The effects of weather and mobility on respiratory viruses dynamics before and during the COVID-19 pandemic in the USA and Canada.

The flu season is caused by a combination of different pathogens, including influenza viruses (IVS), that cause the flu, and non-influenza respiratory viruses (NIRVs), that cause common colds or influenza-like illness. These viruses exhibit similar dynamics and meteorological conditions have historically been regarded as a principal modulator of their epidemiology, with outbreaks in the winter and almost no circulation during the summer, in temperate regions. However, after the emergence of SARS-CoV2, in late 2019, the dynamics of these respiratory viruses were strongly perturbed worldwide: some infections displayed near-eradication, while others experienced temporal shifts or occurred "off-season". This disruption raised questions regarding the dominant role of weather while also providing an unique opportunity to investigate the roles of different determinants on the epidemiological dynamics of IVs and NIRVs. Here, we employ statistical analysis and modelling to test the effects of weather and mobility in viral dynamics, before and during the COVID-19 pandemic. Leveraging epidemiological surveillance data on several respiratory viruses, from Canada and the USA, from 2016 to 2023, we found that whereas in the pre-COVID-19 pandemic period, weather had a strong effect, in the pandemic period the effect of weather was strongly reduced and mobility played a more relevant role. These results, together with previous studies, indicate that behavioral changes resulting from the non-pharmacological interventions implemented to control SARS-CoV2, interfered with the dynamics of other respiratory viruses, and that the past dynamical equilibrium was disturbed, and perhaps permanently altered, by the COVID-19 pandemic.

Embryonal life histories: Desiccation plasticity and diapause in the Argentinean pearlfish Austrolebias bellottii.

Embryos of annual killifish diapause in soil egg banks while ponds are dry. Their rates of development and survival in different developmental stages determine the numbers and stages of embryos at rewetting. In the Argentinean pearlfish Austrolebias bellottii, we investigated plasticity for desiccation in such embryonal life history components across phases of mild desiccation and rewetting and also effects of life history on hatching. In comparison with nonannuals, our data suggest that incidences of diapause have become relatively independent of the occurrence of desiccation, as if they have become genetically assimilated. We found limited survival effects of desiccation, limited developmental delays, and an acceleration of development into the prehatching stage. This response can be adaptive when desiccation informs that an opportunity to hatch approaches. Embryos arrest development in the prehatching stage (diapause DIII) or in the dispersed-cell phase (diapause DI). Parental pair variation in rates of development and survival in the earliest developmental stages affects the fraction of embryos that are in DI at rewetting and the number surviving. Given such effects on life history fitness components, rates during embryonal development seem "visible" to selection and the developmental system can thus adapt when pair variation contains a heritable component. In agreement with expectations for the presence of diversified bet-hedging, some embryos hatched and others not in over half of the clutches with several developed embryos at the moment of rewetting. Hatching probabilities increased for eggs produced later in the experiment, and they increased when embryos were rewetted a second time after two months. This response is opposite of what is expected when age-dependent hatching would be adapted to exploit opportunities for completing another generation before the dry season.

Desiccation plasticity in the embryonic life histories of non-annual rivulid species.

BACKGROUND: Diapause is a developmental arrest present in annual killifish, whose eggs are able to survive long periods of desiccation when the temporary ponds they inhabit dry up. Diapause can occur in three different developmental stages. These differ, within and between species, in their responsiveness to different environmental cues. A role of developmental plasticity and genetic assimilation in diapause evolution has been previously suggested but not experimentally explored. We investigated whether plastic developmental delays or arrests provoked by an unusual and extreme environment could be the ancestral condition for diapause. This would be in agreement with plasticity evolution playing a role in the emergence of diapause in this group. We have used a comparative experimental approach and exposed embryos of non-annual killifish belonging to five different species from the former genus Rivulus to brief periods of desiccation. We have estimated effects on developmental and mortality rates during and after the desiccation treatment. RESULTS: Embryos of these non-annual rivulids decreased their developmental rates in early stages of development in response to desiccation and this effect persisted after the treatment. Two pairs of two different species had sufficient sample sizes to investigate rates of development in later stages well. In one of these, we found cohorts of embryos in the latest stages of development that did not hatch over a period of more than 1 month without mortality. Several properties of this arrest are also used to characterize diapause III in annual killifish. Such a cohort is present in control conditions and increases in frequency in the desiccation treatment. CONCLUSIONS: The presence of plasticity for developmental timing and a prolonged developmental arrest in non-annual rivulids, suggest that a plastic developmental delay or diapause might have been present in the shared ancestor of annual and non-annual South American killifish and that the evolution of plasticity could have played a role in the emergence of the diapauses. Further comparative experimental studies and field research are needed to better understand how diapause and its plasticity evolved in this group.

Switching axial progenitors from producing trunk to tail tissues in vertebrate embryos.

The vertebrate body is made by progressive addition of new tissue from progenitors at the posterior embryonic end. Axial extension involves different mechanisms that produce internal organs in the trunk but not in the tail. We show that Gdf11 signaling is a major coordinator of the trunk-to-tail transition. Without Gdf11 signaling, the switch from trunk to tail is significantly delayed, and its premature activation brings the hindlimbs and cloaca next to the forelimbs, leaving extremely short trunks. Gdf11 activity includes activation of Isl1 to promote formation of the hindlimbs and cloaca-associated mesoderm as the most posterior derivatives of lateral mesoderm progenitors. Gdf11 also coordinates reallocation of bipotent neuromesodermal progenitors from the anterior primitive streak to the tail bud, in part by reducing the retinoic acid available to the progenitors. Our findings provide a perspective to understand the evolution of the vertebrate body plan.

