Browsing by Author "Rivera, Carlos"

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    First report and genetic characterization of Seneca Valley virus (SVV) in Chile
    (SPRINGER INTERNATIONAL PUBLISHING AG, 2022) Bennett, Benjamin; Urzua-Encina, Constanza; Pardo-Roa, Catalina; Ariyama, Naomi; Lecocq, Claudio; Rivera, Carlos; Badia, Catalina; Suarez, Paulina; Agredo, Michel; Aguayo, Carolina; Avila, Claudia; Araya, Hugo; Perez, Patricio; Berrios, Felipe; Aguero, Belen; Mendieta, Vanessa; Pituco, Edviges Maristela; de Almeida, Iassudara Garcia; Medina, Rafael; Brito, Barbara; Johow, Magdalena; Neira Ramirez, Victor
    Seneca Valley virus (SVV) is a non-enveloped RNA virus and the only member of the Senecavirus A (SVA) species, in the Senecavirus genus, Picornaviridae family. SVV infection causes vesicular lesions in the oral cavity, snout and hooves of pigs. This infection is clinically indistinguishable from trade-restrictions-related diseases such as foot-and-mouth disease. Other clinical manifestations include diarrhoea, anorexia, lethargy, neurological signs and mortality in piglets during their first week of age. Before this study, Chile was considered free of vesicular diseases of swine, including SVV. In April 2022, a suspected case of vesicular disease in a swine farm was reported in Chile. The SVV was confirmed and other vesicular diseases were ruled out. An epidemiological investigation and phylogenetic analyses were performed to identify the origin and extent of the outbreak. Three hundred ninety-five samples from 44 swine farms were collected, including faeces (208), oral fluid (28), processing fluid (14), fresh semen (61), environmental samples (80) and tissue from lesions (4) for real-time RT-PCR detection. Until June 2022, the SVV has been detected in 16 out of 44 farms, all epidemiologically related to the index farm. The closest phylogenetic relationship of the Chilean SVV strain is with viruses collected from swine in California in 2017. The direct cause of the SVV introduction has not yet been identified; however, the phylogenetic analyses suggest the USA as the most likely source. Since the virus remains active in the environment, transmission by fomites such as contaminated feed cannot be discarded. Further studies are needed to determine the risk of the introduction of novel SVV and other transboundary swine pathogens to Chile.
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    Mass mortality event in South American sea lions (Otaria flavescens) correlated to highly pathogenic avian influenza (HPAI) H5N1 outbreak in Chile
    (2023) Ulloa, Mauricio; Fernandez, Antonio; Ariyama, Naomi; Colom-Rivero, Ana; Rivera, Carlos; Nunez, Paula; Sanhueza, Paola; Johow, Magdalena; Araya, Hugo; Torres, Juan Carlos; Gomez, Paola; Munoz, Gabriela; Aguero, Belen; Alegria, Raul; Medina, Rafael; Neira, Victor; Sierra, Eva
    In Chile, since January 2023, a sudden and pronounced increase in strandings and mortality has been observed among South American (SA) sea lions (Otaria flavescens), prompting significant concern. Simultaneously, an outbreak of highly pathogenic avian influenza H5N1 (HPAIV H5N1) in avian species has emerged since December 2022. To investigate the cause of this unexpected mortality, we conducted a comprehensive epidemiological and pathologic study. One hundred sixty-nine SA sea lions were sampled to ascertain their HPAIV H5N1 status, and long-term stranding trends from 2009 to 2023 were analyzed. In addition, two animals were necropsied. Remarkably, a significant surge in SA sea lion strandings was observed initiating in January 2023 and peaking in June 2023, with a count of 4,545 stranded and deceased animals. Notably, this surge in mortality correlates geographically with HPAIV outbreaks affecting wild birds. Among 168 sampled SA sea lions, 34 (20%) tested positive for Influenza A virus, and 21 confirmed for HPAIV H5N1 2.3.4.4b clade in tracheal/rectal swab pools. Clinical and pathological evaluations of the two necropsied stranded sea lions revealed prevalent neurological and respiratory signs, including disorientation, tremors, ataxia, and paralysis, as well as acute dyspnea, tachypnea, profuse nasal secretion, and abdominal breathing. The lesions identified in necropsied animals aligned with observed clinical signs. Detection of the virus via immunohistochemistry (IHC) and real-time PCR in the brain and lungs affirmed the findings. The findings provide evidence between the mass mortality occurrences in SA sea lions and HPAIV, strongly indicating a causal relationship. Further studies are needed to better understand the pathogenesis and transmission.
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    PIASγ controls stability and facilitates SUMO-2 conjugation to CoREST family of transcriptional co-repressors
    (2018) Sáez Ardura, Julián Esteban; Arredondo Ramírez, Cristian Andrés; Rivera, Carlos; Andrés Coke, María Estela
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    Pilocarpine-induced seizures associate with modifications of LSD1/CoREST/HDAC1/2 epigenetic complex and repressive chromatin in mice hippocampus
    (2021) Noches, Veronica; Rivera, Carlos; Gonzalez, Marcela P.; Merello, Gianluca; Olivares-Costa, Montserrat; Estela Andres, Maria
    Epilepsy is a neurological disorder of genetic or environmental origin characterized by recurrent spontaneous seizures. A rodent model of temporal lobe epilepsy is induced by a single administration of pilocarpine, a nonselective cholinergic muscarinic receptor agonist. The molecular changes associated with pilocarpine-induced seizures are still poorly described. Epigenetic multiprotein complexes that regulate gene expression by changing the structure of chromatin impose transcriptional memories. Among the epigenetic enzymes relevant to the epileptogenic process is lysine-specific demethylase 1 (LSD1, KDM1A), which regulates the expression of genes that control neuronal excitability. LSD1 forms complexes with the CoREST family of transcriptional corepressors, which are molecular bridges that bring HDAC1/2 and LSD1 enzymes to deacetylate and demethylate the tail of nucleosomal histone H3. To test the hypothesis that LSD1-complexes are involved in initial modifications associated with pilocarpine-induced epilepsy, we studied the expression of main components of LSD1-complexes and the associated epigenetic marks on isolated neurons and the hippocampus of pilocarpine-treated mice. Using a single injection of 300 mg/kg of pilocarpine and after 24 h, we found that protein levels of LSD1, CoREST2, and HDAC1/2 increased, while CoREST1 decreased in the hippocampus. In addition, we observed increased histone H3 lysine 9 di- and trimethylation (H3K9me2/3) and decreased histone H3 lysine 4 di and trimethylation (H3K4me2/3). Similar findings were observed in cultured hippocampal neurons and HT-22 hippocampal cell line treated with pilocarpine. In conclusion, our data show that muscarinic receptor activation by pilocarpine induces a global repressive state of chromatin and prevalence of LSD1-CoREST2 epigenetic complexes, modifications that could underlie the pathophysiological processes leading to epilepsy.
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    Unveiling RCOR1 as a rheostat at transcriptionally permissive chromatin
    (2022) Rivera, Carlos; Lee, Hun-Goo; Lappala, Anna; Wang, Danni; Noches, Veronica; Olivares-Costa, Montserrat; Sjoberg-Herrera, Marcela; Lee, Jeannie T.; Andres, Maria Estela
    The classical neuronal-gene corepressor RCOR1/CoREST is paradoxically enriched in transcriptionally active chromatin. Here the authors show RCOR1 is recruited during promoter-proximal pausing and negatively regulates the nascent-transcript synthesis. They also show that an RCOR1-LSD1- HDAC1 complex removes lysine acetylation from RNA polymerase II to repress transcription.