Regulation of HIV1 replication by interferon alpha: From laboratory bench to bedside

Gendelman, Howard Eliot; Baldwin, Tonia; Baca-Regen, Lisa; Swindells, Susan; Loomis, Lawrence D.; Skurkovich, S. V.

doi:10.1016/s0923-2494(05)80054-9

Cited by 8 publications

(3 citation statements)

References 33 publications

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“…Central nervous system (CNS) HIV infection appears to begin with the transmigration of peripheral HIV-infected cells (eg, monocytes or macrophages) across the blood brain barrier (BBB) ( 38 , 46 , 47 , 53 , 57 , 82 , 89 , 100 , 104 ) and consequently infection, primarily of microglia, the resident macrophages of the brain ( 24 , 32 , 37 , 40 , 50 , 55 , 64 ). Activation of microglia and the release of chemokine, cytokines and neurotoxins in conjunction with secreted HIV protein can damage the brain ( 36 , 56 , 76 , 85 , 103 ).…”

Section: Introductionmentioning

confidence: 99%

Imaging Neuroinflammation? A Perspective from MR Spectroscopy

et al. 2014

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Neuroinflammatory mechanisms contribute to the brain pathology resulting from human immunodeficiency virus (HIV) infection. Magnetic resonance spectroscopy (MRS) has been touted as a suitable method for discriminating in vivo markers of neuroinflammation. The present MRS study was conducted in four groups: alcohol dependent (A, n = 37), HIV-infected (H, n = 33), alcohol dependent + HIV infected (HA, n = 38) and healthy control (C, n = 62) individuals to determine whether metabolites would change in a pattern reflecting neuroinflammation. Significant four-group comparisons were evident only for striatal choline-containing compounds (Cho) and myo-inositol (mI), which follow-up analysis demonstrated were due to higher levels in HA compared with C individuals. To explore the potential relevance of elevated Cho and mI, correlations between blood markers, medication status and alcohol consumption were evaluated in H + HA subjects. Having an acquired immune deficiency syndrome (AIDS)-defining event or hepatitis C was associated with higher Cho; lower Cho levels, however, were associated with low thiamine levels and with highly active antiretroviral HIV treatment (HAART). Higher levels of mI were related to greater lifetime alcohol consumed, whereas HAART was associated with lower mI levels. The current results suggest that competing mechanisms can influence in vivo Cho and mI levels, and that elevations in these metabolites cannot necessarily be interpreted as reflecting a single underlying mechanism, including neuroinflammation.

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Section: Introductionmentioning

confidence: 99%

Imaging Neuroinflammation? A Perspective from MR Spectroscopy

et al. 2014

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“…Another candidate for immune therapy is IFN-c~, not primarily because of its immune modulatory potential but because of its anti-viral capacities [57]. IFN-c~ is produced in increased amounts during natural HIV-1 infection, and resistance to IFN-c~ of HIV-1 variants was demonstrated in the course of infection.…”

Section: Cytokines and Immune Modulationmentioning

confidence: 99%

“…IFN-c~ is produced in increased amounts during natural HIV-1 infection, and resistance to IFN-c~ of HIV-1 variants was demonstrated in the course of infection. Thus, it was proposed that IFN-c~ therapy would only be useful in early stages of HIV-1 infection [57]. A phase I trial of IFN-c~ in combination with IL-2 showed few side effects and preliminary evidence for immune modulation and anti-viral activity [55].…”

Section: Cytokines and Immune Modulationmentioning

confidence: 99%