Elevated Biomarkers of Inflammation and Coagulation in Patients with HIV Are Associated with Higher Framingham and VACS Risk Index Scores

Mooney, Sarah; Tracy, Russell P.; Osler, Turner M.; Grace, Christopher

doi:10.1371/journal.pone.0144312

Cited by 44 publications

(37 citation statements)

References 32 publications

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“…In addition, the subtype C group had less severe historical levels of immunosuppression as measured by nadir CD4. Because low nadir CD4 has been shown in previous studies to be associated with increased soluble biomarkers of inflammation and chemotaxis in HIV (Gisslen et al, 1994; Mooney et al, 2015; Noel et al, 2014), we included nadir CD4 in a multivariate model (Vittinghoff, 2012). The statistically adjusted the effect size estimates presented in Table 4 show no subtype differences.…”

Section: Discussionmentioning

confidence: 99%

“…We used a multivariable linear regression (adjusted analysis), controlling for plasma HIV viral load suppression, which was statistically different between the subtypes, and nadir CD4 count. Because low nadir CD4 has been shown in previous studies to be associated with increased soluble biomarkers of inflammation and chemotaxis in HIV (Gisslen et al, 1994; Mooney et al, 2015; Noel et al, 2014), we included nadir CD4 in the multivariable model (Vittinghoff, 2011). Results were considered statistically significant at the 5% alpha level.…”

Section: Methodsmentioning

confidence: 99%

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Biomarkers of chemotaxis and inflammation in cerebrospinal fluid and serum in individuals with HIV-1 subtype C versus B

et al. 2016

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A defective chemokine motif in the HIV-1 Tat protein has been hypothesized to alter central nervous system cellular trafficking and inflammation, rendering HIV-1 subtype C less neuropathogenic than B. To evaluate this hypothesis, we compared biomarkers of cellular chemotaxis and inflammation in cerebrospinal fluid (CSF) and serum in individuals infected with HIV-1 subtypes B (n=27) and C (n=25) from Curitiba, Brazil. None had opportunistic infections. Chemokines (MCP-1, MIP-1α, MIP-1β, RANTES, IP-10) and cytokines (TNF-α, IFN-y, IL-1β, IL-2, IL-4, IL-6, IL-7, IL-10) were measured using the multiplex bead suspension array immunoassays or ELISA HD. CSF and serum biomarker concentrations were compared between subtype B and C groups and HIV-positive and HIV-negative subjects (N=19) using an independent group t-test (unadjusted analysis) and linear regression (adjusted analysis), controlling for nadir CD4 and CSF and plasma HIV RNA suppression. CSF levels of cytokines and chemokines were significantly (p< 0.05) elevated in HIV-positive versus HIV-negative participants for 7/13 biomarkers measured, but levels did not differ for subtypes B and C. Serum levels were significantly elevated for 4/13 markers, with no significant differences between subtypes B and C. Although pleocytosis was much more frequent in HIV-positive than in HIV-negative individuals (27% vs. 0%), subtypes B and C did not differ (32% and 22%; p = 0.23). We did not find molecular evidence to support the hypothesis that intrathecal chemotaxis and inflammation is less in HIV-1 subtype C than in subtype B. Biomarker changes in CSF were more robust than in serum, suggesting compartmentalization of the immunological response to HIV.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Biomarkers of chemotaxis and inflammation in cerebrospinal fluid and serum in individuals with HIV-1 subtype C versus B

et al. 2016

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“…We used a multivariable linear regression (adjusted analysis), controlling for plasma HIV viral load suppression, and nadir CD4 count, which has been shown in previous studies to be associated with increased soluble biomarkers of inflammation and chemotaxis in HIV (Gisslen et al, 1994; Mooney et al, 2015; Noel et al, 2014). In a second moment results were adjusted for Q Alb for the comparison of groups HIV+ and HIV-; and Q Alb in addition to suppressed plasma and CSF viral load, and CD4 nadir for the comparison of the groups with and without CSF pleocytosis.…”

