Skip to main content
Erschienen in: Current HIV/AIDS Reports 3/2014

01.09.2014 | Central Nervous System and Cognition (I Grant, Section Editor)

Chronic Inflammation and the Role for Cofactors (Hepatitis C, Drug Abuse, Antiretroviral Drug Toxicity, Aging) in HAND Persistence

verfasst von: Alexander J. Gill, Dennis L. Kolson

Erschienen in: Current HIV/AIDS Reports | Ausgabe 3/2014

Einloggen, um Zugang zu erhalten

Abstract

HIV-associated neurocognitive disorders (HAND) is a group of syndromes of varying degrees of cognitive impairment affecting up to 50 % of HIV-infected individuals. The neuropathogenesis of HAND is thought to be driven by HIV invasion and productive replication within brain perivascular macrophages and endogenous microglia, and to some degree by restricted infection of astrocytes. The persistence of HAND in individuals experiencing suppression of systemic HIV viral load with antiretroviral therapy (ART) is incompletely explained, and suggested factors include chronic inflammation, persistent HIV replication in brain macrophages, effects of aging on brain vulnerability, and co-morbid conditions including hepatitis C (HCV) co-infection, substance abuse, and CNS toxicity of ART, among other factors. This review discusses several of these conditions: chronic inflammation, co-infection with HCV, drugs of abuse, aging, and antiretroviral drug effects. Effectively managing these co-morbid conditions in individuals with and without HAND is critical for improving neurocognitive outcomes and decreasing HIV-associated morbidity.
Literatur
1.
Zurück zum Zitat Antinori A, Arendt G, Becker JT, et al. Updated research nosology for HIV-associated neurocognitive disorders. Neurology. 2007;69:1789–99.PubMedCrossRef Antinori A, Arendt G, Becker JT, et al. Updated research nosology for HIV-associated neurocognitive disorders. Neurology. 2007;69:1789–99.PubMedCrossRef
2.••
Zurück zum Zitat Canizares S, Cherner M, Ellis RJ. HIV and aging: effects on the central nervous system. Semin Neurol. 2014;34:27–34. This is a comprehensive review of published (and some unpublished) studies HIV, aging, and associated risk factors, including APOE e4 allele status, metabolic syndrome and other factors. The strengths and weaknesses of published studies are effectively discussed.PubMedCrossRef Canizares S, Cherner M, Ellis RJ. HIV and aging: effects on the central nervous system. Semin Neurol. 2014;34:27–34. This is a comprehensive review of published (and some unpublished) studies HIV, aging, and associated risk factors, including APOE e4 allele status, metabolic syndrome and other factors. The strengths and weaknesses of published studies are effectively discussed.PubMedCrossRef
3.
Zurück zum Zitat Price RW, Spudich SS, Peterson J, et al. Evolving character of chronic central nervous system HIV infection. Semin Neurol. 2014;34:7–13.PubMedCrossRef Price RW, Spudich SS, Peterson J, et al. Evolving character of chronic central nervous system HIV infection. Semin Neurol. 2014;34:7–13.PubMedCrossRef
4.••
Zurück zum Zitat Hearps AC, Martin GE, Rajasuriar R, et al. Inflammatory co-morbidities in HIV+ individuals: learning lessons from healthy ageing. Curr HIV/AIDS Rep. 2014;11:20–34. This review thoroughly discusses the interactions among inflammation, immune activation and associated HIV morbidity. The role for microbial translocation is integrated and a particularly thoughtful discussion of therapeutic targeting of the inflammatory response is presented.PubMedCrossRef Hearps AC, Martin GE, Rajasuriar R, et al. Inflammatory co-morbidities in HIV+ individuals: learning lessons from healthy ageing. Curr HIV/AIDS Rep. 2014;11:20–34. This review thoroughly discusses the interactions among inflammation, immune activation and associated HIV morbidity. The role for microbial translocation is integrated and a particularly thoughtful discussion of therapeutic targeting of the inflammatory response is presented.PubMedCrossRef
6.
Zurück zum Zitat The Antiretroviral Therapy Cohort Collaboration. Life expectancy of individuals on combination antiretroviral therapy in high-income countries: a collaborative analysis of 14 cohort studies. Lancet. 2008;372:293–9.PubMedCentralCrossRef The Antiretroviral Therapy Cohort Collaboration. Life expectancy of individuals on combination antiretroviral therapy in high-income countries: a collaborative analysis of 14 cohort studies. Lancet. 2008;372:293–9.PubMedCentralCrossRef
7.••
Zurück zum Zitat Marchetti G, Tincati C, Silvestri G. Microbial translocation in the pathogenesis of HIV infection and AIDS. Clin Microbiol Rev. 2013;26:2–18. A comprehensive review of the process of microbial translocation across the gut mucosa, associated host responses, and the implications for SIV and HIV disease pathogenesis.PubMedCentralPubMedCrossRef Marchetti G, Tincati C, Silvestri G. Microbial translocation in the pathogenesis of HIV infection and AIDS. Clin Microbiol Rev. 2013;26:2–18. A comprehensive review of the process of microbial translocation across the gut mucosa, associated host responses, and the implications for SIV and HIV disease pathogenesis.PubMedCentralPubMedCrossRef
8.••
Zurück zum Zitat Mutlu EA, Keshavarzian A, Losurdo J, et al. A compositional look at the human gastrointestinal microbiome and immune activation parameters in HIV infected subjects. PLoS Pathog. 2014;10:e1003829. Analysis of the GI microbiome in HIV+ and HIV- individuals revealed less diversity, loss of commensal bacteria, and gain of some potential pathogenic bacterial taxa in HIV+ individuals. This study validates several earlier studies and further supports the hypothesis that changes in the gut microbiome due to HIV infection directly link to pathogenic immune activation. Therapeutic implications are discussed.PubMedCentralPubMedCrossRef Mutlu EA, Keshavarzian A, Losurdo J, et al. A compositional look at the human gastrointestinal microbiome and immune activation parameters in HIV infected subjects. PLoS Pathog. 2014;10:e1003829. Analysis of the GI microbiome in HIV+ and HIV- individuals revealed less diversity, loss of commensal bacteria, and gain of some potential pathogenic bacterial taxa in HIV+ individuals. This study validates several earlier studies and further supports the hypothesis that changes in the gut microbiome due to HIV infection directly link to pathogenic immune activation. Therapeutic implications are discussed.PubMedCentralPubMedCrossRef
9.
