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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.
One of the most important insights of Optimality Theory (Prince & Smolensky 1993) is that phonological processes can be reduced to the interaction between faithfulness and universal markedness principles. In the most constrained version of the theory, all phonological processes should be thus reducible. This hypothesis is tested by alternations that appear to be phonological but in which universal markedness principles appear to play no role. If we are to pursue the claim that all phonological processes depend on the interaction of faithfulness and markedness, then processes that are not dependent on markedness must lie outside phonology. In this paper I will examine a group of such processes, the initial consonant mutations of the Celtic languages, and argue that they belong entirely to the morphology of the languages, not the phonology.
The phenomenon of phonological opacity has been the subject of much debate in recent years, with scholars opposed to the Optimality Theory (OT) research program arguing that opacity proves OT must be false, while the solutions proposed within OT, such as sympathy theory and stratal OT , have proved to be unsatisfying to many OT proponents, who have found these proposals to be inconsistent with the parallelist approach to phonological processes otherwise characteristic of OT. In this paper I reexamine one of the best known cases of opacity, that found in three processes of Tiberian Hebrew (TH), and argue that these processes only appear to be opaque, because previous analyses have treated them as pure phonology, rather than as an interaction between phonology and morphology. Once it is recognized that certain words of TH are lexically marked to end with a syllabic trochee, and that the goal of paradigm uniformity exerts grammatical pressure on phonology, the three processes no longer present a problem to parallelist OT. The results suggest the possibility that all crosslinguistic instances of apparent opacity can be explained in terms of the phonology-morphology interface and that purely phonological opacity does not exist. If this claim is true, then parallelist OT can be defended against its detractors without the need for additional mechanisms like sympathy theory and stratal OT.