T Cell Subsets in HIV Infected Patients after Successful Combination Antiretroviral Therapy: Impact on Survival after 12 Years

Rönsholt, Frederikke Falkencrone; Ostrowski, Sisse Rye; Katzenstein, Terese L.; Ullum, Henrik; Gerstoft, Jan

doi:10.1371/journal.pone.0039356

Cited by 11 publications

(6 citation statements)

References 31 publications

(27 reference statements)

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“…Other studies have reported alterations in the T-cell subsets in treated PWH, but results have been conflicting. Thus, elevated proportions of immune activation, senescence and apoptosis have been reported (8,10,22,23), while other studies found comparable proportion of activated (24,25) or senescent T-cells in PWH and controls (8,10,26). However, most of the previous studies on T-cell proportions were small and did not adjust for lifestyle.…”

Section: Discussionmentioning

confidence: 96%

Impact of Age and HIV Status on Immune Activation, Senescence and Apoptosis

et al. 2020

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Introduction: Residual immune dysfunctions, resembling those that occur during normal aging, may persist even in well-treated people with HIV (PWH), and accelerated aging has been proposed. We aimed to determine if HIV infection is an independent risk factor for T-cell immune dysfunctions including increased immune activation, senescence and apoptosis. Moreover, in PWH we aimed to identify the associations between age and immune activation, senescence and apoptosis. Materials and Methods: We included 780 PWH with suppressed viral replication (<50 copies/mL) and absence of hepatitis B and hepatitis C co-infection and 65 uninfected controls from the Copenhagen Co-morbidity in HIV Infection (COCOMO) Study. Flow cytometry was used to determine T-cell activation (CD38+HLA-DR+), senescence (CD28-CD57+), and apoptosis (CD28-CD95+). T-cell subsets are reported as proportions of CD4+ and CD8+ T-cells. We defined an elevated proportion of a given T-cell subset as above the 75th percentile. Regression models were used to determine the association between HIV status and T-cell subset and in PWH to determine the association between age or HIV-specific risk factors and T-cell subsets. Furthermore, an interaction between HIV status and age on T-cell subsets was investigated with an interaction term in models including both PWH and controls. Models were adjusted for age, sex, BMI, and smoking status. Results: In adjusted models a positive HIV status was associated with elevated proportions of CD8+ activated (p = 0.009), CD4+ senescent (p = 0.004), CD4+ apoptotic (p = 0.002), and CD8+ apoptotic (p = 0.003) T-cells. In PWH a 10-year increase in age was associated with higher proportions of CD4+ and CD8+ senescent (p = 0.001 and p < 0.001) and CD4+ and CD8+ apoptotic T-cells (p < 0.001 and p < 0.001). However, no interaction between HIV status and age was found.

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Section: Discussionmentioning

confidence: 96%

Impact of Age and HIV Status on Immune Activation, Senescence and Apoptosis

et al. 2020

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“…One of these patients experienced a viraemic bleep of 8888 copies/mL on the day of sampling and was excluded, leaving 70 patients who participated in the present study. The patients who died during the follow up period and their causes of death have been described previously [4].…”

Section: Methodsmentioning

confidence: 99%

Persistent Inflammation and Endothelial Activation in HIV-1 Infected Patients after 12 Years of Antiretroviral Therapy

et al. 2013

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ObjectiveThe study investigated markers of inflammation and endothelial activation in HIV infected patients after 12 years of successful combination antiretroviral treatment (cART).MethodsInflammation and endothelial activation were assessed by measuring levels of immunoglobulins, β2-microglobulin, interleukin (IL) 8, tumor necrosis factor α (TNFα), vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), sE-Selectin, and sP-Selectin.ResultsHIV infected patients had higher levels of β2-microglobulin, IL-8, TNFα, and sICAM-1 than uninfected controls, and HIV infected patients lacked correlation between platelet counts and sP-Selectin levels found in uninfected controls.ConclusionDiscrete signs of systemic and vascular inflammation persist even after very long term cART.

