scholarly journals Overexpression of PD-1 on Peripheral Blood Lymphocytes in Patients with Idiopathic Pulmonary Arterial Hypertension and Its Association with High Viral Loads of Epstein-Barr Virus and Poor Clinical Parameters

2020 ◽  
Vol 9 (6) ◽  
pp. 1966 ◽  
Author(s):  
Michał Tomaszewski ◽  
Ewelina Grywalska ◽  
Andrzej Tomaszewski ◽  
Piotr Błaszczak ◽  
Marcin Kurzyna ◽  
...  
Keyword(s):  
T Cells ◽  
Immune System ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Epstein Barr Virus ◽  
Idiopathic Pulmonary Arterial Hypertension ◽  
Barr Virus ◽  
Ebv Infection ◽  
Pulmonary Arterial ◽  
Epstein Barr

Idiopathic pulmonary arterial hypertension (IPAH) is a rare but severe disease with the elevated blood pressure in the pulmonary arteries without a known trigger of vascular remodelling. It leads to the right heart failure with reduced survival. Changes in the immunological landscape of the lungs and the periphery are common in IPAH patients, suggesting an immune system dysfunction. A cohort of 25 IPAH patients was enrolled in our study to investigate a link between the patient’s clinical status, immune parameters of the blood, and the Epstein–Barr virus (EBV) infection. We found significant alterations of the patients’ peripheral blood parameters. Therein, T lymphocytes and NK cell counts were decreased in the IPAH patients’ blood, while the proportion of regulatory T cells was increased. Additionally, levels of proinflammatory cytokines interleukin-6 (IL-6), IL-2, and interferon-gamma (IFN-γ) were elevated. We identified a weak correlation between EBV loads and IPAH patients’ clinical state (r = 0.54) and between EBV loads and overexpression of PD-1 on helper T cells (r = 0.56). We speculate that a significant dysregulation of the immune system homeostasis observed in IPAH patients may contribute to increased susceptibility of those patients to EBV infection, yet further longitudinal studies are required to characterize this relation in detail.

scholarly journals Chemotherapy Improved Pulmonary Arterial Hypertension in a Patient with Chronic-Active Epstein-Barr Virus Infection

2020 ◽  
Vol 61 (1) ◽  
pp. 191-194
Author(s):  
Satoshi Akagi ◽  
Takashi Miki ◽  
Yasuhisa Sando ◽  
Nobuharu Fujii ◽  
Toshihiro Sarashina ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Virus Infection ◽  
Arterial Hypertension ◽  
Epstein Barr Virus ◽  
Epstein Barr Virus Infection ◽  
Barr Virus ◽  
Pulmonary Arterial ◽  
Epstein Barr ◽  
Barr Virus Infection

Pulmonary arterial hypertension associated with chronic active Epstein-Barr virus infection

2015 ◽  
Vol 57 (4) ◽  
pp. 731-734 ◽  
Author(s):  
Yutaka Fukuda ◽  
Nobuo Momoi ◽  
Mitsuko Akaihata ◽  
Katsutoshi Nagasawa ◽  
Masaki Mitomo ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Virus Infection ◽  
Arterial Hypertension ◽  
Epstein Barr Virus ◽  
Epstein Barr Virus Infection ◽  
Barr Virus ◽  
Pulmonary Arterial ◽  
Epstein Barr ◽  
Barr Virus Infection

scholarly journals MicroRNAs of Epstein-Barr Virus Attenuate T-Cell-Mediated Immune ControlIn Vivo

mBio ◽  
2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Anita Murer ◽  
Julia Rühl ◽  
Andrea Zbinden ◽  
Riccarda Capaul ◽  
Wolfgang Hammerschmidt ◽  
...  
Keyword(s):  
T Cells ◽  
Immune System ◽  
T Cell ◽  
Immune Responses ◽  
Epstein Barr Virus ◽  
Tumor Formation ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

ABSTRACTThe human persistent and oncogenic Epstein-Barr virus (EBV) was one of the first viruses that were described to express viral microRNAs (miRNAs). These have been proposed to modulate many host and viral functions, but their predominant rolein vivohas remained unclear. We compared recombinant EBVs expressing or lacking miRNAs duringin vivoinfection of mice with reconstituted human immune system components and found that miRNA-deficient EBV replicates to lower viral titers with decreased frequencies of proliferating EBV-infected B cells. In response, activated cytotoxic EBV-specific T cells expand to lower frequencies than during infection with miRNA-expressing EBV. However, when we depleted CD8+T cells the miRNA-deficient virus reached similar viral loads as wild-type EBV, increasing by more than 200-fold in the spleens of infected animals. Furthermore, CD8+T cell depletion resulted in lymphoma formation in the majority of animals after miRNA-deficient EBV infection, while no tumors emerged when CD8+T cells were present. Thus, miRNAs mainly serve the purpose of immune evasion from T cellsin vivoand could become a therapeutic target to render EBV-associated malignancies more immunogenic.IMPORTANCEEpstein-Barr virus (EBV) infects the majority of the human population and usually persists asymptomatically within its host. Nevertheless, EBV is the causative agent for infectious mononucleosis (IM) and for lymphoproliferative disorders, including Burkitt and Hodgkin lymphomas. The immune system of the infected host is thought to prevent tumor formation in healthy virus carriers. EBV was one of the first viruses described to express miRNAs, and many host and viral targets were identified for thesein vitro. However, their role during EBV infectionin vivoremained unclear. This work is the first to describe that EBV miRNAs mainly increase viremia and virus-associated lymphomas through dampening antigen recognition by adaptive immune responses in mice with reconstituted immune responses. Currently, there is no prophylactic or therapeutic treatment to restrict IM or EBV-associated malignancies; thus, targeting EBV miRNAs could promote immune responses and limit EBV-associated pathologies.

