ABSTRACT
Type I interferon (IFN-I) signalling represents a major target for modulation in a virus' bid for latency. IFN-I perturbations are also present in such as Alzheimer's disease (AD) and multiple sclerosis (MS), where viral infections are known to increase symptomatic burden. IFN-I modulation such as via IFNß-1a, an established MS treatment, has been researched to a limited extent to both AD and COVID-19. In this mini review, we present emerging research on trained immunity as a pathogenetic basis for Alzheimer's disease and the emerging context for IFNß-1a repositioning, via mechanisms shared with multiple sclerosis and induced by viral infections.
Subject(s)
Alzheimer Disease , COVID-19 , Multiple Sclerosis , Virus Diseases , Humans , Interferon-betaABSTRACT
Since the outbreak of COVID-19, the world has raced to understand and accurately diagnose infection caused by SARS-CoV-2. Today, hundreds of commercial antibody tests are on the market despite often lacking proper validation and with unsatisfactory sensitivity and/or specificity. In addition, many questions related to the humoral response remain unresolved, although research is carried out at an unprecedented speed. Despite the shortcomings, serological assays have an important part to play in combating the pandemic by aiding in diagnosis and sero-epidemiological studies. However, careful attention must be paid to the application of serology and the interpretation of serological data-especially in low prevalence regions, both at an individual and at a population level. In this article, we argue that serological results are often misinterpreted, and in the eagerness to be first, methodological rigor is often taking a backseat.