How did Sweden Fail the Pandemic?

Sweden has since the start of the pandemic a COVID-19 mortality rate that is 4 to 10 times higher than in the other Nordic countries. Also, measured as age-standardized all-cause excess mortality in the first half of 2020 compared to previous years Sweden failed in comparison with the other Nordic countries, but only among the elderly. Sweden has large socioeconomic and ethnic inequalities in COVID-19 mortality. Geographical, ethnic, and socioeconomic inequalities in mortality can be due to differential exposure to the virus, differential immunity, and differential survival. Most of the country differences are due to differential exposure, but the socioeconomic disparities are mainly driven by differential survival due to an unequal burden of comorbidity. Sweden suffered from an unfortunate timing of tourists returning from virus hotspots in the Alps and Sweden's government response came later and was much more limited than elsewhere. The government had an explicit priority to protect the elderly in nursing and care homes but failed to do so. The staff in elderly care are less qualified and have harder working conditions in Sweden, and they lacked adequate care for the clients. Sweden has in recent years diverged from the Scandinavian welfare model by strong commercialization of primary care and elderly care.

Pneumococcal colonization impairs nasal and lung mucosal immune responses to Live Attenuated Influenza Vaccination in adults

ABSTRACTInfluenza virus infections affect millions of people annually. Current available vaccines provide varying rates of protection. There is a knowledge gap on how the nasal microbiota, particularly established pneumococcal colonization, shapes the response to influenza vaccination. In this study, we inoculated healthy adults with live S. pneumoniae and vaccinated them three days later with either TIV or LAIV. Vaccine-induced immune responses were assessed in nose, blood and lung. Nasal pneumococcal colonization had no impact upon TIV-induced antibody responses to influenza, which manifested in all compartments. However, pre-existing pneumococcal colonization dampened LAIV-mediated mucosal antibody responses, primarily IgA in the nose and IgG in the lung. Pulmonary influenza-specific cellular responses were more apparent in the LAIV group compared to either TIV or an unvaccinated group. These results indicate that TIV and LAIV elicit differential immunity to adults and that LAIV immunogenicity is diminished by the nasal presence of S. pneumoniae. This important confounder should be considered when assessing LAIV efficacy.

AN EPIDEMIC MODEL STRUCTURED BY HOST IMMUNITY

In this paper we introduce a physiologically structured SIR epidemic model where the individuals are distributed according to their immune status. An individual immune status is assumed to increase during the infectious period and remain unchanged after the recovery. Recovered individuals can become reinfected at a rate which is a decreasing function of their immune status. We find that the possibility of reinfection of recovered individuals results in subthreshold endemic equilibria. The differential immunity of the infectious individuals leads to multiple nontrivial equilibria in the superthreshold case. We present an example that has exactly three nontrivial equilibria. We also analyze the local stability of equilibria.