Zurück zum Zitat Brenchley JM, Price DA, Schacker TW, et al. Microbial translocation is a cause of systemic immune activation in chronic HIV infection. Nat Med. 2006;12:1365–71.PubMedCrossRef Brenchley JM, Price DA, Schacker TW, et al. Microbial translocation is a cause of systemic immune activation in chronic HIV infection. Nat Med. 2006;12:1365–71.PubMedCrossRef
10.
Zurück zum Zitat Ancuta P, Kamat A, Kunstman KJ, et al. Microbial translocation is associated with increased monocyte activation and dementia in AIDS patients. PLoS One. 2008;3:e2516.PubMedCentralPubMedCrossRef Ancuta P, Kamat A, Kunstman KJ, et al. Microbial translocation is associated with increased monocyte activation and dementia in AIDS patients. PLoS One. 2008;3:e2516.PubMedCentralPubMedCrossRef
11.
Zurück zum Zitat Hamann L, Alexander C, Stamme C, et al. Acute-phase concentrations of lipopolysaccharide (LPS)-binding protein inhibit innate immune cell activation by different LPS chemotypes via different mechanisms. Infect Immun. 2005;73:193–200.PubMedCentralPubMedCrossRef Hamann L, Alexander C, Stamme C, et al. Acute-phase concentrations of lipopolysaccharide (LPS)-binding protein inhibit innate immune cell activation by different LPS chemotypes via different mechanisms. Infect Immun. 2005;73:193–200.PubMedCentralPubMedCrossRef
12.
Zurück zum Zitat Neuhaus J, Jacobs Jr DR, Baker JV, et al. Markers of inflammation, coagulation, and renal function are elevated in adults with HIV infection. J Infect Dis. 2010;201:1788–95.PubMedCentralPubMedCrossRef Neuhaus J, Jacobs Jr DR, Baker JV, et al. Markers of inflammation, coagulation, and renal function are elevated in adults with HIV infection. J Infect Dis. 2010;201:1788–95.PubMedCentralPubMedCrossRef
13.
Zurück zum Zitat Tien PC, Choi AI, Zolopa AR, et al. Inflammation and mortality in HIV-infected adults: analysis of the FRAM study cohort. J Acquir Immune Defic Syndr. 2010;55:316–22.PubMedCentralPubMedCrossRef Tien PC, Choi AI, Zolopa AR, et al. Inflammation and mortality in HIV-infected adults: analysis of the FRAM study cohort. J Acquir Immune Defic Syndr. 2010;55:316–22.PubMedCentralPubMedCrossRef
14.
Zurück zum Zitat Han J, Wang B, Han N, et al. CD14(high)CD16(+) rather than CD14(low)CD16(+) monocytes correlate with disease progression in chronic HIV-infected patients. J Acquir Immune Defic Syndr. 2009;52:553–9.PubMedCrossRef Han J, Wang B, Han N, et al. CD14(high)CD16(+) rather than CD14(low)CD16(+) monocytes correlate with disease progression in chronic HIV-infected patients. J Acquir Immune Defic Syndr. 2009;52:553–9.PubMedCrossRef
15.
Zurück zum Zitat Ellery PJ, Tippett E, Chiu YL, et al. The CD16+ monocyte subset is more permissive to infection and preferentially harbors HIV-1 in vivo. J Immunol. 2007;178:6581–9.PubMedCrossRef Ellery PJ, Tippett E, Chiu YL, et al. The CD16+ monocyte subset is more permissive to infection and preferentially harbors HIV-1 in vivo. J Immunol. 2007;178:6581–9.PubMedCrossRef
16.
Zurück zum Zitat Douek DC. Disrupting T-cell homeostasis: how HIV-1 infection causes disease. AIDS Rev. 2003;5:172–7.PubMed Douek DC. Disrupting T-cell homeostasis: how HIV-1 infection causes disease. AIDS Rev. 2003;5:172–7.PubMed
17.
Zurück zum Zitat Wallet MA, Rodriguez CA, Yin L, et al. Microbial translocation induces persistent macrophage activation unrelated to HIV-1 levels or T-cell activation following therapy. AIDS. 2010;24:1281–90.PubMedCentralPubMedCrossRef Wallet MA, Rodriguez CA, Yin L, et al. Microbial translocation induces persistent macrophage activation unrelated to HIV-1 levels or T-cell activation following therapy. AIDS. 2010;24:1281–90.PubMedCentralPubMedCrossRef
18.
Zurück zum Zitat Gori A, Tincati C, Rizzardini G, et al. Early impairment of gut function and gut flora supporting a role for alteration of gastrointestinal mucosa in human immunodeficiency virus pathogenesis. J Clin Microbiol. 2008;46:757–8.PubMedCentralPubMedCrossRef Gori A, Tincati C, Rizzardini G, et al. Early impairment of gut function and gut flora supporting a role for alteration of gastrointestinal mucosa in human immunodeficiency virus pathogenesis. J Clin Microbiol. 2008;46:757–8.PubMedCentralPubMedCrossRef
19.•
Zurück zum Zitat Castro P, Plana M, Gonzalez R, et al. Influence of episodes of intermittent viremia (“blips”) on immune responses and viral load rebound in successfully treated HIV-infected patients. AIDS Res Hum Retroviruses. 2013;29:68–76. A retrospective analysis of a randomized, double-blinded, placebo-controlled study of HIV-infected individuals on stable cART and receiving vaccinations. All patients had monthly viral loads. Planned cART interruption for 6 months after 12 months of cART during the study. Those with ‘blips’ above 200 copies/ml during cART had higher viral rebound, worse CD4+ T cell recovery, and increased levels of immune activation markers.PubMedCentralPubMedCrossRef Castro P, Plana M, Gonzalez R, et al. Influence of episodes of intermittent viremia (“blips”) on immune responses and viral load rebound in successfully treated HIV-infected patients. AIDS Res Hum Retroviruses. 2013;29:68–76. A retrospective analysis of a randomized, double-blinded, placebo-controlled study of HIV-infected individuals on stable cART and receiving vaccinations. All patients had monthly viral loads. Planned cART interruption for 6 months after 12 months of cART during the study. Those with ‘blips’ above 200 copies/ml during cART had higher viral rebound, worse CD4+ T cell recovery, and increased levels of immune activation markers.PubMedCentralPubMedCrossRef
20.••
Zurück zum Zitat Grennan JT, Loutfy MR, Su D, et al. Magnitude of virologic blips is associated with a higher risk for virologic rebound in HIV-infected individuals: a recurrent events analysis. J Infect Dis. 2012;205:1230–8. A large observational cohort study (3550 HIV+ patients with confirmed virological suppression) that demonstrated a correlation between HIV viral load ‘blip’ amplitude and subsequent virologic rebound. This study emphasizes the importance of determining ‘effective’ virological suppression to potentially determine future risk of disease progression.PubMedCentralPubMedCrossRef Grennan JT, Loutfy MR, Su D, et al. Magnitude of virologic blips is associated with a higher risk for virologic rebound in HIV-infected individuals: a recurrent events analysis. J Infect Dis. 2012;205:1230–8. A large observational cohort study (3550 HIV+ patients with confirmed virological suppression) that demonstrated a correlation between HIV viral load ‘blip’ amplitude and subsequent virologic rebound. This study emphasizes the importance of determining ‘effective’ virological suppression to potentially determine future risk of disease progression.PubMedCentralPubMedCrossRef
