Relationship between cytomegalovirus infection and procoagulant changes in human immunodeficiency virus‐infected patients

Mulder, René; Tichelaar, Ynse Ieuwe Gerardus Vladimir; Sprenger, Herman; Mulder, André B.; Lijfering, Willem M.

doi:10.1111/j.1469-0691.2010.03415.x

Cited by 14 publications

(11 citation statements)

References 15 publications

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“…Further, CMV viremia was more prevalent among cases than controls. Active CMV infection was recently associated with hypercoagulability independent of stage of HIV disease [42]. These findings suggest that CMV disease, rather than immunodeficiency alone, may result in a heightened inflammatory state leading to activation of the coagulation cascade in co-infected patients.…”

Section: Discussionmentioning

confidence: 99%

Markers of endothelial dysfunction, coagulation and tissue fibrosis independently predict venous thromboembolism in HIV

Musselwhite

Sheikh

Norton

et al. 2011

Aids

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Objective HIV infection is associated with coagulation abnormalities and significantly increased risk of venous thrombosis. It has been shown that higher plasma levels of coagulation and inflammatory biomarkers predicted mortality in HIV. We investigated the relationship between venous thrombosis and HIV-related characteristics, traditional risk factors of hypercoagulability and pre-event levels of biomarkers. Design A retrospective case-control study of 23 HIV-infected individuals who experienced an incident venous thromboembolic (VTE) event while enrolled in National Institutes of Health studies from 1995–2010 and 69 age and sex-matched HIV-infected individuals without known VTE. Methods Biomarkers of inflammation, endothelial dysfunction, coagulation, tissue fibrosis, and cytomegalovirus (CMV) reactivation were assessed by ELISA-based assays and PCR using plasma obtained prior to the event. Results VTE events were related to nadir CD4 count, lifetime history of multiple opportunistic infections, CMV disease, CMV viremia, immunological AIDS, active infection and provocation (i.e. recent hospitalization, surgery or trauma). VTE events were independently associated with increased plasma levels of P-selectin, P=0.002; D-dimer, P=0.01; and hyaluronic acid, P=0.009 in a multivariate analysis. No significant differences in antiretroviral or interleukin 2 exposures, plasma HIV viremia, or other traditional risk factors were observed. Conclusion Severe immunodeficiency, active infection and provocation are associated with venous thromboembolic disease in HIV. Biomarkers of endothelial dysfunction, coagulation and tissue fibrosis may help identify HIV-infected patients at elevated risk of VTE.

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Section: Discussionmentioning

confidence: 99%

Markers of endothelial dysfunction, coagulation and tissue fibrosis independently predict venous thromboembolism in HIV

Musselwhite

Sheikh

Norton

et al. 2011

Aids

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“…Regarding HIV-infected patients active cytomegalovirus infection has decreased substantially, in current HAART era, to less than 6 cases/100 person-years 87. In one study it was associated with a procoagulant state independently of stage of HIV disease 88.…”

Section: Viral Risk Factorsmentioning

confidence: 99%

Hiv-Associated Venous Thromboembolism

Bibas

Biava²,

Antinori³

2011

Mediterr J Hematol Infect Dis

136

172

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HIV infection has been recognized as a prothrombotic condition and this association has now been proven by a large number of studies with a reported VTE frequency among HIV-infected patients ranging from 0.19% to 7,63 %/year. HIV infection is associated with a two to tenfold increased risk of venous thrombosis in comparison with a general population of the same age. Some risk factors demonstrated a strongest association with VTE such as, low CD4+ cell count especially in the presence of clinical AIDS, protein S deficiency, and protein C deficiency. Whereas other risk factors are still controversial like protease inhibitor therapy, presence of active opportunistic infections and presence of antiphospholipid antibodies, including anticardiolipin antibodies and lupus anticoagulant. Physicians caring for HIV positive patients should be able to recognize and treat not only the well-known opportunistic infections and malignancies associated with this chronic disease, but also be alert to the less well-known complications such as thromboses. Pulmonary embolism should be included in the differential diagnosis when patients with HIV/AIDS have unexplained dyspnea or hypoxemia. In younger individuals with VTE, especially men, without other identifiable risk factors for VTE, HIV should be considered. Because interactions between warfarin and antiretrovirals is possible, health care providers should also be alert to the potential of dangerously high or low INRs when they are giving anticoagulants to patients with HIV infection who are undergoing antiretroviral therapy.

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“…Recently, PROS1 has also been identified to function as a cofactor for tissue factor pathway inhibitor (TFPI), accelerating the inhibition of activated factor Xa (FXa) [5]. GAS6 and PROS1 have been associated with a wide variety of conditions and disorders, including thrombosis [6,7], systemic lupus erythematus [8,9], kidney disorders [10,11], sepsis [12,13], cancer [14,15], pregnancy [16], infections such as human immunodeficiency virus [17] and during the use of oral contraceptives [18]. Interestingly, both proteins exhibit different expression profiles.…”

Section: Introductionmentioning

confidence: 99%

Understanding the functional difference between growth arrest-specific protein 6 and protein S: an evolutionary approach

et al. 2014

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Although protein S (PROS1) and growth arrest-specific protein 6 (GAS6) proteins are homologous with a high degree of structural similarity, they are functionally different. The objectives of this study were to identify the evolutionary origins from which these functional differences arose. Bioinformatics methods were used to estimate the evolutionary divergence time and to detect the amino acid residues under functional divergence between GAS6 and PROS1. The properties of these residues were analysed in the light of their three-dimensional structures, such as their stability effects, the identification of electrostatic patches and the identification potential protein–protein interaction. The divergence between GAS6 and PROS1 probably occurred during the whole-genome duplications in vertebrates. A total of 78 amino acid sites were identified to be under functional divergence. One of these sites, Asn463, is involved in N-glycosylation in GAS6, but is mutated in PROS1, preventing this post-translational modification. Sites experiencing functional divergence tend to express a greater diversity of stabilizing/destabilizing effects than sites that do not experience such functional divergence. Three electrostatic patches in the LG1/LG2 domains were found to differ between GAS6 and PROS1. Finally, a surface responsible for protein–protein interactions was identified. These results may help researchers to analyse disease-causing mutations in the light of evolutionary and structural constraints, and link genetic pathology to clinical phenotypes.

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Relationship between cytomegalovirus infection and procoagulant changes in human immunodeficiency virus‐infected patients

Cited by 14 publications

References 15 publications

Markers of endothelial dysfunction, coagulation and tissue fibrosis independently predict venous thromboembolism in HIV

Markers of endothelial dysfunction, coagulation and tissue fibrosis independently predict venous thromboembolism in HIV

Hiv-Associated Venous Thromboembolism

Understanding the functional difference between growth arrest-specific protein 6 and protein S: an evolutionary approach

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