Huddling with families after disaster: Human resilience and social disparity.

Disasters, from hurricanes to pandemics, tremendously impact human lives and behaviors. Physical closeness to family post-disaster plays a critical role in mental healing and societal sustainability. Nonetheless, little is known about whether and how family colocation alters after a disaster, a topic of immense importance to a post-disaster society. We analyze 1 billion records of population-scale, granular, individual-level mobile location data to quantify family colocation, and examine the magnitude, dynamics, and socioeconomic heterogeneity of the shift in family colocation from the pre- to post-disaster period. Leveraging Hurricane Florence as a natural experiment, and Geographic Information System (GIS), machine learning, and statistical methods to investigate the shift across the landfall (treated) city of Wilmington, three partially treated cites on the hurricane's path, and two control cities off the path, we uncover dramatic (18.9%), widespread (even among the partially treated cities), and enduring (over at least 3 months) escalations in family colocation. These findings reveal the powerful psychological and behavioral impacts of the disaster upon the broader populations, and simultaneously remarkable human resilience via behavioral adaptations during disastrous times. Importantly, the disaster created a gap across socioeconomic groups non-existent beforehand, with the disadvantaged displaying weaker lifts in family colocation. This sheds important lights on policy making and policy communication to promote sustainable family colocation, healthy coping strategies against traumatic experiences, social parity, and societal recovery.

Aspulvins A-H, Aspulvinone Analogues with SARS-CoV-2 Mpro Inhibitory and Anti-inflammatory Activities from an Endophytic Cladosporium sp.

Eight new aspulvinone analogues, aspulvins A-H (1-8) and aspulvinones D, M, O, and R (9-12), were isolated from cultures of the endophytic fungus Cladosporium sp. 7951. Detailed spectroscopic analyses were conducted to determine the structures of the new compounds. All isolates displayed different degrees of inhibitory activity against the severe acute respiratory syndrome coronavirus 2 main protease (SARS-CoV-2 Mpro) at 10 µM. Notably, compounds 9, 10, and 12 showed potential SARS-CoV-2 Mpro inhibition with IC50 values of 10.3 ± 0.6, 9.4 ± 0.6, and 7.7 ± 0.6 µM, respectively. For all compounds except 3 and 4, the anti-inflammatory activity occurred by inhibiting the release of lactate dehydrogenase (LDH) with IC50 values ranging from 0.7 to 7.4 µM. Compound 10 showed the most potent anti-inflammatory activity by inhibiting Casp-1 cleavage, IL-1ß maturation, NLRP3 inflammasome activation, and pyroptosis. The findings reveal that the aspulvinone analogues 9, 10, and 12 could be promising candidates for coronavirus disease 2019 (COVID-19) treatment as they inhibit SARS-CoV-2 infection and reduce inflammatory reactions caused by SARS-CoV-2.

Evidence for a mouse origin of the SARS-CoV-2 Omicron variant.

The rapid accumulation of mutations in the SARS-CoV-2 Omicron variant that enabled its outbreak raises questions as to whether its proximal origin occurred in humans or another mammalian host. Here, we identified 45 point mutations that Omicron acquired since divergence from the B.1.1 lineage. We found that the Omicron spike protein sequence was subjected to stronger positive selection than that of any reported SARS-CoV-2 variants known to evolve persistently in human hosts, suggesting a possibility of host-jumping. The molecular spectrum of mutations (i.e., the relative frequency of the 12 types of base substitutions) acquired by the progenitor of Omicron was significantly different from the spectrum for viruses that evolved in human patients but resembled the spectra associated with virus evolution in a mouse cellular environment. Furthermore, mutations in the Omicron spike protein significantly overlapped with SARS-CoV-2 mutations known to promote adaptation to mouse hosts, particularly through enhanced spike protein binding affinity for the mouse cell entry receptor. Collectively, our results suggest that the progenitor of Omicron jumped from humans to mice, rapidly accumulated mutations conducive to infecting that host, then jumped back into humans, indicating an inter-species evolutionary trajectory for the Omicron outbreak.