21.
Zurück zum Zitat Canestri A, Lescure FX, Jaureguiberry S, et al. Discordance between cerebral spinal fluid and plasma HIV replication in patients with neurological symptoms who are receiving suppressive antiretroviral therapy. Clin Infect Dis. 2010;50:773–8.PubMedCrossRef Canestri A, Lescure FX, Jaureguiberry S, et al. Discordance between cerebral spinal fluid and plasma HIV replication in patients with neurological symptoms who are receiving suppressive antiretroviral therapy. Clin Infect Dis. 2010;50:773–8.PubMedCrossRef
22.
Zurück zum Zitat Gelman BBMDJ. HIV-1 neuropathology. In: Gendelman HEGI, Everall IP, Fox HS, Gelbard HA, Lipton SA, Swindells S, editors. The neurology of AIDS. Oxford: Oxford University Press; 2012. p. 518–35. Gelman BBMDJ. HIV-1 neuropathology. In: Gendelman HEGI, Everall IP, Fox HS, Gelbard HA, Lipton SA, Swindells S, editors. The neurology of AIDS. Oxford: Oxford University Press; 2012. p. 518–35.
23.
Zurück zum Zitat Anthony IC, Ramage SN, Carnie FW, et al. Accelerated Tau deposition in the brains of individuals infected with human immunodeficiency virus-1 before and after the advent of highly active anti-retroviral therapy. Acta Neuropathol. 2006;111:529–38.PubMedCrossRef Anthony IC, Ramage SN, Carnie FW, et al. Accelerated Tau deposition in the brains of individuals infected with human immunodeficiency virus-1 before and after the advent of highly active anti-retroviral therapy. Acta Neuropathol. 2006;111:529–38.PubMedCrossRef
24.
Zurück zum Zitat Silva AC, Rodrigues BS, Micheletti AM, et al. Neuropathology of AIDS: an autopsy review of 284 cases from Brazil comparing the findings Pre- and Post-HAART (Highly Active Antiretroviral Therapy) and Pre- and postmortem correlation. AIDS Res Treat. 2012;2012:186850.PubMedCentralPubMedCrossRef Silva AC, Rodrigues BS, Micheletti AM, et al. Neuropathology of AIDS: an autopsy review of 284 cases from Brazil comparing the findings Pre- and Post-HAART (Highly Active Antiretroviral Therapy) and Pre- and postmortem correlation. AIDS Res Treat. 2012;2012:186850.PubMedCentralPubMedCrossRef
25.
Zurück zum Zitat Neaton JD, Neuhaus J, Emery S. Soluble biomarkers and morbidity and mortality among people infected with HIV: summary of published reports from 1997 to 2010. Curr Opin HIV AIDS. 2010;5:480–90.PubMedCentralPubMedCrossRef Neaton JD, Neuhaus J, Emery S. Soluble biomarkers and morbidity and mortality among people infected with HIV: summary of published reports from 1997 to 2010. Curr Opin HIV AIDS. 2010;5:480–90.PubMedCentralPubMedCrossRef
27.
Zurück zum Zitat Lyons JL, Uno H, Ancuta P, et al. Plasma sCD14 is a biomarker associated with impaired neurocognitive test performance in attention and learning domains in HIV infection. J Acquir Immune Defic Syndr. 2011;57:371–9.PubMedCentralPubMedCrossRef Lyons JL, Uno H, Ancuta P, et al. Plasma sCD14 is a biomarker associated with impaired neurocognitive test performance in attention and learning domains in HIV infection. J Acquir Immune Defic Syndr. 2011;57:371–9.PubMedCentralPubMedCrossRef
28.
Zurück zum Zitat Burdo TH, Lo J, Abbara S, et al. Soluble CD163, a novel marker of activated macrophages, is elevated and associated with noncalcified coronary plaque in HIV-infected patients. J Infect Dis. 2011;204:1227–36.PubMedCentralPubMedCrossRef Burdo TH, Lo J, Abbara S, et al. Soluble CD163, a novel marker of activated macrophages, is elevated and associated with noncalcified coronary plaque in HIV-infected patients. J Infect Dis. 2011;204:1227–36.PubMedCentralPubMedCrossRef
29.
Zurück zum Zitat Burdo TH, Lentz MR, Autissier P, et al. Soluble CD163 made by monocyte/macrophages is a novel marker of HIV activity in early and chronic infection prior to and after anti-retroviral therapy. J Infect Dis. 2011;204:154–63.PubMedCentralPubMedCrossRef Burdo TH, Lentz MR, Autissier P, et al. Soluble CD163 made by monocyte/macrophages is a novel marker of HIV activity in early and chronic infection prior to and after anti-retroviral therapy. J Infect Dis. 2011;204:154–63.PubMedCentralPubMedCrossRef
30.•
Zurück zum Zitat Burdo TH, Woods A, Letendre S, et al. Elevated sCD163 is a Marker of Neurocognitive Impairment in HIV-infected Individuals on Effective ART. AIDS. 2013;27:1387–95. Thirty four virally suppressed HIV+ patients (15 with HAND, 19 with normal neurocognitive testing) and 34 HIV negative matched controls were assessed for plasma sCD163 at consecutive visits 7-32 months apart. Neuropyschological impairment correlated significantly with plasma sCD163 levels, consistent with a causal link between monocyte activation and neurocognitive dysfunction in the setting of viral suppression.PubMedCrossRef Burdo TH, Woods A, Letendre S, et al. Elevated sCD163 is a Marker of Neurocognitive Impairment in HIV-infected Individuals on Effective ART. AIDS. 2013;27:1387–95. Thirty four virally suppressed HIV+ patients (15 with HAND, 19 with normal neurocognitive testing) and 34 HIV negative matched controls were assessed for plasma sCD163 at consecutive visits 7-32 months apart. Neuropyschological impairment correlated significantly with plasma sCD163 levels, consistent with a causal link between monocyte activation and neurocognitive dysfunction in the setting of viral suppression.PubMedCrossRef
31.
Zurück zum Zitat Kamat A, Lyons JL, Misra V, et al. Monocyte activation markers in cerebrospinal fluid associated with impaired neurocognitive testing in advanced HIV infection. J Acquir Immune Defic Syndr. 2012;60:234–43.PubMedCentralPubMedCrossRef Kamat A, Lyons JL, Misra V, et al. Monocyte activation markers in cerebrospinal fluid associated with impaired neurocognitive testing in advanced HIV infection. J Acquir Immune Defic Syndr. 2012;60:234–43.PubMedCentralPubMedCrossRef
32.
Zurück zum Zitat Simioni S, Cavassini M, Annoni JM, et al. Cognitive dysfunction in HIV patients despite long-standing suppression of viremia. AIDS. 2010;24:1243–50.PubMed Simioni S, Cavassini M, Annoni JM, et al. Cognitive dysfunction in HIV patients despite long-standing suppression of viremia. AIDS. 2010;24:1243–50.PubMed
33.
Zurück zum Zitat Heaton RK, Franklin DR, Ellis RJ, et al. HIV-associated neurocognitive disorders before and during the era of combination antiretroviral therapy: differences in rates, nature, and predictors. J Neurovirol. 2011;17:3–16.PubMedCentralPubMedCrossRef Heaton RK, Franklin DR, Ellis RJ, et al. HIV-associated neurocognitive disorders before and during the era of combination antiretroviral therapy: differences in rates, nature, and predictors. J Neurovirol. 2011;17:3–16.PubMedCentralPubMedCrossRef
