@article {809, title = {Molecular and phylogenetic characterization of the monkeypox outbreak in the South of Spain.}, journal = {Health Sci Rep}, volume = {7}, year = {2024}, month = {2024 Mar}, pages = {e1965}, abstract = {

BACKGROUND AND AIM: Until the May 2022 Monkeypox (MPXV) outbreak, which spread rapidly to many non-endemic countries, the virus was considered a viral zoonosis limited to some African countries. The Andalusian circuit of genomic surveillance was rapidly applied to characterize the MPXV~outbreak in the South of Spain.

METHODS: Whole genome sequencing was used to obtain the genomic profiles of samples collected across the south of Spain, representative of all the provinces of Andalusia. Phylogenetic analysis was used to study the relationship of the isolates and the available sequences of the 2022 outbreak.

RESULTS: Whole genome sequencing of a total of 160 MPXV~viruses from the different provinces that reported cases were obtained. Interestingly, we report the sequences of MPXV~viruses obtained from two patients who died. While one of the isolates bore no noteworthy mutations that explain a potential heightened virulence, in another patient the second consecutive genome sequence, performed after the administration of tecovirimat, uncovered a mutation within the A0A7H0DN30 gene, known to be a prime target for tecovirimat in its Vaccinia counterpart. In general, a low number of mutations were observed in the sequences reported, which were very similar to the reference of the 2022 outbreak (OX044336), as expected from a DNA virus. The samples likely correspond to several introductions of the circulating MPXV~viruses from the last outbreak. The virus sequenced from one of the two patients that died presented a mutation in a gene that bears potential connections to drug resistance. This mutation was absent in the initial sequencing before treatment.

}, issn = {2398-8835}, doi = {10.1002/hsr2.1965}, author = {Casimiro-Soriguer, Carlos S and Perez-Florido, Javier and Lara, Mar{\'\i}a and Camacho-Martinez, Pedro and Merino-Diaz, Laura and Pupo-Ledo, Inmaculada and de Salazar, Adolfo and Fuentes, Ana and Vi{\~n}uela, Laura and Chueca, Natalia and Martinez-Martinez, Luis and Lorusso, Nicola and Lepe, Jose A and Dopazo, Joaquin and Garc{\'\i}a, Federico} } @article {815, title = {Mutational landscape of risk variants in comorbid depression and obesity: a next-generation sequencing approach.}, journal = {Mol Psychiatry}, year = {2024}, month = {2024 May 28}, abstract = {

Major depression (MD) and obesity are complex genetic disorders that are frequently comorbid. However, the study of both diseases concurrently remains poorly addressed and therefore the underlying genetic mechanisms involved in this comorbidity remain largely unknown. Here we examine the contribution of common and rare variants to this comorbidity through a next-generation sequencing (NGS) approach. Specific genomic regions of interest in MD and obesity were sequenced in a group of 654 individuals from the PISMA-ep epidemiological study. We obtained variants across the entire frequency spectrum and assessed their association with comorbid MD and obesity, both at variant and gene levels. We identified 55 independent common variants and a burden of rare variants in 4 genes (PARK2, FGF21, HIST1H3D and RSRC1) associated with the comorbid phenotype. Follow-up analyses revealed significantly enriched gene-sets associated with biological processes and pathways involved in metabolic dysregulation, hormone signaling and cell cycle regulation. Our results suggest that, while risk variants specific to the comorbid phenotype have been identified, the genes functionally impacted by the risk variants share cell biological processes and signaling pathways with MD and obesity phenotypes separately. To the best of our knowledge, this is the first study involving a targeted sequencing approach toward the study of the comorbid MD and obesity. The framework presented here allowed a deep characterization of the genetics of the co-occurring MD and obesity, revealing insights into the mutational and functional profile that underlies this comorbidity and contributing to a better understanding of the relationship between these two disabling disorders.

}, issn = {1476-5578}, doi = {10.1038/s41380-024-02609-2}, author = {P{\'e}rez-Guti{\'e}rrez, Ana M and Carmona, Rosario and Loucera, Carlos and Cervilla, Jorge A and Guti{\'e}rrez, Blanca and Molina, Esther and L{\'o}pez-L{\'o}pez, Daniel and Perez-Florido, Javier and Zarza-Rebollo, Juan Antonio and L{\'o}pez-Isac, Elena and Dopazo, Joaquin and Martinez-Gonzalez, Luis Javier and Rivera, Margarita} }