Amniotic fluid deficiency and congenital abnormalities both influence fluctuating asymmetry in developing limbs of human deceased fetuses.

Fluctuating asymmetry (FA), as an indirect measure of developmental instability (DI), has been intensively studied for associations with stress and fitness. Patterns, however, appear heterogeneous and the underlying causes remain largely unknown. One aspect that has received relatively little attention in the literature is the consequence of direct mechanical effects on asymmetries. The crucial prerequisite for FA to reflect DI is that environmental conditions on both sides should be identical. This condition may be violated during early human development if amniotic fluid volume is deficient, as the resulting mechanical pressures may increase asymmetries. Indeed, we showed that limb bones of deceased human fetuses exhibited increased asymmetry, when there was not sufficient amniotic fluid (and, thus, space) in the uterine cavity. As amniotic fluid deficiency is known to cause substantial asymmetries and abnormal limb development, these subtle asymmetries are probably at least in part caused by the mechanical pressures. On the other hand, deficiencies in amniotic fluid volume are known to be associated with other congenital abnormalities that may disturb DI. More specifically, urogenital abnormalities can directly affect/reduce amniotic fluid volume. We disentangled the direct mechanical effects on FA from the indirect effects of urogenital abnormalities, the latter presumably representing DI. We discovered that both factors contributed significantly to the increase in FA. However, the direct mechanical effect of uterine pressure, albeit statistically significant, appeared less important than the effects of urogenital abnormalities, with an effect size only two-third as large. We, thus, conclude that correcting for the relevant direct factors allowed for a representative test of the association between DI and stress, and confirmed that fetuses form a suitable model system to increase our understanding in patterns of FA and symmetry development.

Evo-Devo of the Human Vertebral Column: On Homeotic Transformations, Pathologies and Prenatal Selection.

Homeotic transformations of vertebrae are particularly common in humans and tend to come associated with malformations in a wide variety of organ systems. In a dataset of 1,389 deceased human foetuses and infants a majority had cervical ribs and approximately half of these individuals also had missing twelfth ribs or lumbar ribs. In ~10 % of all cases there was an additional shift of the lumbo-sacral boundary and, hence, homeotic transformations resulted in shifts of at least three vertebral boundaries. We found a strong coupling between the abnormality of the vertebral patterns and the amount and strength of associated malformations, i.e., the longer the disturbance of the vertebral patterning has lasted, the more associated malformations have developed and the more organ systems are affected. The germ layer of origin of the malformations was not significantly associated with the frequency of vertebral patterns. In contrast, we find significant associations with the different developmental mechanisms that are involved in the causation of the malformations, that is, segmentation, neural crest development, left-right patterning, etc. Our results, thus, suggest that locally perceived developmental signals are more important for the developmental outcome than the origin of the cells. The low robustness of vertebral A-P patterning apparent from the large number of homeotic transformations is probably caused by the strong interactivity of developmental processes and the low redundancy of involved morphogens during early organogenesis. Additionally, the early irreversibility of the specification of the A-P identity of vertebrae probably adds to the vulnerability of the process by limiting the possibility for recovery from developmental disturbances. The low developmental robustness of vertebral A-P patterning contrasts with a high robustness of the A-P patterning of the vertebral regions. Not only the order is invariable, also the variation in the number of vertebrae per region is small. This robustness is in agreement with the evolutionary stability of vertebral regions in tetrapods. Finally, we propose a new hypothesis regarding the constancy of the presacral number of vertebrae in mammals.

Breaking evolutionary and pleiotropic constraints in mammals: On sloths, manatees and homeotic mutations.

BACKGROUND: Mammals as a rule have seven cervical vertebrae, except for sloths and manatees. Bateson proposed that the change in the number of cervical vertebrae in sloths is due to homeotic transformations. A recent hypothesis proposes that the number of cervical vertebrae in sloths is unchanged and that instead the derived pattern is due to abnormal primaxial/abaxial patterning. RESULTS: We test the detailed predictions derived from both hypotheses for the skeletal patterns in sloths and manatees for both hypotheses. We find strong support for Bateson's homeosis hypothesis. The observed vertebral and rib patterns cannot be explained by changes in primaxial/abaxial patterning. Vertebral patterns in sloths and manatees are similar to those in mice and humans with abnormal numbers of cervical vertebrae: incomplete and asymmetric homeotic transformations are common and associated with skeletal abnormalities. In sloths the homeotic vertebral shift involves a large part of the vertebral column. As such, similarity is greatest with mice mutant for genes upstream of Hox. CONCLUSIONS: We found no skeletal abnormalities in specimens of sister taxa with a normal number of cervical vertebrae. However, we always found such abnormalities in conspecifics with an abnormal number, as in many of the investigated dugongs. These findings strongly support the hypothesis that the evolutionary constraints on changes of the number of cervical vertebrae in mammals is due to deleterious pleitropic effects. We hypothesize that in sloths and manatees low metabolic and activity rates severely reduce the usual stabilizing selection, allowing the breaking of the pleiotropic constraints. This probably also applies to dugongs, although to a lesser extent.