34.
Zurück zum Zitat Heaton RK, Clifford DB, Franklin Jr DR, et al. HIV-associated neurocognitive disorders persist in the era of potent antiretroviral therapy: CHARTER Study. Neurology. 2010;75:2087–96.PubMedCentralPubMedCrossRef Heaton RK, Clifford DB, Franklin Jr DR, et al. HIV-associated neurocognitive disorders persist in the era of potent antiretroviral therapy: CHARTER Study. Neurology. 2010;75:2087–96.PubMedCentralPubMedCrossRef
35.••
Zurück zum Zitat Mothobi NZ, Brew BJ. Neurocognitive dysfunction in the highly active antiretroviral therapy era. Curr Opin Infect Dis. 2012;25:4–9. This review summarizes findings of CHARTER studies and discusses the ‘paradoxical’ lack of efficacy of HAART in effectively preventing HAND. Particular attention is given to possible CNS ART neurotoxicity.PubMedCrossRef Mothobi NZ, Brew BJ. Neurocognitive dysfunction in the highly active antiretroviral therapy era. Curr Opin Infect Dis. 2012;25:4–9. This review summarizes findings of CHARTER studies and discusses the ‘paradoxical’ lack of efficacy of HAART in effectively preventing HAND. Particular attention is given to possible CNS ART neurotoxicity.PubMedCrossRef
36.
Zurück zum Zitat Letendre S, Marquie-Beck J, Capparelli E, et al. Validation of the CNS Penetration-Effectiveness rank for quantifying antiretroviral penetration into the central nervous system. Arch Neurol. 2008;65:65–70.PubMedCentralPubMedCrossRef Letendre S, Marquie-Beck J, Capparelli E, et al. Validation of the CNS Penetration-Effectiveness rank for quantifying antiretroviral penetration into the central nervous system. Arch Neurol. 2008;65:65–70.PubMedCentralPubMedCrossRef
37.
Zurück zum Zitat Robertson KR, Su Z, Margolis DM, et al. Neurocognitive effects of treatment interruption in stable HIV-positive patients in an observational cohort. Neurology. 2010;74:1260–6.PubMedCentralPubMedCrossRef Robertson KR, Su Z, Margolis DM, et al. Neurocognitive effects of treatment interruption in stable HIV-positive patients in an observational cohort. Neurology. 2010;74:1260–6.PubMedCentralPubMedCrossRef
38.
Zurück zum Zitat Marra CM, Zhao Y, Clifford DB, et al. Impact of combination antiretroviral therapy on cerebrospinal fluid HIV RNA and neurocognitive performance. AIDS. 2009;23:1359–66.PubMedCentralPubMedCrossRef Marra CM, Zhao Y, Clifford DB, et al. Impact of combination antiretroviral therapy on cerebrospinal fluid HIV RNA and neurocognitive performance. AIDS. 2009;23:1359–66.PubMedCentralPubMedCrossRef
39.•
Zurück zum Zitat Perez-Valero I, Gonzalez-Baeza A, Estebanez M, et al. Neurocognitive impairment in patients treated with protease inhibitor monotherapy or triple drug antiretroviral therapy. PLoS One. 2013;8:e69493. This is the first prospective study of PI monotherapy in comparison to triple ART associations with neurocognitive functioning. No differences in functioning were seen, suggesting that PI monotherapy does not have an increased risk for neurotoxicity.PubMedCentralPubMedCrossRef Perez-Valero I, Gonzalez-Baeza A, Estebanez M, et al. Neurocognitive impairment in patients treated with protease inhibitor monotherapy or triple drug antiretroviral therapy. PLoS One. 2013;8:e69493. This is the first prospective study of PI monotherapy in comparison to triple ART associations with neurocognitive functioning. No differences in functioning were seen, suggesting that PI monotherapy does not have an increased risk for neurotoxicity.PubMedCentralPubMedCrossRef
40.
Zurück zum Zitat Parikh N, Nonnemacher MR, Pirrone V, et al. Substance abuse, HIV-1 and hepatitis. Curr HIV Res. 2012;10:557–71.PubMedCentralPubMed Parikh N, Nonnemacher MR, Pirrone V, et al. Substance abuse, HIV-1 and hepatitis. Curr HIV Res. 2012;10:557–71.PubMedCentralPubMed
41.••
Zurück zum Zitat Byrnes V, Miller A, Lowry D, et al. Effects of anti-viral therapy and HCV clearance on cerebral metabolism and cognition. J Hepatol. 2012;56:549–56. This study describes evidence that effective HCV antiviral treatment (sustained HCV suppression) can improve neurocognitive functioning and MRS parameters of neuronal injury and glial activation in HIV/HCV co-infection. It is a limited, small study that should prompt thoughtful discussions and larger definitive trials.PubMedCrossRef Byrnes V, Miller A, Lowry D, et al. Effects of anti-viral therapy and HCV clearance on cerebral metabolism and cognition. J Hepatol. 2012;56:549–56. This study describes evidence that effective HCV antiviral treatment (sustained HCV suppression) can improve neurocognitive functioning and MRS parameters of neuronal injury and glial activation in HIV/HCV co-infection. It is a limited, small study that should prompt thoughtful discussions and larger definitive trials.PubMedCrossRef
42.
Zurück zum Zitat Weissenborn K, Tryc AB, Heeren M, et al. Hepatitis C virus infection and the brain. Metab Brain Dis. 2009;24:197–210.PubMedCrossRef Weissenborn K, Tryc AB, Heeren M, et al. Hepatitis C virus infection and the brain. Metab Brain Dis. 2009;24:197–210.PubMedCrossRef
43.
Zurück zum Zitat Chak E, Talal AH, Sherman KE, et al. Hepatitis C virus infection in USA: an estimate of true prevalence. Liver Int. 2011;31:1090–101.PubMedCrossRef Chak E, Talal AH, Sherman KE, et al. Hepatitis C virus infection in USA: an estimate of true prevalence. Liver Int. 2011;31:1090–101.PubMedCrossRef
44.
Zurück zum Zitat Sherman KE, Thomas D, Chung RT. Human immunodeficiency virus and liver disease forum 2012. Hepatology. 2014;59:307–17.PubMedCrossRef Sherman KE, Thomas D, Chung RT. Human immunodeficiency virus and liver disease forum 2012. Hepatology. 2014;59:307–17.PubMedCrossRef
45.
Zurück zum Zitat Letendre SL, Cherner M, Ellis RJ, et al. The effects of hepatitis C, HIV, and methamphetamine dependence on neuropsychological performance: biological correlates of disease. AIDS. 2005;19 Suppl 3:S72–8.PubMedCrossRef Letendre SL, Cherner M, Ellis RJ, et al. The effects of hepatitis C, HIV, and methamphetamine dependence on neuropsychological performance: biological correlates of disease. AIDS. 2005;19 Suppl 3:S72–8.PubMedCrossRef
47.
Zurück zum Zitat Wilkinson J, Radkowski M, Eschbacher JM, et al. Activation of brain macrophages/microglia cells in hepatitis C infection. Gut. 2010;59:1394–400.PubMedCrossRef Wilkinson J, Radkowski M, Eschbacher JM, et al. Activation of brain macrophages/microglia cells in hepatitis C infection. Gut. 2010;59:1394–400.PubMedCrossRef
