Publications by authors named "Marlies Boeren"
Article Synopsis
- * The study analyzed how human neural-like cells (neurospheroids) respond to VZV infection compared to Sendai virus (SeV), finding that SeV triggers a strong immune response while VZV appears to evade detection.
- * The research indicates that VZV not only avoids activating the immune system but also disrupts cellular integrity and prompts stress response mechanisms in the long term.
The role of T cell receptor (TCR) diversity in infectious disease susceptibility is not well understood. We use a systems immunology approach on three cohorts of herpes zoster (HZ) patients and controls to investigate whether TCR diversity against varicella-zoster virus (VZV) influences the risk of HZ. We show that CD4 T cell TCR diversity against VZV glycoprotein E (gE) and immediate early 63 protein (IE63) after 1-week culture is more restricted in HZ patients.
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- * A study analyzed genetic data from UK Biobank patients with shingles, focusing on immune responses and risk factors, uncovering significant links between susceptibility and human leukocyte antigens (HLAs).
- * Key findings indicate that variations in the major histocompatibility complex play a crucial role in developing shingles, alongside increased immune responses related to type I interferon, offering new insights into how VZV reactivation affects the immune system.
Lack of strong innate immune reactivity renders macrophages alone unable to control productive Varicella-Zoster Virus infection in an isogenic human iPSC-derived neuronal co-culture model.
Front Immunol
June 2023
Article Synopsis
- Researchers are using human induced pluripotent stem cell (hiPSC)-derived neural models to study the interactions between the Varicella-Zoster Virus (VZV) and the immune system in neurons.
- A new study explored whether macrophages could help activate an antiviral response in VZV-infected hiPSC-neurons, but found the macrophages were ineffective in suppressing the infection.
- RNA sequencing results showed a weak immune response in both infected neurons and co-cultured macrophages, indicating that other immune cells, like T-cells, may be necessary for a strong antiviral response against VZV.
Article Synopsis
- Varicella-zoster virus (VZV) infection mechanisms in human neurons are not well understood due to a lack of effective models for study.
- Researchers created a human-induced pluripotent stem cell (hiPSC)-derived neuronal model that allows for realistic VZV infection, demonstrating that these neurons fail to activate an effective interferon-mediated antiviral response.
- The study reveals that while hiPSC-neurons do not produce interferon-α (IFNα) on their own, they respond well to it when provided externally, suggesting that other cell types in the body may play a crucial role in controlling VZV infection by producing IFNα.
Herpesviruses hijack the MHC class I (MHC I) and class II (MHC II) antigen-presentation pathways to manipulate immune recognition by T cells. First, we illustrate herpes simplex virus-1 (HSV-1) and varicella-zoster virus (VZV) MHC immune evasion strategies. Next, we describe MHC-T cell interactions in HSV-1- and VZV- infected neural ganglia.
View Article and Find Full Text PDFDespite the considerable impact of stroke on both the individual and on society, a neuroprotective therapy for stroke patients is missing. This is partially due to the current lack of a physiologically relevant human in vitro stroke model. To address this problem, we have developed a luminescent human iPSC-derived neurospheroid model that enables real-time read-out of neural viability after ischemia-like conditions.
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- Respiratory syncytial virus (RSV) makes a lot of babies sick and there's no vaccine to prevent it yet.
- Scientists are studying two important proteins, G and F, in RSV that help the virus multiply and see how changes in these proteins might help create a vaccine.
- They found out that certain small changes in the F protein can lead to better immune responses and possibly improve vaccine effectiveness in the future.
Prevention of severe lower respiratory tract infections in infants caused by the human respiratory syncytial virus (hRSV) remains a major public health priority. Currently, the major focus of vaccine development relies on the RSV fusion (F) protein since it is the main target protein for neutralizing antibodies induced by natural infection. The protein conserves 5 N-glycosylation sites, two of which are located in the F2 subunit (N27 and N70), one in the F1 subunit (N500) and two in the p27 peptide (N116 and N126).
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