Virologic Markers of Human Immunodeficiency Virus Type 1 in Cerebrospinal Fluid

Spector, Stephen A.; Hsia, Karen; Pratt, D.L.; Lathey, Janet L.; McCutchan, J. Allen; Alcaraz, John E.; Atkinson, J. Hampton; Gulevich, Steven; Wallace, Mark R.; Grant, Igor

doi:10.1093/infdis/168.1.68

Cited by 51 publications

(19 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The virus in the CSF of the subjects examined by Ellis et al (1997) was, however, cell-free virus. A previous study also noted that HIV-1 isolated from the CSF was found in the supernatant rather than in the cellular fraction (Spector et al, 1993) suggesting that the CSF/plasma relationship is attributable to cellfree virus, and might be indirectly related to lymphocytic pleocytosis.…”

Section: Discussionmentioning

confidence: 90%

Cocaine opens the blood-brain barrier to HIV-1 invasion

Zhang¹,

Looney²,

Taub³

et al. 1998

J Neurovirol

110

View full text Add to dashboard Cite

Cocaine abuse has been associated with vasculitis and stroke, and is suspected to in¯uence the progression of AIDS dementia. Cocaine may enhance HIV-1 neuroinvasion by actions directed at the blood-brain barrier. HIV-1 appears to penetrate the human brain microvascular endothelial cell barrier by a paracellular route breached by tumor necrosis factor-a (TNF-a). Cocaine's effects on the blood-brain barrier were investigated using human brain microvascular endothelial cells and peripheral blood monocytes. Cocaine (10 75 M and 10 76 M) increased molecular permeability of the barrier and viral invasion by the macrophage-tropic HIV-1 JR ± FL into the brain chamber. Cocaine also augmented apoptosis of brain endothelial cells and monocytes, increased secretion of four chemokines (interleukin-8, interferon-inducible protein-10, macrophage in¯ammatory protein-1a, and monocyte chemoattractant protein-1) and the cytokine, TNF-a, by human monocytes. TNF-a enhanced invasion of the brain compartment by macrophage-tropic, lymphotropic, and bitropic HIV-1 strains. These data indicate that HIV-1 neuroinvasion can be increased by (a) cocaine's direct effects on brain microvascular endothelial cells and (b) paracrine effects of cocaine-induced pro-in¯ammatory cytokines and chemokines on the blood-brain barrier.

show abstract

Section: Discussionmentioning

confidence: 90%

Cocaine opens the blood-brain barrier to HIV-1 invasion

Zhang¹,

Looney²,

Taub³

et al. 1998

J Neurovirol

110

View full text Add to dashboard Cite

show abstract

“…Western blot analyses also indicated that clinically available inhibitors of HMG-coenzyme A reductase, atorvastatin and simvastatin, inhibited HIV-1-induced release of Hsp70 from neurons. (78,87). Several studies have shown that there is a potential interaction between alcohol and several other drugs of abuse and HIV-1 infection (26,30,51).…”

Section: Coculturing Of Infected T Cells With Neurons or Neurons Expomentioning

confidence: 99%

Cholesterol-Depleting Statin Drugs Protect Postmitotically Differentiated Human Neurons against Ethanol- and Human Immunodeficiency Virus Type 1-Induced Oxidative Stress In Vitro

Acheampong

Parveen

Mengistu

et al. 2007

J Virol

View full text Add to dashboard Cite

The AIDS-related dementia characterized by cognitive dysfunction, motor neuron disease, coordination abnormalities, and other neurological signs and symptoms develops in many human immunodeficiency virus type 1 (HIV-1)-infected individuals (17, 58). The molecular mechanisms involved in these HIV-1-associated dysfunctions of the central nervous system (CNS) remain incompletely explained and controversial (42,45). Studies have demonstrated that although the major reservoirs for productive infection within the CNS of HIV-1-infected individuals are microglia and monocytes/macrophages, infection of other CNSbased cell types, such as microvascular endothelial cells and neurons, also appears to occur (44,57,92). The role of lymphocytes in AIDS dementia has also been described previously (59,67,68). Of note, viral replication in cerebrospinal fluid is considered to be a marker for the severity of AIDS-related neurodegeneration (16,20). The CNS tissues are protected from the periphery by a structure known as blood-brain barrier (BBB), which limits the passage of solutes as well as infections into the brain (10). The tight junctions of brain microvascular endothelial cells strengthen the functional impermeability of BBB. Under certain pathological conditions, the BBB becomes compromised, providing access for infections/infected cells into the brain (64). The passage of HIV-1 entry into the brains of AIDS patients in vivo is not quite clear and is supposed to involve both free viruses and virally infected cells (4,89,91).HIV-1-infected individuals are under chronic oxidative stress, and antioxidants have proved to ameliorate infectionassociated oxidative stress. (81, 84). Oxidative stress involves

show abstract

“…HIV-1 enters the CNS early in the course of disease (Resnick et al, 1988;Spector et al, 1993) and establishes productive infection in the brain, detectable in perivascular macrophages and microglia. Despite the absence of productive infection of neurons, HIV-1 infection is associated with neuronal loss in distinct regions of the brain, including the frontal cortex, substantia nigra, cerebellum, and striatum (Everall et al, 1993).…”

Section: Introductionmentioning

confidence: 99%