48.
49.
Zurück zum Zitat Bladowska J, Zimny A, Knysz B, et al. Evaluation of early cerebral metabolic, perfusion and microstructural changes in HCV-positive patients: a pilot study. J Hepatol. 2013;59:651–7.PubMedCrossRef Bladowska J, Zimny A, Knysz B, et al. Evaluation of early cerebral metabolic, perfusion and microstructural changes in HCV-positive patients: a pilot study. J Hepatol. 2013;59:651–7.PubMedCrossRef
50.
Zurück zum Zitat Jernigan TL, Archibald SL, Fennema-Notestine C, et al. Clinical factors related to brain structure in HIV: the CHARTER study. J Neurovirol. 2011;17:248–57.PubMedCentralPubMedCrossRef Jernigan TL, Archibald SL, Fennema-Notestine C, et al. Clinical factors related to brain structure in HIV: the CHARTER study. J Neurovirol. 2011;17:248–57.PubMedCentralPubMedCrossRef
51.
Zurück zum Zitat Vassallo M, Dunais B, Durant J, et al. Relevance of lipopolysaccharide levels in HIV-associated neurocognitive impairment: the Neuradapt study. J Neurovirol. 2013;19:376–82.PubMedCrossRef Vassallo M, Dunais B, Durant J, et al. Relevance of lipopolysaccharide levels in HIV-associated neurocognitive impairment: the Neuradapt study. J Neurovirol. 2013;19:376–82.PubMedCrossRef
52.
Zurück zum Zitat Garvey LJ, Pavese N, Ramlackhansingh A, et al. Acute HCV/HIV coinfection is associated with cognitive dysfunction and cerebral metabolite disturbance, but not increased microglial cell activation. PLoS One. 2012;7:e38980.PubMedCentralPubMedCrossRef Garvey LJ, Pavese N, Ramlackhansingh A, et al. Acute HCV/HIV coinfection is associated with cognitive dysfunction and cerebral metabolite disturbance, but not increased microglial cell activation. PLoS One. 2012;7:e38980.PubMedCentralPubMedCrossRef
53.
Zurück zum Zitat Clifford DB, Smurzynski M, Park LS, et al. Effects of active HCV replication on neurologic status in HIV RNA virally suppressed patients. Neurology. 2009;73:309–14.PubMedCentralPubMedCrossRef Clifford DB, Smurzynski M, Park LS, et al. Effects of active HCV replication on neurologic status in HIV RNA virally suppressed patients. Neurology. 2009;73:309–14.PubMedCentralPubMedCrossRef
54.
Zurück zum Zitat Garvey LJ, Pflugrad H, Thiyagarajan A, et al. Effects of active HCV replication on neurologic status in HIV RNA virally suppressed patients. Neurology. 2010;74:779. author reply 779-780.PubMedCrossRef Garvey LJ, Pflugrad H, Thiyagarajan A, et al. Effects of active HCV replication on neurologic status in HIV RNA virally suppressed patients. Neurology. 2010;74:779. author reply 779-780.PubMedCrossRef
55.
Zurück zum Zitat Clifford DB, Evans SR, Yang Y, et al. The neuropsychological and neurological impact of hepatitis C virus co-infection in HIV-infected subjects. AIDS. 2005;19 Suppl 3:S64–71.PubMedCrossRef Clifford DB, Evans SR, Yang Y, et al. The neuropsychological and neurological impact of hepatitis C virus co-infection in HIV-infected subjects. AIDS. 2005;19 Suppl 3:S64–71.PubMedCrossRef
56.••
Zurück zum Zitat Muir AJ. The rapid evolution of treatment strategies for hepatitis C. Am J Gastroenterol. 2014;109:628–35. This review describes the groundbreaking discovery of the first anti-HCV drug to win FDA approval for treatment of HIV/HCV co-infected individuals. This interferon-sparing drug may be used as monotherapy or combined therapy with other HCV inhibitors with the realistic hope of high efficacy in curing HCV infection.PubMedCrossRef Muir AJ. The rapid evolution of treatment strategies for hepatitis C. Am J Gastroenterol. 2014;109:628–35. This review describes the groundbreaking discovery of the first anti-HCV drug to win FDA approval for treatment of HIV/HCV co-infected individuals. This interferon-sparing drug may be used as monotherapy or combined therapy with other HCV inhibitors with the realistic hope of high efficacy in curing HCV infection.PubMedCrossRef
57.
Zurück zum Zitat Martin-Thormeyer EM, Paul RH. Drug abuse and hepatitis C infection as comorbid features of HIV associated neurocognitive disorder: neurocognitive and neuroimaging features. Neuropsychol Rev. 2009;19:215–31.PubMedCentralPubMedCrossRef Martin-Thormeyer EM, Paul RH. Drug abuse and hepatitis C infection as comorbid features of HIV associated neurocognitive disorder: neurocognitive and neuroimaging features. Neuropsychol Rev. 2009;19:215–31.PubMedCentralPubMedCrossRef
58.
Zurück zum Zitat Nath A. Human immunodeficiency virus-associated neurocognitive disorder: pathophysiology in relation to drug addiction. Ann N Y Acad Sci. 2010;1187:122–8.PubMedCrossRef Nath A. Human immunodeficiency virus-associated neurocognitive disorder: pathophysiology in relation to drug addiction. Ann N Y Acad Sci. 2010;1187:122–8.PubMedCrossRef
59.
Zurück zum Zitat Beyrer C, Wirtz AL, Baral S, et al. Epidemiologic links between drug use and HIV epidemics: an international perspective. J Acquir Immune Defic Syndr. 2010;55 Suppl 1:S10–6.PubMedCrossRef Beyrer C, Wirtz AL, Baral S, et al. Epidemiologic links between drug use and HIV epidemics: an international perspective. J Acquir Immune Defic Syndr. 2010;55 Suppl 1:S10–6.PubMedCrossRef
60.
Zurück zum Zitat Substance Abuse and Mental Health Services Administration CfBHSaQ. The NSDUH Report: HIV/AIDS and Substance Use. 2010. Rockville. Substance Abuse and Mental Health Services Administration CfBHSaQ. The NSDUH Report: HIV/AIDS and Substance Use. 2010. Rockville.
62.••
Zurück zum Zitat Byrd DA, Fellows RP, Morgello S, et al. Neurocognitive impact of substance use in HIV infection. J Acquir Immune Defic Syndr. 2011;58:154–62. This is large cohort study by the CHARTER group examed the relationship between substance abuse history and neurocognitive impairment. The majority of the individuals with substance abuse had sustained abstinence from drug use at time of neurocognitive analysis. The study found no significant effect of substance use status on neurocognitive impairment, suggesting that drugs of abuse may have a limited legacy effect on neurocognitive impairment in HIV+ individuals.PubMedCentralPubMedCrossRef Byrd DA, Fellows RP, Morgello S, et al. Neurocognitive impact of substance use in HIV infection. J Acquir Immune Defic Syndr. 2011;58:154–62. This is large cohort study by the CHARTER group examed the relationship between substance abuse history and neurocognitive impairment. The majority of the individuals with substance abuse had sustained abstinence from drug use at time of neurocognitive analysis. The study found no significant effect of substance use status on neurocognitive impairment, suggesting that drugs of abuse may have a limited legacy effect on neurocognitive impairment in HIV+ individuals.PubMedCentralPubMedCrossRef
63.
Zurück zum Zitat Banerjee A, Strazza M, Wigdahl B, et al. Role of mu-opioids as cofactors in human immunodeficiency virus type 1 disease progression and neuropathogenesis. J Neurovirol. 2011;17:291–302.PubMedCentralPubMedCrossRef Banerjee A, Strazza M, Wigdahl B, et al. Role of mu-opioids as cofactors in human immunodeficiency virus type 1 disease progression and neuropathogenesis. J Neurovirol. 2011;17:291–302.PubMedCentralPubMedCrossRef
64.
Zurück zum Zitat Iudicello JE, Woods SP, Vigil O, et al. Longer term improvement in neurocognitive functioning and affective distress among methamphetamine users who achieve stable abstinence. J Clin Exp Neuropsychol. 2010;32:704–18.PubMedCentralPubMedCrossRef Iudicello JE, Woods SP, Vigil O, et al. Longer term improvement in neurocognitive functioning and affective distress among methamphetamine users who achieve stable abstinence. J Clin Exp Neuropsychol. 2010;32:704–18.PubMedCentralPubMedCrossRef
65.
Zurück zum Zitat Wang X, Wang Y, Ye L, et al. Modulation of intracellular restriction factors contributes to methamphetamine-mediated enhancement of acquired immune deficiency syndrome virus infection of macrophages. Curr HIV Res. 2012;10:407–14.PubMedCentralPubMedCrossRef Wang X, Wang Y, Ye L, et al. Modulation of intracellular restriction factors contributes to methamphetamine-mediated enhancement of acquired immune deficiency syndrome virus infection of macrophages. Curr HIV Res. 2012;10:407–14.PubMedCentralPubMedCrossRef
66.
Zurück zum Zitat Reynolds JL, Law WC, Mahajan SD, et al. Morphine and galectin-1 modulate HIV-1 infection of human monocyte-derived macrophages. J Immunol. 2012;188:3757–65.PubMedCentralPubMedCrossRef Reynolds JL, Law WC, Mahajan SD, et al. Morphine and galectin-1 modulate HIV-1 infection of human monocyte-derived macrophages. J Immunol. 2012;188:3757–65.PubMedCentralPubMedCrossRef
67.
Zurück zum Zitat Dave RS, Khalili K. Morphine treatment of human monocyte-derived macrophages induces differential miRNA and protein expression: impact on inflammation and oxidative stress in the central nervous system. J Cell Biochem. 2010;110:834–45.PubMedCentralPubMedCrossRef Dave RS, Khalili K. Morphine treatment of human monocyte-derived macrophages induces differential miRNA and protein expression: impact on inflammation and oxidative stress in the central nervous system. J Cell Biochem. 2010;110:834–45.PubMedCentralPubMedCrossRef
68.
Zurück zum Zitat Mantri CK, Pandhare Dash J, Mantri JV, et al. Cocaine enhances HIV-1 replication in CD4+ T cells by down-regulating MiR-125b. PLoS One. 2012;7:e51387.PubMedCentralPubMedCrossRef Mantri CK, Pandhare Dash J, Mantri JV, et al. Cocaine enhances HIV-1 replication in CD4+ T cells by down-regulating MiR-125b. PLoS One. 2012;7:e51387.PubMedCentralPubMedCrossRef
69.
Zurück zum Zitat Kim SG, Jung JB, Dixit D, et al. Cocaine exposure enhances permissiveness of quiescent T cells to HIV infection. J Leukoc Biol. 2013;94:835–43.PubMedCrossRef Kim SG, Jung JB, Dixit D, et al. Cocaine exposure enhances permissiveness of quiescent T cells to HIV infection. J Leukoc Biol. 2013;94:835–43.PubMedCrossRef
70.•
Zurück zum Zitat Mantri CK, Mantri JV, Pandhare J, et al. Methamphetamine inhibits HIV-1 replication in CD4+ T cells by modulating anti-HIV-1 miRNA expression. Am J Pathol. 2014;184:92–100. This study presents evidence of an inhibitory effect of methamphetamine on HIV replication in CD4+ T lymphocytes through miRNA regulation, in contrast to other published reports of methamphetamine enhancement of HIV replication. These conflicting results are discussed in detail, and appropriate caution is urged when extrapolating in vitro results in such studies to pathogenic mechanisms in vivo.PubMedCrossRef Mantri CK, Mantri JV, Pandhare J, et al. Methamphetamine inhibits HIV-1 replication in CD4+ T cells by modulating anti-HIV-1 miRNA expression. Am J Pathol. 2014;184:92–100. This study presents evidence of an inhibitory effect of methamphetamine on HIV replication in CD4+ T lymphocytes through miRNA regulation, in contrast to other published reports of methamphetamine enhancement of HIV replication. These conflicting results are discussed in detail, and appropriate caution is urged when extrapolating in vitro results in such studies to pathogenic mechanisms in vivo.PubMedCrossRef
71.
Zurück zum Zitat Gaskill PJ, Calderon TM, Coley JS, et al. Drug induced increases in CNS dopamine alter monocyte, macrophage and T cell functions: implications for HAND. J Neuroimmune Pharmacol. 2013;8:621–42.PubMedCrossRef Gaskill PJ, Calderon TM, Coley JS, et al. Drug induced increases in CNS dopamine alter monocyte, macrophage and T cell functions: implications for HAND. J Neuroimmune Pharmacol. 2013;8:621–42.PubMedCrossRef
72.
Zurück zum Zitat Gaskill PJ, Calderon TM, Luers AJ, et al. Human immunodeficiency virus (HIV) infection of human macrophages is increased by dopamine: a bridge between HIV-associated neurologic disorders and drug abuse. Am J Pathol. 2009;175:1148–59.PubMedCentralPubMedCrossRef Gaskill PJ, Calderon TM, Luers AJ, et al. Human immunodeficiency virus (HIV) infection of human macrophages is increased by dopamine: a bridge between HIV-associated neurologic disorders and drug abuse. Am J Pathol. 2009;175:1148–59.PubMedCentralPubMedCrossRef
73.
Zurück zum Zitat Czub S, Koutsilieri E, Sopper S, et al. Enhancement of central nervous system pathology in early simian immunodeficiency virus infection by dopaminergic drugs. Acta Neuropathol. 2001;101:85–91.PubMed Czub S, Koutsilieri E, Sopper S, et al. Enhancement of central nervous system pathology in early simian immunodeficiency virus infection by dopaminergic drugs. Acta Neuropathol. 2001;101:85–91.PubMed
74.
Zurück zum Zitat Czub S, Czub M, Koutsilieri E, et al. Modulation of simian immunodeficiency virus neuropathology by dopaminergic drugs. Acta Neuropathol. 2004;107:216–26.PubMedCrossRef Czub S, Czub M, Koutsilieri E, et al. Modulation of simian immunodeficiency virus neuropathology by dopaminergic drugs. Acta Neuropathol. 2004;107:216–26.PubMedCrossRef
75.
