The spread of anti-establishment politics across Central and Eastern Europe may hold lessons for West European countries.

A number of European countries have witnessed increasing support for anti-establishment parties, most notably in Italy, where Beppe Grillo’s ‘Five Star Movement’ gained over 25 per cent of the vote in this year’s elections. Seán Hanley and Allan Sikk write that while such movements may be new to Western European politics, several anti-establishment parties have experienced similar breakthroughs in Central and Eastern European countries over the last decade. Outlining the results of a study on these parties, they formulate a typology for the conditions under which anti-establishment movements emerge

Economy, corruption or floating voters? Explaining the breakthroughs of Anti-Establishment Reform Parties in Eastern Europe

This paper discusses a new group of parties that we term anti-establishment reform parties (AERPs), which combine moderate social and economic policies with anti-establishment appeals and a desire to change the way politics is conducted. We analyse the electoral breakthroughs of AERPs in Eastern Europe (CEE), the region where AERPs have so been most successful. Examples include the Simeon II National Movement, GERB (Bulgaria), Res Publica (Estonia), New Era (Latvia), TOP09 and Public Affairs (Czech Republic) and Positive Slovenia. We examine the conditions under which such parties broke through in nine CEE states in 1997-2012 using Fuzzy Set Qualitative Comparative Analysis (fsQCA). We find five sufficient causal paths combining high or rising corruption, rising unemployment and party system instability. Rising corruption plays a key role in most pathways but, unexpectedly, AERP breakthroughs are more closely associated with economic good times than bad

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

A prenylated dsRNA sensor protects against severe COVID-19

Inherited genetic factors can influence the severity of COVID-19, but the molecular explanation underpinning a genetic association is often unclear. Intracellular antiviral defenses can inhibit the replication of viruses and reduce disease severity. To better understand the antiviral defenses relevant to COVID-19, we used interferon-stimulated gene (ISG) expression screening to reveal that OAS1, through RNase L, potently inhibits SARS-CoV-2. We show that a common splice-acceptor SNP (Rs10774671) governs whether people express prenylated OAS1 isoforms that are membrane-associated and sense specific regions of SARS-CoV-2 RNAs, or only express cytosolic, nonprenylated OAS1 that does not efficiently detect SARS-CoV-2. Importantly, in hospitalized patients, expression of prenylated OAS1 was associated with protection from severe COVID-19, suggesting this antiviral defense is a major component of a protective antiviral response

'Sagt, wie soll man Stalin danken?' Kurt Maetzig's Ehe im schatten (1947), Roman einer jungen ehe (1952) and the cultural politics of post-war Germany

In Ehe im Schatten and Roman einer jungen Ehe Kurt Maetzig analyses the role of the artist and the changing conceptualisation of aesthetics at two contrasting moments of political crisis. Set during the Third Reich, Ehe im Schatten criticises any attempt to separate art and politics, and exposes the limitations of bourgeois classical drama as a form of political resistance. But despite its radical subject-matter, the film's melodramatic format highlights the difficulties post-war directors working for DEFA faced in breaking with the traditions of cinematography established by Ufa during the 1940s. Five years later, and in a very different political context, Maetzig revisits these issues in Roman einer jungen Ehe. Although the later film mobilises concepts of socialist realism in order to redefine aesthetic agendas in the early 1950s, it too relies on moments of exaggerated pathos to achieve its aims. While the film's idealisation of working-class life in the GDR of the early 1950s was soon undermined by the political events of 1953 and 1956, its presentation of works by, among others, Lessing, Seghers, Zuckmayer, Simonov and Sartre offers a detailed and distinctive perspective on the changing dynamics of cultural politics during the immediate post-war period

East German Film and the Holocaust

Elizabeth Ward, New York, Oxford, Berghahn, 2021, 245 pp., Price $135.00/£99.00 (hardback), ISBN 978-1-78920-747-7