Inflammation, Coagulation and Cardiovascular Disease in HIV-Infected Individuals

Duprez, Daniel; Neuhaus, Jacqueline; Kuller, Lewis H.; Tracy, Russell P.; Belloso, Waldo; Wit, Stéphane De; Drummond, Fraser; Lane, H. Clifford; Ledergerber, Bruno; Lundgren, Jens D.; Nixon, Daniel E.; Paton, Nicholas I.; Prineas, Ronald J.

doi:10.1371/journal.pone.0044454

Cited by 462 publications

(411 citation statements)

References 40 publications

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“…Several studies confirm the SMART study in fact that the D-dimers has a strong correlated with cardiovascular disease [12]. D-dimer levels forecast the present of thrombosis whatever venous or arterial in all individuals and with those affected by HIV infection [3] [12]- [18].…”

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confidence: 65%

Estimation and Assessment of Plasma D-Dimer Levels in HIV Patients

Himmat¹,

Gaufri²

2016

JBM

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Background: The elevation of plasma D-dimer levels is fully described and associated with the increase of the mortality of patients with HIV. The present study was aimed to estimate and assess the plasma D-dimer levels in HIV patient. Material and Methods: A case control study done in May 2015. A total of 100 subjects were enrolled in this study; 50 were patients professionally diagnosed by HIV; 25 (50%) were males and 25 (50%) were females; their mean age is 35 years. Further 50 normal healthy individuals as normal control group: their gender and age were matched with patient groups. The platelets poor plasma (PPP) was immediately prepared from citrated blood, then the plasma D-dimer level was measured using (MISPA-i 2 Reagent) Switzerland. Data were analyzed using statistical packing for social sciences program (SPSS) 20. Results: The D-dimer levels was significantly higher in patient with HIV compared with the normal healthy control group (Mean and STD 502.2 ± 287.8 vs 251.8 ± 152.7 P. value 0.01). Conclusion: The D-dimer level was significantly higher in patient with HIV compared with those in normal healthy control group.

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confidence: 65%

Estimation and Assessment of Plasma D-Dimer Levels in HIV Patients

Himmat¹,

Gaufri²

2016

JBM

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“…Levels of T-cell activation and innate system activation are often higher than that observed in well-matched uninfected adults (5,6). These persistent abnormalities may contribute to abnormal vaccine responses (7,8), a higher than normal incidence of non-AIDS-related cancers (9,10) and increased risk for clinical conditions associated with chronic inflammation (e.g., cardiac disease, clotting disorders, pulmonary hypertension, emphysema, and stroke) (11)(12)(13)(14)(15)(16)(17)(18). Thus, improvements over current approaches to treatment of HIV infection that more fully restore normal immune function might significantly improve health and life expectancy.…”

mentioning

confidence: 99%

Persistent HIV-1 replication is associated with lower antiretroviral drug concentrations in lymphatic tissues

Fletcher

Staskus²,

Wietgrefe³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

567

589

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Antiretroviral therapy can reduce HIV-1 to undetectable levels in peripheral blood, but the effectiveness of treatment in suppressing replication in lymphoid tissue reservoirs has not been determined. Here we show in lymph node samples obtained before and during 6 mo of treatment that the tissue concentrations of five of the most frequently used antiretroviral drugs are much lower than in peripheral blood. These lower concentrations correlated with continued virus replication measured by the slower decay or increases in the follicular dendritic cell network pool of virions and with detection of viral RNA in productively infected cells. The evidence of persistent replication associated with apparently suboptimal drug concentrations argues for development and evaluation of novel therapeutic strategies that will fully suppress viral replication in lymphatic tissues. These strategies could avert the long-term clinical consequences of chronic immune activation driven directly or indirectly by low-level viral replication to thereby improve immune reconstitution.drug levels | pharmacokinetics | FDC network C ombination antiviral therapy (ART) to suppress HIV-1 replication and reduce plasma viremia to below the limits of detection in peripheral blood (PB) has reduced mortality and dramatically improved quality of life for patients. However, immune reconstitution, measured by changes in the size of populations of CD4 T cells, is often incomplete, even after years of therapy (1-3). During apparently effective therapy, CD4 T-cell populations in PB mononuclear cells (PBMCs), lymph node (LN), and gut-associated lymphoid tissue (GALT) remain abnormally low and innate and adaptive immunity is not fully restored (4). Levels of T-cell activation and innate system activation are often higher than that observed in well-matched uninfected adults (5, 6). These persistent abnormalities may contribute to abnormal vaccine responses (7, 8), a higher than normal incidence of non-AIDS-related cancers (9, 10) and increased risk for clinical conditions associated with chronic inflammation (e.g., cardiac disease, clotting disorders, pulmonary hypertension, emphysema, and stroke) (11-18). Thus, improvements over current approaches to treatment of HIV infection that more fully restore normal immune function might significantly improve health and life expectancy.To that end, we explore here the hypothesis that antiretroviral drug (ARV) concentrations might be insufficient to fully suppress replication in the lymphoid tissue compartments, which are the principal sites where virus is produced, stored as complexes on the follicular dendritic cell network (FDCn) (19-21), and persists in latently infected cells during ART (19,20,22). This hypothesis builds first on the link between the size of the reservoir and the degree of inflammation, arguing that persistent virus production during ART could sustain immune activation (IA) and downstream pathological consequences (23, 24), and second on drug distribution studies in animal models of AIDS in which ...

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“…A further detailed assessment of CAD risk factors is then to be performed, including smoking history, family history of CAD, and fasting determinations of total cholesterol, highdensity lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol, triglycerides, Framingham Risk Score (FRS) or the atherosclerotic cardiovascular disease (ASCVD) risk assessment. As mentioned, recent analysis has suggested that chronic inflammation can partially attribute to the increased cardiovascular risk correlated with HIV infection [38,39]. The underlying mechanism of this disease process is currently being studied and remains unclear.…”

Section: Diagnosismentioning

confidence: 99%