Zurück zum Zitat Marcondes MC, Flynn C, Watry DD, et al. Methamphetamine increases brain viral load and activates natural killer cells in simian immunodeficiency virus-infected monkeys. Am J Pathol. 2010;177:355–61.PubMedCentralPubMedCrossRef Marcondes MC, Flynn C, Watry DD, et al. Methamphetamine increases brain viral load and activates natural killer cells in simian immunodeficiency virus-infected monkeys. Am J Pathol. 2010;177:355–61.PubMedCentralPubMedCrossRef
76.
Zurück zum Zitat Bokhari SM, Hegde R, Callen S, et al. Morphine potentiates neuropathogenesis of SIV infection in rhesus macaques. J Neuroimmune Pharmacol. 2011;6:626–39.PubMedCentralPubMedCrossRef Bokhari SM, Hegde R, Callen S, et al. Morphine potentiates neuropathogenesis of SIV infection in rhesus macaques. J Neuroimmune Pharmacol. 2011;6:626–39.PubMedCentralPubMedCrossRef
77.
Zurück zum Zitat Weed M, Adams RJ, Hienz RD, et al. SIV/macaque model of HIV infection in cocaine users: minimal effects of cocaine on behavior, virus replication, and CNS inflammation. J Neuroimmune Pharmacol. 2012;7:401–11.PubMedCentralPubMedCrossRef Weed M, Adams RJ, Hienz RD, et al. SIV/macaque model of HIV infection in cocaine users: minimal effects of cocaine on behavior, virus replication, and CNS inflammation. J Neuroimmune Pharmacol. 2012;7:401–11.PubMedCentralPubMedCrossRef
79.
Zurück zum Zitat Liu X, Silverstein PS, Singh V, et al. Methamphetamine increases LPS-mediated expression of IL-8, TNF-alpha and IL-1beta in human macrophages through common signaling pathways. PLoS One. 2012;7:e33822.PubMedCentralPubMedCrossRef Liu X, Silverstein PS, Singh V, et al. Methamphetamine increases LPS-mediated expression of IL-8, TNF-alpha and IL-1beta in human macrophages through common signaling pathways. PLoS One. 2012;7:e33822.PubMedCentralPubMedCrossRef
80.
Zurück zum Zitat Cisneros IE, Ghorpade A. HIV-1, methamphetamine and astrocyte glutamate regulation: combined excitotoxic implications for neuro-AIDS. Curr HIV Res. 2012;10:392–406.PubMedCentralPubMedCrossRef Cisneros IE, Ghorpade A. HIV-1, methamphetamine and astrocyte glutamate regulation: combined excitotoxic implications for neuro-AIDS. Curr HIV Res. 2012;10:392–406.PubMedCentralPubMedCrossRef
81.
Zurück zum Zitat Yang Y, Yao H, Lu Y, et al. Cocaine potentiates astrocyte toxicity mediated by human immunodeficiency virus (HIV-1) protein gp120. PLoS One. 2010;5:e13427.PubMedCentralPubMedCrossRef Yang Y, Yao H, Lu Y, et al. Cocaine potentiates astrocyte toxicity mediated by human immunodeficiency virus (HIV-1) protein gp120. PLoS One. 2010;5:e13427.PubMedCentralPubMedCrossRef
82.•
Zurück zum Zitat Strazza M, Pirrone V, Wigdahl B, et al. Breaking down the barrier: the effects of HIV-1 on the blood-brain barrier. Brain Res. 2011;1399:96–115. A review of the effects of HIV infection on the BBB, specifically addressing the role of HIV proteins, monocyte chemotaxis across the BBB, and the compounding effects of drug abuse.PubMedCentralPubMedCrossRef Strazza M, Pirrone V, Wigdahl B, et al. Breaking down the barrier: the effects of HIV-1 on the blood-brain barrier. Brain Res. 2011;1399:96–115. A review of the effects of HIV infection on the BBB, specifically addressing the role of HIV proteins, monocyte chemotaxis across the BBB, and the compounding effects of drug abuse.PubMedCentralPubMedCrossRef
83.
Zurück zum Zitat Martins T, Baptista S, Goncalves J, et al. Methamphetamine transiently increases the blood-brain barrier permeability in the hippocampus: role of tight junction proteins and matrix metalloproteinase-9. Brain Res. 2011;1411:28–40.PubMed Martins T, Baptista S, Goncalves J, et al. Methamphetamine transiently increases the blood-brain barrier permeability in the hippocampus: role of tight junction proteins and matrix metalloproteinase-9. Brain Res. 2011;1411:28–40.PubMed
84.
Zurück zum Zitat Dhillon NK, Peng F, Bokhari S, et al. Cocaine-mediated alteration in tight junction protein expression and modulation of CCL2/CCR2 axis across the blood-brain barrier: implications for HIV-dementia. J Neuroimmune Pharmacol. 2008;3:52–6.PubMedCrossRef Dhillon NK, Peng F, Bokhari S, et al. Cocaine-mediated alteration in tight junction protein expression and modulation of CCL2/CCR2 axis across the blood-brain barrier: implications for HIV-dementia. J Neuroimmune Pharmacol. 2008;3:52–6.PubMedCrossRef
85.
Zurück zum Zitat Sharma HS, Ali SF. Alterations in blood-brain barrier function by morphine and methamphetamine. Ann N Y Acad Sci. 2006;1074:198–224.PubMedCrossRef Sharma HS, Ali SF. Alterations in blood-brain barrier function by morphine and methamphetamine. Ann N Y Acad Sci. 2006;1074:198–224.PubMedCrossRef
86.
Zurück zum Zitat Yousif S, Saubamea B, Cisternino S, et al. Effect of chronic exposure to morphine on the rat blood-brain barrier: focus on the P-glycoprotein. J Neurochem. 2008;107:647–57.PubMedCrossRef Yousif S, Saubamea B, Cisternino S, et al. Effect of chronic exposure to morphine on the rat blood-brain barrier: focus on the P-glycoprotein. J Neurochem. 2008;107:647–57.PubMedCrossRef
87.
Zurück zum Zitat Mellins CA, Havens JF, McDonnell C, et al. Adherence to antiretroviral medications and medical care in HIV-infected adults diagnosed with mental and substance abuse disorders. AIDS Care. 2009;21:168–77.PubMedCrossRef Mellins CA, Havens JF, McDonnell C, et al. Adherence to antiretroviral medications and medical care in HIV-infected adults diagnosed with mental and substance abuse disorders. AIDS Care. 2009;21:168–77.PubMedCrossRef
88.
Zurück zum Zitat Roux P, Carrieri MP, Villes V, et al. The impact of methadone or buprenorphine treatment and ongoing injection on highly active antiretroviral therapy (HAART) adherence: evidence from the MANIF2000 cohort study. Addiction. 2008;103:1828–36.PubMedCrossRef Roux P, Carrieri MP, Villes V, et al. The impact of methadone or buprenorphine treatment and ongoing injection on highly active antiretroviral therapy (HAART) adherence: evidence from the MANIF2000 cohort study. Addiction. 2008;103:1828–36.PubMedCrossRef
89.
Zurück zum Zitat Carrico AW. Substance use and HIV disease progression in the HAART era: implications for the primary prevention of HIV. Life Sci. 2011;88:940–7.PubMedCrossRef Carrico AW. Substance use and HIV disease progression in the HAART era: implications for the primary prevention of HIV. Life Sci. 2011;88:940–7.PubMedCrossRef
90.
Zurück zum Zitat Deeks SG. Immune dysfunction, inflammation, and accelerated aging in patients on antiretroviral therapy. Top HIV Med. 2009;17:118–23.PubMed Deeks SG. Immune dysfunction, inflammation, and accelerated aging in patients on antiretroviral therapy. Top HIV Med. 2009;17:118–23.PubMed
91.