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“…In regions endemic for NCC, coinfected patients with HIV most frequently have multiple parenchymal lesions seen in 61% to 79.3% of cases [21]. In addition, anthelminthic and antiretroviral treatments (ARTs) could influence the course of the disease as well as the host responses and subsequent clinical presentations [3,18].…”

Section: Epidemiology and Clinical Presentation Of Tsct And Nccmentioning

confidence: 99%

“…Despite the presence of symptoms in NCC and HIV patients, little is known about the influence of HIV infection on the frequency, clinical course, and pathogenesis of NCC. A few number of NCC patients coinfected with HIV with very low CD4 + cell counts and high viral loads commonly do not develop cerebral symptoms, but, after initiation of ART, these patients develop a profound pathologic inflammatory reaction characterized by a sudden increase in activated immune memory CD4 + CD45RO + cells with a significant CD8 + cytotoxic T cell response associated with CSF inflammation [3,74]. Nevertheless, very early initiation of ART in HIV infection only has been shown to normalize CSF immune activation markers such as neopterin, CXCL10, CCL2, and IL-6 and related inflammation [75].…”

Section: Anthelmintic Treatment Hiv and Impacts On The Immune Respomentioning

confidence: 99%

“…The reason(s) for this might also be linked to parasite-induced anti-inflammatory immunity in the host, as discussed in the section "Immune regulation during NCC." Among other important parameters, the location (parenchyma and extraparenchyma) and type of cysts, the immune environment of the parasite as well as the interplay between the host immune cells and the excretory-secretory (ES) parasite proteins or bystander viral infections, such as HIV, are possibly important causes of the exacerbation in the infection and the different clinical presentations observed in endemic regions [3,4]. Parenchymal and extraparenchymal NCC are two distinct diseases from clinical, immunological, and pathophysiological perspectives.…”

Section: Introductionmentioning

confidence: 99%

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Host immune responses during Taenia solium Neurocysticercosis infection and treatment

et al. 2020

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Taenia solium cysticercosis and taeniasis (TSCT), caused by the tapeworm T. solium, is a foodborne and zoonotic disease classified since 2010 by WHO as a neglected tropical isease. It causes considerable impact on health and economy and is one of the leading causes of acquired epilepsy in most endemic countries of Latin America, Sub-Saharan Africa, and Asia. There is some evidence that the prevalence of TSCT in high-income countries has recently increased, mainly due to immigration from endemic areas. In regions endemic for TSCT, human cysticercosis can manifest clinically as neurocysticercosis (NCC), resulting in epileptic seizures and severe progressive headaches, amongst other neurological signs and/or symptoms. The development of these symptoms results from a complex interplay between anatomical cyst localization, environmental factors, parasite's infective potential, host genetics, and, especially, host immune responses. Treatment of individuals with active NCC (presence of viable cerebral cysts) with anthelmintic drugs together with steroids is usually effective and, in the majority, reduces the number and/or size of cerebral lesions as well as the neurological symptoms. However, in some cases, treatment may profoundly enhance anthelmintic inflammatory responses with ensuing symptoms, which, otherwise, would have remained silent as long as the cysts are viable. This intriguing silencing process is not yet fully understood but may involve active modulation of host responses by cyst-derived immunomodulatory components released directly into the surrounding brain tissue or by the induction of regulatory networks including regulatory T cells (Treg) or regulatory B cells (Breg). These processes might be disturbed once the cysts undergo treatment-induced apoptosis and necrosis or in a coinfection setting such as HIV. Herein, we review the current literature regarding the immunology and pathogenesis of NCC with a highlight on the mobilization of immune cells during human NCC and their interaction with viable and degenerating cysticerci. Moreover, the immunological parameters associated with NCC in people living with HIV/AIDS and treatments are discussed.

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T Cell Subsets in HIV Infected Patients after Successful Combination Antiretroviral Therapy: Impact on Survival after 12 Years

Cited by 11 publications

References 31 publications

Impact of Age and HIV Status on Immune Activation, Senescence and Apoptosis

Impact of Age and HIV Status on Immune Activation, Senescence and Apoptosis

Persistent Inflammation and Endothelial Activation in HIV-1 Infected Patients after 12 Years of Antiretroviral Therapy

Host immune responses during Taenia solium Neurocysticercosis infection and treatment

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