[Vaccination and cardiovascular diseases].

Respiratory tract infections with influenza, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and respiratory syncytial (RS) viruses and pneumococci as well as endogenous reactivation of varicella zoster viruses presenting as herpes zoster, are associated with adverse cardiovascular outcomes, such as myocardial infarction or hospitalization for heart failure. Effective prevention of these events, particularly through influenza and pneumococcal vaccination, is well established and cost-effective. Despite guideline recommendations to vaccinate older patients and people at risk, vaccination rates in these population groups remain suboptimal and below average in international comparison.

Association of respiratory infections and the impact of vaccinations on cardiovascular diseases.

Influenza, pneumococcal, severe acute respiratory syndrome coronavirus 2, and respiratory syncytial virus infections are important causes of high morbidity and mortality in the elderly. Beyond the burden of infectious diseases, they are also associated with several non-infectious complications like cardiovascular events. A growing body of evidence in prospective studies and meta-analyses has shown the impact of influenza and pneumococcal vaccines on types of cardiovascular outcomes in the general population.

Reactive Oxidative Species-Modulated Ca Release Regulates β Integrin Activation on CD4 CD28 T Cells of Acute Coronary Syndrome Patients.

The number and activity of T cell subsets in the atherosclerotic plaques are critical for the prognosis of patients with acute coronary syndrome. β Integrin activation is pivotal for T cell recruitment and correlates with future cardiac events. Despite this knowledge, differential regulation of adhesiveness in T cell subsets has not been explored yet.

High-resolution analysis of Merkel Cell Polyomavirus in Merkel Cell Carcinoma reveals distinct integration patterns and suggests NHEJ and MMBIR as underlying mechanisms.

Merkel Cell Polyomavirus (MCPyV) is the etiological agent of the majority of Merkel Cell Carcinomas (MCC). MCPyV positive MCCs harbor integrated, defective viral genomes that constitutively express viral oncogenes. Which molecular mechanisms promote viral integration, if distinct integration patterns exist, and if integration occurs preferentially at loci with specific chromatin states is unknown.