Section: Methodsmentioning

confidence: 99%

Blood-CSF barrier and compartmentalization of CNS cellular immune response in HIV infection

Almeida

Rotta

Ribeiro

et al. 2016

Journal of Neuroimmunology

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HIV infection is persistent in the CNS, to evaluate the compartmentalization of the CNS immune response to HIV, we compared soluble markers of cellular immunity in the blood and CSF among HIV- (n=19) and HIV+ (n=68), as well as among HIV participants with or without CSF pleocytosis. Dysfunction of the blood cerebrospinal fluid barrier (BCSFB) was common in HIV participants. CSF levels of TNFα, IFNγ, IL-2, IL-6, IL-7, IL-10, IP-10, MIP-1α, MIP-1β, and RANTES were significantly higher in participants with CSF pleocytosis (p<0.05); serum levels of these biomarkers were comparable. The CNS immune response is compartmentalized, and remains so despite the BCSFB dysfunction during HIV infection; it is markedly reduced by virology suppression, although BCSFB dysfunction persists on this subgroup.

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“…The soluble biomarkers chosen have been shown in previous studies as persistently elevated despite HIV suppression [37] or have been associated with non-AIDS chronic diseases or mortality in HIV-infected individuals. [7, 8, 38] T cell activation is also associated with HIV disease progression [39] as well as impaired vascular health among virally suppressed individuals. [40] Plasma levels of sCD14 remained elevated in the HIV(+) group despite viral suppression and CD4 + T cell reconstitution.…”

Section: Resultsmentioning

confidence: 99%

Subclinical herpesvirus shedding among HIV-1-infected men on antiretroviral therapy

Agudelo-Hernandez

Chen

Bullotta

et al. 2017

Aids

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Design We evaluated the subclinical shedding of 6 different herpesviruses in antiretroviral drug-treated HIV(+) men who have sex with men (MSM), and determined how this is associated with markers of inflammation and immune activation. Methods We obtained blood, semen, throat washing, urine, and stool from 15 antiretroviral-treated HIV-1-infected MSM with CD4+ T cell reconstitution, and 12 age-matched HIV(−) MSM from the Multicenter AIDS Cohort Study at 4 timepoints over 24 weeks to measure DNA levels of cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus 1 and 2, human herpesvirus 6 (HHV6), and HHV8. T cell activation and plasma levels of soluble markers of inflammation and activation were also measured at the corresponding timepoints. Results HIV(+) participants had a trend for higher total herpesvirus shedding rate. HIV(+) participants also had a significantly higher rate of shedding EBV and CMV compared to the HIV(−) group. Herpesvirus shedding was mostly seen in throat washings. In the HIV(+) group, herpesvirus shedding rate inversely correlated with plasma levels of interferon gamma-induced protein 10 (IP-10) and soluble CD163 (sCD163). CMV DNA levels negatively correlated with levels of T cell activation. There was a trend for a positive correlation between EBV shedding rate and plasma soluble CD14. HHV6 shedding rate negatively correlated with plasma levels of interleukin-6, sCD163, and IP-10. Correlations were not observed among HIV(−) individuals. Conclusions Among treated HIV-infected MSM, there are higher subclinical shedding rates of some herpesviruses that occurs in different body compartments and negatively correlates with levels of inflammation and immune activation.

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Elevated Biomarkers of Inflammation and Coagulation in Patients with HIV Are Associated with Higher Framingham and VACS Risk Index Scores

Cited by 44 publications

References 32 publications

Biomarkers of chemotaxis and inflammation in cerebrospinal fluid and serum in individuals with HIV-1 subtype C versus B

Biomarkers of chemotaxis and inflammation in cerebrospinal fluid and serum in individuals with HIV-1 subtype C versus B

Blood-CSF barrier and compartmentalization of CNS cellular immune response in HIV infection

Subclinical herpesvirus shedding among HIV-1-infected men on antiretroviral therapy

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