Early-career general practitioners' career intentions in Estonia: A qualitative study.

BACKGROUND: The shortage of general practitioners (GPs) is a worsening problem in many countries and poses a threat to the services provided by primary care and by extension for the entire healthcare system. Issues with GP workforce recruitment and retention can be reasons for this shortage. OBJECTIVES: To describe GP trainees and newly qualified GPs experiences and perceptions on how their training and early experiences of work influence their career intentions in primary care in Estonia. METHODS: A qualitative study with GP trainees (n = 12) and newly qualified GPs (n = 13) using semi-structured group interviews (n = 6) was conducted. Interviews were conducted from October until November 2020. Data were analysed using thematic analysis with NVivo Software. RESULTS: Although early-career GPs in Estonia envision their future roles as GP practice owners with patient list, this is often postponed due to various reasons. Early-career GPs expressed a sense of unpreparedness to fill all the roles of GPs' and found the process of establishing a GP practice and taking on a patient lists very complicated. They value work-life balance and prefer workplaces, which offer flexible working conditions. CONCLUSION: Potential strategies were identified to enhance the willingness of early-career GPs to continue their career as GP practice owners with patient list: improving the GP training program by placing more emphasis on managing skills and making the process of establishing GP practice and taking on a patient list less bureaucratic and more accessible.

This study highlights the career intentions of GP trainees and newly qualified GPs in Estonia.Participants of this study perceive the many different roles of being a GP as very challenging.Understanding early-career GPs ideas about the future work environments can be helpful in shaping future workforce strategies.

Lack of functional TCR-epitope interaction is associated with herpes zoster through reduced downstream T cell activation.

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. Single-cell RNA and TCR sequencing of VZV-specific T cells shows that T cell activation pathways are significantly decreased after stimulation with VZV peptides in convalescent HZ patients. TCR clustering indicates that TCRs from HZ patients co-cluster more often together than TCRs from controls. Collectively, our results suggest that not only lower VZV-specific TCR diversity but also reduced functional TCR affinity for VZV-specific proteins in HZ patients leads to lower T cell activation and consequently affects the susceptibility for viral reactivation.

Unravelling the immune signature of herpes zoster: Insights into pathophysiology and the HLA risk profile.

The varicella-zoster virus (VZV) infects over 95% of the population. VZV reactivation causes herpes zoster (HZ), known as shingles, primarily affecting the elderly and immunocompromised individuals. However, HZ can also occur in otherwise healthy individuals. We analyzed the immune signature and risk profile in HZ patients using a genome-wide association study across different UK Biobank HZ cohorts. Additionally, we conducted one of the largest HZ HLA association studies to date, coupled with transcriptomic analysis of pathways underlying HZ susceptibility. Our findings highlight the significance of the MHC locus for HZ development, identifying five protective and four risk HLA alleles. This demonstrates that HZ susceptibility is largely governed by variations in the MHC. Furthermore, functional analyses revealed the upregulation of type I interferon and adaptive immune responses. These findings provide fresh molecular insights into the pathophysiology and the activation of innate and adaptive immune responses triggered by symptomatic VZV reactivation.