viremia/protease

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Relapse of Kaposi's Sarcoma and HHV-8 viremia in an HIV-infected patient switching from protease inhibitor to integrase inhibitor-based antiretroviral therapy.

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Combination antiretroviral therapy (cART) reduced the incidence of Kaposi's Sarcoma (KS), mainly mediated by the suppression of HIV replication and the recovery of the immune system. The effect of specific classes of antiretrovirals on KS remains unclear. However, both in vitro and clinical studies

Inflammatory, procoagulant markers and HIV residual viremia in patients receiving protease inhibitor monotherapy or triple drug therapy: a cross-sectional study.

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BACKGROUND Protease inhibitor monotherapy is associated with more frequent episodes of viral rebounds above 50 copies/mL than triple therapy. OBJECTIVE To evaluate if, compared to triple-drug therapy, protease inhibitor monotherapy is associated with increased levels of inflammatory/procoagulant

Low level HIV viremia is more frequent under protease-inhibitor containing firstline therapy than under NNRTI-regimens.

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BACKGROUND An association of persistent low level viremia (LLV) below 500 copies/mL and a higher risk of therapy failure is still point of controversial discussion. Furthermore, it seems that LLV occurs more frequently in patients with protease-inhibitor regimens than in NNRTI- / or

Viremia copy-years as a predictive marker of all-cause mortality in HIV-1-infected patients initiating a protease inhibitor-containing antiretroviral treatment.

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BACKGROUND Viremia copy-years (VCY) has been reported as a short-term predictor of mortality. We evaluated the association of this parameter with 10-year outcome within the APROCO-COPILOTE cohort. METHODS Prospective data from 1281 HIV-1-infected patients who started a first protease

Characterization of low level viraemia in HIV-infected patients receiving boosted protease inhibitor-based antiretroviral regimens.

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To understand the pathogenesis of low level viraemia (LLV) in HIV-infected patients on boosted protease inhibitors (PI/b), we enrolled 34 subjects with a median HIV-RNA 79 copies/mL and followed them for 15 months. Samples for next generation sequencing were collected at three time-points. Two

Impact of treatment with human immunodeficiency virus (HIV) protease inhibitors on hepatitis C viremia in patients coinfected with HIV.

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The impact of human immunodeficiency virus (HIV) protease inhibitors on hepatitis C (HCV) viremia was assessed in 19 patients infected with both HIV and HCV. HIV and HCV RNA levels were measured before and during treatment with protease inhibitors. Before treatment, mean levels of HCV RNA were 5.3

Systemic inflammation and residual viraemia in HIV-positive adults on protease inhibitor monotherapy: a cross-sectional study.

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BACKGROUND Increased levels of markers of systemic inflammation have been associated with serious non-AIDS events even in patients on fully suppressive antiretroviral therapy. We explored residual viremia and systemic inflammation markers in patients effectively treated with ritonavir-boosted

Intermittent episodes of detectable HIV viremia in patients receiving nonnucleoside reverse-transcriptase inhibitor-based or protease inhibitor-based highly active antiretroviral therapy regimens are equivalent in incidence and prognosis.

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BACKGROUND Intermittent episodes of detectable human immunodeficiency virus (HIV) viremia (hereafter referred to as "blips") are generally not predictive of subsequent virologic failure. Limited data are available for patients treated with nonnucleoside reverse-transcriptase inhibitor (NNRTI)-based

Detectability of HIV residual viremia despite therapy is highly associated with treatment with a protease inhibitor-based combination ART.

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Background: HIV persistence despite therapy contributes to chronic immune activation and inflammation, increasing the risk of aging-associated events in HIV-infected individuals.Objectives: To better understand the complex link between clinical and treatment features and HIV

Intermittent viremia during first-line, protease inhibitors-containing therapy: significance and relationship with drug resistance.

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BACKGROUND In HIV-infected patients on first-line antiretroviral therapy, the significance of intermittent viremia and their relationship with drug resistance remain unclear. OBJECTIVE To study the virological characteristics of intermittent viremia (IV) and the association between IV and later

Genotypic and phenotypic cross-resistance patterns to lopinavir and amprenavir in protease inhibitor-experienced patients with HIV viremia.

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Genotypic correlates of reduced phenotypic susceptibility to amprenavir (APV) and lopinavir (LPV) were examined in 271 HIV isolates from 207 protease inhibitor (PI)-experienced subjects. All samples were from LPV-naive subjects; two were from APV-experienced subjects. Using a fold resistance (FR) of

Maintaining reduced viral fitness and CD4 response in HIV-infected patients with viremia receiving a boosted protease inhibitor.

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When fully suppressive regimens are not available, incompletely suppressive regimens also provide immunologic benefits. In this study, with stable background therapy, human immunodeficiency virus (HIV)-infected patients who were randomized to receive atazanavir or boosted atazanavir, compared with

Time to HIV-1 RNA suppression below 5 copies/ml during first-line protease inhibitor-based antiretroviral treatment - any impact of residual viremia on treatment success?

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When antiretroviral treatment suppresses HIV RNA levels to below 50 copies/ml, traces of viremia may still be detected with more sensitive assays. In the ARTEMIS trial, 689 antiretroviral treatment-naive patients were randomized to tenofovir/emtricitabine plus either darunavir/ritonavir (n = 343) or

Lack of benefit of protease inhibitors on HCV viremia in HIV-infected patients.

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Evolution of protease and reverse transcriptase inhibitor resistance-associated mutations in HIV-1-infected protease inhibitor-treated patients with persistent low viraemia.

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