Background Variations in the age patterns and magnitudes of excess deaths, as well as differences in population sizes and age structures, make cross-national comparisons of the cumulative mortality impacts of the COVID-19 pandemic challenging. Life expectancy is a widely used indicator that provides a clear and cross-nationally comparable picture of the population-level impacts of the pandemic on mortality. Methods Life tables by sex were calculated for 29 countries, including most European countries, Chile and the USA, for 2015–2020. Life expectancy at birth and at age 60 years for 2020 were contextualized against recent trends between 2015 and 2019. Using decomposition techniques, we examined which specific age groups contributed to reductions in life expectancy in 2020 and to what extent reductions were attributable to official COVID-19 deaths. Results Life expectancy at birth declined from 2019 to 2020 in 27 out of 29 countries. Males in the USA and Lithuania experienced the largest losses in life expectancy at birth during 2020 (2.2 and 1.7 years, respectively), but reductions of more than an entire year were documented in 11 countries for males and 8 among females. Reductions were mostly attributable to increased mortality above age 60 years and to official COVID-19 deaths. Conclusions The COVID-19 pandemic triggered significant mortality increases in 2020 of a magnitude not witnessed since World War II in Western Europe or the breakup of the Soviet Union in Eastern Europe. Females from 15 countries and males from 10 ended up with lower life expectancy at birth in 2020 than in 2015.

Interferon stimulates the expression of a number of genes encoding enzymes with antiviral activities, including myxovirus resistance-1 (MxA), 2-5-oligoadenylate synthetase 1 (OAS-1) and double-stranded RNA-dependent protein kinase (PKR). We examined whether polymorphisms in these genes influenced the outcome of hepatitis C virus (HCV) infection. We observed a lower frequency of the GG genotype at position À88 in the MxA gene promoter in self-limiting HCV infection (OR ¼ 0.56; 95% CI: 0.35-0.8; P ¼ 0.010) and in nonresponders to therapy (OR ¼ 0.49; 95% CI: 0.25-0.95; P ¼ 0.020). This genotype predominantly influenced the outcome of treatment in patients with viral genotype 1 (OR ¼ 0.22 95% CI: 0.07-0.67; P ¼ 0.002). A polymorphism in the 3 0 -untranslated region of the OAS-1 gene was associated with outcome of infection (GG genotype less frequent in self-limiting infection: OR ¼ 0.43; 95% CI: 0.21-0.86; P ¼ 0.010). A polymorphism at position À168 in the promoter region of the PKR gene was associated with self-limiting infection (CT genotype: OR ¼ 2.75; 95% CI: 1.45-5.24; P ¼ 0.002). Further associations were found with a CGG trinucleotide repeat in the 5 0 UTR region of the PKR gene. Polymorphisms in the interferon-induced genes, MxA, OAS-1 and PKR appear thus associated with HCV outcome.