GL11

This lecture describes the extraordinary journey from genotyping Mtb strains to suddenly assessing SARS-CoV-2 variants intensively during the last two years. A journey that can be expressed in one sentence “same same but different”.

Classical infectious disease epidemiology methods enable us to study the incidence, spread and dynamics of infectious diseases in populations over time, taking into account host, pathogen and environmental factors and devise smart intervention strategies. Adding modern molecular genotyping tools, such as phylogenomics, enable us to track the specific pathogens more accurately and study the genome (RNA/DNA) in details. Thus, classical + molecular infectious disease epidemiology, enables us to associate specific genes/mutations with specific pathogen properties such as e.g. receptor binding, antibody response and diagnostic impact. Ideally, it enables us to predict whether specific strains/variants will be more harmful than others, the so-called “variants of concern”. For SARS-CoV-2, variants with reduced effect of neutralizing antibodies, increased transmissibility, increased disease severity, and/or diagnostic impairment. For M. tuberculosis; strains with increased multi-drug resistance, increased virulence and/or increased transmission.

Mutations are the spice of life! Mutations occurs naturally following infection. The vast majority of mutations do not affect the pathogens ability to spread or cause disease, as they do not alter major proteins involved in infection. However, these non-significant mutations are outcompeted by mutations that are beneficial for the pathogen. Therefore, it remains an important priority to monitor circulating pathogens for key mutation(s) discovering the next pandemic threat in due time.