Zurück zum Zitat Xu J, Ikezu T. The comorbidity of HIV-associated neurocognitive disorders and Alzheimer's disease: a foreseeable medical challenge in post-HAART era. J Neuroimmune Pharmacol. 2009;4:200–12.PubMedCentralPubMedCrossRef Xu J, Ikezu T. The comorbidity of HIV-associated neurocognitive disorders and Alzheimer's disease: a foreseeable medical challenge in post-HAART era. J Neuroimmune Pharmacol. 2009;4:200–12.PubMedCentralPubMedCrossRef
92.
Zurück zum Zitat Achim CL, Adame A, Dumaop W, et al. Increased accumulation of intraneuronal amyloid beta in HIV-infected patients. J Neuroimmune Pharmacol. 2009;4:190–9.PubMedCentralPubMedCrossRef Achim CL, Adame A, Dumaop W, et al. Increased accumulation of intraneuronal amyloid beta in HIV-infected patients. J Neuroimmune Pharmacol. 2009;4:190–9.PubMedCentralPubMedCrossRef
93.
Zurück zum Zitat Khanlou N, Moore DJ, Chana G, et al. Increased frequency of alpha-synuclein in the substantia nigra in human immunodeficiency virus infection. J Neurovirol. 2009;15:131–8.PubMedCentralPubMedCrossRef Khanlou N, Moore DJ, Chana G, et al. Increased frequency of alpha-synuclein in the substantia nigra in human immunodeficiency virus infection. J Neurovirol. 2009;15:131–8.PubMedCentralPubMedCrossRef
94.
Zurück zum Zitat Soontornniyomkij V, Moore DJ, Gouaux B, et al. Cerebral beta-amyloid deposition predicts HIV-associated neurocognitive disorders in APOE epsilon4 carriers. AIDS. 2012;26:2327–35.PubMedCentralPubMedCrossRef Soontornniyomkij V, Moore DJ, Gouaux B, et al. Cerebral beta-amyloid deposition predicts HIV-associated neurocognitive disorders in APOE epsilon4 carriers. AIDS. 2012;26:2327–35.PubMedCentralPubMedCrossRef
95.
Zurück zum Zitat Smith DB, Simmonds P, Bell JE. Brain viral burden, neuroinflammation and neurodegeneration in HAART-treated HIV positive injecting drug users. J Neurovirol. 2014;20:28–38.PubMedCrossRef Smith DB, Simmonds P, Bell JE. Brain viral burden, neuroinflammation and neurodegeneration in HAART-treated HIV positive injecting drug users. J Neurovirol. 2014;20:28–38.PubMedCrossRef
96.
Zurück zum Zitat Fields J, Dumaop W, Rockenstein E, et al. Age-dependent molecular alterations in the autophagy pathway in HIVE patients and in a gp120 tg mouse model: reversal with beclin-1 gene transfer. J Neurovirol. 2013;19:89–101.PubMedCentralPubMedCrossRef Fields J, Dumaop W, Rockenstein E, et al. Age-dependent molecular alterations in the autophagy pathway in HIVE patients and in a gp120 tg mouse model: reversal with beclin-1 gene transfer. J Neurovirol. 2013;19:89–101.PubMedCentralPubMedCrossRef
97.••
Zurück zum Zitat Salminen A, Kaarniranta K, Kauppinen A, et al. Impaired autophagy and APP processing in Alzheimer's disease: the potential role of Beclin 1 interactome. Prog Neurobiol. 2013;106–107:33–54. An exhaustive review of autophagy, APP processing and the unique role for Beclin-1, a critical component of the autophagosome. Although dealing primarily with AD, it presents an interesting discussion of the implications for several viral diseases, including HIV CNS infection.PubMedCrossRef Salminen A, Kaarniranta K, Kauppinen A, et al. Impaired autophagy and APP processing in Alzheimer's disease: the potential role of Beclin 1 interactome. Prog Neurobiol. 2013;106–107:33–54. An exhaustive review of autophagy, APP processing and the unique role for Beclin-1, a critical component of the autophagosome. Although dealing primarily with AD, it presents an interesting discussion of the implications for several viral diseases, including HIV CNS infection.PubMedCrossRef
98.
Zurück zum Zitat Seider TR, Luo X, Gongvatana A, et al. Verbal memory declines more rapidly with age in HIV infected versus uninfected adults. J Clin Exp Neuropsychol. 2014;36:356–67.PubMedCrossRef Seider TR, Luo X, Gongvatana A, et al. Verbal memory declines more rapidly with age in HIV infected versus uninfected adults. J Clin Exp Neuropsychol. 2014;36:356–67.PubMedCrossRef
100.
Zurück zum Zitat Cassol E, Misra V, Dutta A, et al. Cerebrospinal fluid metabolomics reveals altered waste clearance and accelerated aging in HIV patients with neurocognitive impairment. AIDS. 2014;28. Cassol E, Misra V, Dutta A, et al. Cerebrospinal fluid metabolomics reveals altered waste clearance and accelerated aging in HIV patients with neurocognitive impairment. AIDS. 2014;28.
101.•
Zurück zum Zitat Chang L, Holt JL, Yakupov R, et al. Lower cognitive reserve in the aging human immunodeficiency virus-infected brain. Neurobiol Aging. 2013;34:1240–53. This large (n = 122 patients) fMRI study demonstrated poorer regional brain compensation through recruitment of functional attention networks in HIV infected individuals under demand test conditions. Synergistic effects of HIV and aging were proposed.PubMedCentralPubMedCrossRef Chang L, Holt JL, Yakupov R, et al. Lower cognitive reserve in the aging human immunodeficiency virus-infected brain. Neurobiol Aging. 2013;34:1240–53. This large (n = 122 patients) fMRI study demonstrated poorer regional brain compensation through recruitment of functional attention networks in HIV infected individuals under demand test conditions. Synergistic effects of HIV and aging were proposed.PubMedCentralPubMedCrossRef
102.
Zurück zum Zitat Thomas JB, Brier MR, Snyder AZ, et al. Pathways to neurodegeneration: effects of HIV and aging on resting-state functional connectivity. Neurology. 2013;80:1186–93.PubMedCentralPubMedCrossRef Thomas JB, Brier MR, Snyder AZ, et al. Pathways to neurodegeneration: effects of HIV and aging on resting-state functional connectivity. Neurology. 2013;80:1186–93.PubMedCentralPubMedCrossRef
Metadaten
Titel
Chronic Inflammation and the Role for Cofactors (Hepatitis C, Drug Abuse, Antiretroviral Drug Toxicity, Aging) in HAND Persistence
verfasst von
Alexander J. Gill
Dennis L. Kolson
Publikationsdatum
01.09.2014
Verlag
Springer US
Erschienen in
Current HIV/AIDS Reports / Ausgabe 3/2014
Print ISSN: 1548-3568
Elektronische ISSN: 1548-3576
DOI
https://doi.org/10.1007/s11904-014-0210-3

Weitere Artikel der Ausgabe 3/2014

Current HIV/AIDS Reports 3/2014 Zur Ausgabe

Complications of Antiretroviral Therapy (JM Kilby, Section Editor)

Understanding the Etiology and Management of HIV-Associated Peripheral Neuropathy

Complications of Antiretroviral Therapy (JM Kilby, Section Editor)

Drug Interactions and Antiretroviral Drug Monitoring

Complications of Antiretroviral Therapy (JM Kilby, Section Editor)

Bone Alterations Associated with HIV

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.