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Romero, V.

Publications and source records attributed to Romero, V..

3 recordsLinked to original sources

Widespread SARS-CoV-2 infection in free-ranging Neotropical bats suggests repeated human-to-bat spillback

Bats harbor exceptional coronavirus diversity and are considered ancestral sources of several human pathogens. As SARS-CoV-2 transitioned from pandemic emergence to global endemicity in humans, concern has shifted from wildlife-to-human spillover toward reverse zoonosis. However, infection of free-ranging bat populations under natural conditions has not previously been demonstrated. Here, we report widespread detection of SARS-CoV-2 RNA in wild Neotropical bats sampled across Andean and Amazonian ecosystems of Southern Ecuador. RT-qPCR screening of 126 individuals, representing nine taxa, detected SARS-CoV-2 RNA in 34.12% of bats across multiple sites. Partial to near-complete viral genomes recovered from five individuals showed >99% nucleotide identity to contemporary human SARS-CoV-2 lineages and clustered within multiple global phylogenetic clades. Mixed-effects modeling revealed pronounced species-level heterogeneity, a positive association between elevation and infection probability, and higher infection probability in females compared with males. The close phylogenetic affinity of bat-derived genomes to circulating human variants and their distribution across multiple lineages suggest repeated anthropogenic spillback rather than sustained bat-specific circulation. These results expand current understanding of the ecological footprint of the COVID-19 pandemic and highlight the importance of integrating wildlife surveillance into long-term One Health strategies for emerging infectious diseases.

microbiology↗

Surveying armadillo and bat trypanosomes by DNA metabarcoding with Oxford Nanopore Technologies sequencing: the importance of fine-tuning parameters to identify mixed infections

BackgroundThe ecological dynamics between Trypanosoma parasites and their wild mammalian hosts, such as bats and armadillos, are complex. Recent 18S rRNA metabarcoding studies have reported extraordinary levels of hidden parasite diversity and frequent multi-lineage coinfections within individual wild hosts. However, the boundary between genuine biological coinfection and methodological artifact remains difficult to establish. Based on Gauses principle of competitive exclusion, the mammalian bloodstream represents a highly constrained niche where stable coexistence of identical ecological competitors is theoretically rare. We hypothesize that previously reported hyper-diverse Trypanosoma coinfections are largely bioinformatic artifacts, and that true intra-host dynamics instead favor single-lineage dominance. MethodsTo test this hypothesis, we sequenced samples from 27 wild armadillos (Dasypus novemcinctus) and 26 bats from Ecuador. The 18S rRNA gene was amplified via nested PCR and sequenced using an Oxford Nanopore Technologies MinION platform. We developed a progressively stringent bioinformatics pipeline to evaluate coinfection hypotheses. Raw reads were processed through three alignment scenarios: Lenient, Moderate, and Conservative. These scenarios modulate sequence identity, mapping quality (MAPQ), and coverage thresholds to effectively isolate true biological signals from alignment ambiguity. ResultsUnder lenient alignment parameters, the resulting profiles mirrored previous literature, exhibiting massive apparent intra-host multi-lineage diversity. However, as bioinformatic stringency increased to conservative thresholds ([≥] 98% sequence identity, [≥] 99% coverage, and MAPQ [≥] 30), artifactual pseudo-coinfections collapsed. The highly restricted dataset demonstrated overwhelming single-lineage dominance, validating only three active mixed infections out of the retained samples. Furthermore, our rigorous pipeline isolated rare but genuine biological signals, including the detection of Trypanosoma cruzi marinkellei--historically considered a bat-restricted subgenus--within the terrestrial armadillo cohort. We also confirmed the presence of T. cruzi DTU III (TcIII) in Ecuadorian armadillos, representing a significant biogeographical record for the region. ConclusionsOnce methodological noise is computationally stripped away, active multi-strain Trypanosoma coinfections in the host bloodstream are revealed to be ecologically anomalous. Our findings strongly support the principle of competitive exclusion, suggesting established lineages actively suppress competitors. While Oxford Nanopore sequencing offers necessary resolution for wildlife parasitology, fine-tuning algorithmic parameters is critical to accurately represent host-parasite networks and prevent the artificial inflation of intra-host diversity metrics. Author summaryPrevious studies using DNA metabarcoding have reported that wild mammals, such as bats, frequently harbor complex communities of multiple Trypanosoma parasite lineages simultaneously. However, ecological principles suggest that identical competitors struggle to coexist stably within a constrained environment like the host bloodstream. To investigate whether these reported high coinfection rates reflect true biology or methodological artifacts, we sequenced the 18S rRNA gene of Trypanosoma from 26 bats and 27 armadillos in Ecuador. We processed the sequencing data through computational pipelines with progressively stricter filtering parameters. We observed that under lenient filtering, animals appeared to have highly diverse, mixed infections. Conversely, when strict parameters were applied to remove potential analytical noise, the artificial complexity collapsed, revealing that the vast majority of hosts were dominated by a single parasite lineage. We confirmed only three active mixed infections in our highly restricted dataset. Our findings indicate that active multi-strain Trypanosoma coinfections are rare, aligning with the principle of competitive exclusion. These results highlight the necessity of applying rigorous bioinformatic filters to accurately evaluate host-parasite interactions and avoid overestimating diversity metrics.

microbiology↗

Exacerbation of mitochondrial fission in human CD34+ cells halts erythropoiesis and hemoglobin biosynthesis

Erythropoiesis is the most powerful cellular differentiation and proliferation system, with a production of 1011 cells per day. In this fine-tuned process, the hematopoietic stem cells (HSCs) generate erythroid progenitors, which proliferate and mature into erythrocytes. During erythropoiesis, mitochondria are reprogrammed to drive the differentiation process before finally being eliminated by mitophagy. In erythropoiesis, mitochondrial dynamics (MtDy) is expected to be a regulatory key point that has not been described previously. We described that a specific MtDy pattern is occurring in human erythropoiesis from EPO-induced human CD34+ cells, characterized by a predominant mitochondrial fusion at early stages followed by predominant fission at late stages. The fusion protein MFN1 and the fission protein FIS1 are shown to play a key role in the accurate progression of erythropoiesis. Fragmentation of the mitochondrial web by the overexpression of FIS1 (gain of fission) resulted in both the inhibition of hemoglobin biosynthesis and the arrest of erythroid differentiation, keeping cells in immature differentiation stages. These cells showed specific mitochondrial features as compared with control cells, such as an increase in round and large mitochondria morphology, low mitochondrial membrane potential and a drop in the expression of the respiratory complexes II and IV. Interestingly, treatment with the mitochondrial permeability transition pore (mPTP) inhibitor cyclosporin A, rescued mitochondrial morphology, hemoglobin biosynthesis and erythropoiesis. Studies presented in this work revealed MtDy as a hot spot in the regulation of erythroid differentiation which might be signaling downstream for metabolic reprogramming through the aperture/close of the mPTP. Key Points-. Excessive fission disrupts erythroid progression, heme biosynthesis and mitochondrial function, keeping cells mostly in progenitors and proerythroblast stage. -. Mitochondrial Dynamics signaling for erythroid differentiation involves FIS1 and the mPTP

cell biology↗