Biology subjects

Pantoja, C.

Publications and source records attributed to Pantoja, C..

4 recordsLinked to original sources

bioRxiv2026

A baseline for aquatic parasite diversity in West African mangroves: host-parasite records, DNA barcodes, and an experimental design for future use

Macroparasites represent a major fraction of biodiversity and biomass in marine ecosystems, yet remain substantially underrepresented in ecological surveys and food-web models, particularly in the Global South. This study addresses this geographic bias by providing the first comprehensive ecological survey of macroparasite communities of fishes in a West African Marine Protected Area (MPA) and adjacent Open-Access Area (OAA) characterised by mangrove forests. We collected 5,020 parasite specimens from 10 fish and one crab species in the Saloum Delta, Senegal, identifying 27 parasite species across all major taxa. Our findings include 15 new records for Senegal of which 11 are also new for West Africa. Additionally, 64% of host-parasite combinations constitute new host records. We provide 208 DNA barcodes, offering the first molecular data for 31% of these species globally and establishing a reference library for future DNA metabarcoding efforts in the region. Using sample size-corrected biodiversity indices and mixed-model analyses, we detected significant variations in parasite infracommunities and component communities between the MPA and OAA, demonstrating the feasibility of using comparative study designs to monitor fisheries impacts on parasite diversity in the Saloum Delta. Furthermore, the identification of trophically transmitted parasites provided evidence of unstudied food-web connections, e.g. predator-prey linkages between fishes and higher-trophic-level definitive hosts including birds and elasmobranchs. By integrating morphological identification, molecular data, and archiving of voucher specimens into publicly accessible, curated collections, this study establishes a new baseline for marine parasite biodiversity in West Africa and provides a methodological blueprint for surveying understudied regions.

zoology↗

bioRxiv2026

Axonal entry and retrograde transport define HSV-1 latency establishment and reactivation potential in neurons

Herpes simplex virus 1 (HSV-1) establishes life-long latency in peripheral neurons following neuroinvasion, yet the early determinants governing latency versus productive infection remain poorly understood. Available in vitro models bypass the physiological route of infection by directly infecting neuronal cell bodies under antiviral suppression. Here, we established a compartmented axonal infection model that recapitulates HSV-1 neuroinvasion and latency establishment without pharmacological inhibitors. Using primary superior cervical ganglion (SCG) neurons, we demonstrated that low-dose axonal infection consistently establishes latency, whereas higher axonal doses or direct somatic infection led to productive replication. Latently infected neurons exhibit accumulation of the latency-associated transcript (LAT) and can be efficiently reactivated by UV-inactivated virus or VP16 expression. Remarkably, productive infection can be induced during low-dose axonal infection by simultaneous exposure of neuronal cell bodies, but not axons, to replication-deficient virions, implicating tegument delivery in soma overrides latency establishment. Conversely, excess replication-incompetent particles in axons suppress productive outcomes and subsequent reactivations, suggesting competition for retrograde transport. Together, these findings identify axonal entry and transport as critical regulatory checkpoints in HSV-1 latency establishment and suggest that interference with retrograde trafficking may represent a strategy to limit neuroinvasion and life-long reactivations.

microbiology↗

bioRxiv2024

Electromagnetic waves destabilize the SARS-CoV-2 Spike protein and reduce SARS-CoV-2 Virus-Like Particle (SC2-VLP) infectivity

Infection and transmission of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) continues to pose a global public health concern. Using electromagnetic waves represents an alternative strategy to inactivate pathogenic viruses such as SARS-CoV-2 and reduce overall transmission. However, whether electromagnetic waves reduce SARS-CoV-2 infectivity is unclear. Here, we adapted a coplanar waveguide (CPW) to identify electromagnetic waves that could neutralize SARS-CoV-2 virus-like particles (SC2-VLPs). Treatment of SC2-VLPs, particularly at frequencies between 2.5-3.5 GHz at an electric field of 400 V/m for 2 minutes, reduced infectivity. Exposure to a frequency of 3.1 GHz decreased the binding of SC2-VLPs to antibodies directed against the Spike S1 subunit receptor binding domain (RBD). These results suggest that electromagnetic waves alter the conformation of Spike, thereby reducing viral attachment to host cell receptors. Overall, this data provides proof-of-concept in using electromagnetic waves for sanitation and prevention efforts to curb the transmission of SARS-CoV-2 and potentially other pathogenic enveloped viruses.

microbiology↗

bioRxiv2020

Cellular senescence limits acute lung injury induced by mechanical ventilation

The p53/p21 pathway is activated in response to cell stress. However, its role in acute lung injury has not been elucidated. Acute lung injury is associated with disruption of the alveolo-capillary barrier leading to acute respiratory distress syndrome (ARDS). Mechanical ventilation may be necessary to support gas exchange in patients with ARDS, however, high positive airway pressures can cause regional overdistension of alveolar units and aggravate lung injury. Here, we report that acute lung injury and alveolar overstretching activate the p53/p21 pathway to maintain homeostasis and avoid massive cell apoptosis. A systematic pooling of transcriptomic data from animal models of lung injury demonstrates the enrichment of specific p53- and p21-dependent gene signatures and a validated senescence profile. In a clinically relevant, murine model of acid aspiration and mechanical ventilation, we observed changes in the nuclear envelope and the underlying chromatin, DNA damage and activation of the Tp53/p21 pathway. Absence of Cdkn1a decreased the senescent response, but worsened lung injury due to increased cell apoptosis. Conversely, treatment with lopinavir/ritonavir led to Cdkn1a overexpression and ameliorated cell apoptosis and lung injury. The activation of these mechanisms was associated with early markers of senescence, including expression of senescence-related genes and increases in senescence-associated heterochromatin foci in alveolar cells. Autopsy samples from lungs of patients with ARDS revealed increased senescence-associated heterochromatin foci. Collectively, these results suggest that acute lung injury activates p53/p21 as an anti-apoptotic mechanism to ameliorate damage, but with the side effect of induction of senescence.

cell biology↗