One or several betrayals?: Or, when is betrayal treason? Genet, Arlt and the Argentine liberal project

Betrayal is one of the key narrative tropes in the fiction of the Argentine writer Roberto Arlt. The psychological and existential implications of the betrayals found in novels such as El juguete rabioso (1926) and El amor brujo (1933) have attracted much critical comment, as have the links between the betrayals found in Arlt's fiction and the work of Jean Genet. Arlt's oeuvre has been read in relation to the turbulent political context of 1920s and 30s Argentina, in particular the failure of the Liberal Project of economic development through immigration that was introduced after the fall of the dictator Juan Manuel de Rosas in 1852, the economic collapse of 1929 and the ensuing military coup of 1930. Critics have suggested that betrayal in Arlt represents an attack on bourgeois hypocrisy, a middle-class attempt at transcending one's environment, or a reversal of dominant social values. This paper however intends to deepen the understanding of betrayal in Arlt's fiction by examining it as a political gesture, a quality overlooked by many studies. A reading of the political nature of betrayal in Genet's work and an engagement with Bersani's queer reading of Funeral Rites alongside Said's analysis of Genet as an anti-identarian revolutionary, allows the reader of Arlt to reassess the political gesture contained in betrayal, and to move towards a reading of the development in Arlt's fiction either side of the military takeover of 1930, moving from his critique of the rising petit-bourgeois classes in El juguete rabioso (1926) to a clear realisation and encouragement of class consciousness in the short stories of El criador de gorilas (1936)

Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease

Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3,4,5,6,7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease