Comparative developmental biology of populations of three European and one North American Eubazus spp. (Hymenoptera: Braconidae), parasitoids of Pissodes spp. weevils (Coleoptera: Curculionidae)

Observations were made on the developmental responses of the North American braconid species, Eubazus crassigaster, a parasitoid of the white pine weevil, Pissoles strobi, and three European congeneric species, E. semirugosus, E. robustus, and Eubazus sp. Several populations of Eubazus spp. were compared in their phenology in the laboratory and under natural conditions. When reared in the laboratory on non-diapausing Pissodes castaneus, mountain populations of E. semirugosus and E. robustus entered into an obligatory diapause in the host larva, whereas all the other populations tested developed continuously. Diapausing larvae continued their development only after having experienced at least three months at 2°C. Non-diapausing populations of Eubazus spp. significantly differed in the duration of pre-imaginal development, with E. semirugosus being the fastest developing species and E. robustus the slowest. Outdoor rearings of Eubazus spp. on P. castaneus showed that E. crassigaster, Eubazus sp. and the lowland biotype of E. semirugosus emerged in the year of oviposition if this occurred early enough to allow parasitoid development. In contrast, a majority of E. robustus individuals overwintered in the host larvae, regardless of the oviposition date. The diapausing, mountain biotype of E. semirugosus is considered as the most promising candidate for control of P. strobi in Canada, because it is likely to be better adapted to the life cycle of the target host than the other Eubazus spp., including the native E. crassigaste

Insects associated with the Sitka spruce weevil, Pissodes strobi (Col.: Curculionidae) on Sitka spruce, Picea sitchensis in British Columbia, Canada.

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Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease