: The close temporal relationship of the increase of MCP-1 and CSF VL suggests that they are co-regulated, or that one is a stimulus for the other.

Anti-Retroviral Agents↗
PubMed2004

The monocyte chemotactic protein-1 -2578G allele is associated with elevated MCP-1 concentrations in cerebrospinal fluid.

Because monocyte chemotactic protein (MCP)-1 is an important cofactor in HIV neuropathogenesis, we investigated the relationship between MCP-1 genotype and expression in cerebrospinal fluid (CSF). We evaluated a genetic polymorphism in the MCP-1 promoter at position -2578 (alternatively designated -2518) in 98 HIV-infected subjects who had contemporaneously collected plasma and CSF. CSF MCP-1 levels were highest in the G/G genotype group, intermediate in the G/A group, and lowest in the A/A group. MCP-1 levels in plasma only differed by genotype after adjusting for HIV-related factors. Our findings suggest that this MCP-1 promoter polymorphism influences HIV neuropathogenesis by regulating MCP-1 protein expression in the central nervous system (CNS).

Adult↗