scholarly journals Pulmonary Arterial Hypertension Associated with Chronic Active Epstein-Barr Virus Infection

2011 ◽  
Vol 50 (2) ◽  
pp. 119-124 ◽  
Author(s):  
Takahiro Hashimoto ◽  
Yasushi Sakata ◽  
Kentaro Fukushima ◽  
Tetsuo Maeda ◽  
Yoh Arita ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Virus Infection ◽  
Arterial Hypertension ◽  
Epstein Barr Virus ◽  
Epstein Barr Virus Infection ◽  
Barr Virus ◽  
Pulmonary Arterial ◽  
Epstein Barr ◽  
Barr Virus Infection

scholarly journals Selective Induction of Th2-Attracting Chemokines CCL17 and CCL22 in Human B Cells by Latent Membrane Protein 1 of Epstein-Barr Virus

2004 ◽  
Vol 78 (4) ◽  
pp. 1665-1674 ◽  
Author(s):  
Takashi Nakayama ◽  
Kunio Hieshima ◽  
Daisuke Nagakubo ◽  
Emiko Sato ◽  
Masahiro Nakayama ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
Regulatory T Cells ◽  
Epstein Barr Virus ◽  
Cytotoxic T Cells ◽  
Th2 Cells ◽  
Th1 Cells ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

ABSTRACT Chemokines are likely to play important roles in the pathophysiology of diseases associated with Epstein-Barr virus (EBV). Here, we have analyzed the repertoire of chemokines expressed by EBV-infected B cells. EBV infection of B cells induced expression of TARC/CCL17 and MDC/CCL22, which are known to attract Th2 cells and regulatory T cells via CCR4, and also upregulated constitutive expression of MIP-1α/CCL3, MIP-1β/CCL4, and RANTES/CCL5, which are known to attract Th1 cells and cytotoxic T cells via CCR5. Accordingly, EBV-immortalized B cells secreted these chemokines, especially CCL3, CCL4, and CCL22, in large quantities. EBV infection or stable expression of LMP1 also induced CCL17 and CCL22 in a B-cell line, BJAB. The inhibitors of the TRAF/NF-κB pathway (BAY11-7082) and the p38/ATF2 pathway (SB202190) selectively suppressed the expression of CCL17 and CCL22 in EBV-immortalized B cells and BJAB-LMP1. Consistently, transient-transfection assays using CCL22 promoter-reporter constructs demonstrated that two NF-κB sites and a single AP-1 site were involved in the activation of the CCL22 promoter by LMP1. Finally, serum CCL22 levels were significantly elevated in infectious mononucleosis. Collectively, LMP1 induces CCL17 and CCL22 in EBV-infected B cells via activation of NF-κB and probably ATF2. Production of CCL17 and CCL22, which attract Th2 and regulatory T cells, may help EBV-infected B cells evade immune surveillance by Th1 cells. However, the concomitant production of CCL3, CCL4, and CCL5 by EBV-infected B cells may eventually attract Th1 cells and cytotoxic T cells, leading to elimination of EBV-infected B cells at latency III and to selection of those with limited expression of latent genes.

Alterations in circulating helper T-cells in idiopathic pulmonary arterial hypertension

2019 ◽  
Author(s):  
Denise van Uden ◽  
Menno Van Nimwegen ◽  
Thomas Koudstaal ◽  
Peter Heukels ◽  
Jennifer Van Hulst ◽  
...  
Keyword(s):  
T Cells ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Idiopathic Pulmonary Arterial Hypertension ◽  
Helper T Cells ◽  
Pulmonary Arterial

ASSOCIATION OF EPSTEIN-BARR VIRUS WITH LEIOMYOSARCOMAS IN YOUNG PEOPLE WITH AIDS

PEDIATRICS ◽  
1996 ◽  
Vol 98 (2) ◽  
pp. 347-347
Author(s):  
Maritza Navarro ◽  
I. Celine Hanson
Keyword(s):  
Smooth Muscle ◽  
Immune System ◽  
Epstein Barr Virus ◽  
Receptor Expression ◽  
Barr Virus ◽  
Ebv Infection ◽  
Smooth Muscle Tumors ◽  
Epstein Barr ◽  
Negative Controls ◽  
Hiv Negative

EBV was found in all smooth muscle tumors from the six HIV-infected cases, but not in smooth muscle tumors from HIV-negative controls. All tumors studied stained for CD21 (EBV receptor), but levels were higher on tumor cells from HIV-infected cases than controls. This suggests that perturbation of the immune system (as in AIDS) may increase the production of the EBV receptor and/or that EBV infection itself causes increased receptor expression. It is postulated that EBV may contribute to smooth muscle tumorigenesis in HIV infection and potentially in other immunosuppressed states.

Sign in / Sign up

Export Citation Format

Share Document