SARS-CoV-2’s Variants of Concern: A Brief Characterization

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disclose the variants of concern (VOC) including Alpha (B.1.1.7), Beta (B.1.351), Gamma (P1), Delta (B.1.617.2), and Omicron (B.1.1.529). Its spike protein (S) present on the surface of the virus is recognized by the host cell receptor, the angiotensin-2 converting enzyme (ACE2) which promotes their entry into the cell. The mutations presented by VOCs are found in RBD and the N-terminal region of S protein. Therefore, mutations occurring in RBD can modify the biological and immunogenic characteristics of the virus, such as modifying the spike affinity for ACE2, increasing the virus transmissibility, or conferring the ability to escape the immune responses. The raise of a potential new SARS-CoV-2 variant capable of evading the host defenses at the same time maintaining its fitness justifies the importance of continued genetic monitoring of the pandemic coronavirus

Protective role of chlorogenic acid on DNA damage caused by ochratoxin A exposure

Chlorogenic acid (ChlA) has shown short-term protective effects against the cytogenotoxiceffects of ochratoxin A (OTA). The present study evaluated the effect of oraladministration of ChlA in male Wistar rats exposed to OTA. OTA (0.4 mg/kg bw/day), ChlA (5 mg/kg bw/day), or the combination of both, were administered orally toanimals during 28 days. No deaths, decrease in feed consumption or change in the bodyweight of animals were observed in any group. In the OTA-treated group a decrease inlocomotion as well as increased DNA damage in blood, kidney and bone marrow cellswere observed. ChlA alone was not genotoxic for animals. The combination of OTA+ChlA decreased the DNA damage by 37% in blood cells, by 55% in kidney cells andby 80% in bone marrow cells compared to OTA-treated group. In conclusion, oraltreatment with ChlA showed a good protective effect on genotoxicity produced byOTA in rats during 28 days exposure.El ácido clorogé nico (ChlA) mostró efectos protectores a corto plazo contra los efectos citogenotóxicos de ocratoxina A (OTA). En el presente estudio se evaluó si este polifenol mantiene su efecto protector mediante la administración oral en ratas Wistar machos expuestas a OTA. OTA (0,4 mg/kg/día), ChlA (5 mg/kg/día), o la combinación de ambos, fueron administrados a los animales por vía oral durante 28 días. No se observaron muertes, ni disminución en el consumo de alimento, ni cambios en el peso corporal en ningún grupo de animales. En el grupo tratado con OTA se observó disminución en la locomoción, así como daño en el ADN en las cé lulas de sangre, riñó n y mé dula ósea. En los animales que solo recibieron ChlA no se observaron efectos genotóxicos. La combinación de OTA + ChlA disminuyó el daño del ADN en un 37%en las cé lulas sanguíneas, en un 55% en las cé lulas renales y en un 80% en las cé lulas de la mé dula ósea con respecto al grupo tratado con OTA. En conclusión, el tratamiento oral con ChlA mostró buen efecto protector sobre la genotoxicidad producida por OTA en ratas durante 28 días de exposición.Fil: Campra, Noelia Anahí. Universidad Nacional de Río Cuarto. Facultad de Ciencias Exactas Fisicoquímicas y Naturales. Instituto de Biotecnología Ambiental y Salud - Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Biotecnología Ambiental y Salud; ArgentinaFil: Cariddi, Laura Noelia. Universidad Nacional de Río Cuarto. Facultad de Ciencias Exactas Fisicoquímicas y Naturales. Instituto de Biotecnología Ambiental y Salud - Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Biotecnología Ambiental y Salud; ArgentinaFil: Escobar, Franco Matias. Universidad Nacional de Río Cuarto; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; ArgentinaFil: Sabini, Maria Carola. Universidad Nacional de Río Cuarto. Facultad de Ciencias Exactas Fisicoquímicas y Naturales. Instituto de Biotecnología Ambiental y Salud - Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Biotecnología Ambiental y Salud; ArgentinaFil: Freire de lima, Celio Geraldo. Universidade Federal do Rio de Janeiro; BrasilFil: Decote Ricardo, Debora. Universidade Federal do Rio de Janeiro; BrasilFil: Roma, Dardo Andrés. Universidad Nacional de Río Cuarto; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; ArgentinaFil: Mañas, Fernando Javier. Universidad Nacional de Río Cuarto; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; ArgentinaFil: Dalcero, Ana Maria. Universidad Nacional de Río Cuarto; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentin

Rol protector del ácido clorogénico sobre el daño del ADN causado por la exposición a ocratoxina A : Chlorogenic acid and its effect on ochratoxin A

Chlorogenic acid (ChlA) has shown short-term protective effects against the cyto-genotoxic effects of ochratoxin A (OTA). The present study evaluated the effect of oral administration of ChlA in male Wistar rats exposed to OTA. OTA (0.4 mg/kg bw/day), ChlA (5 mg/kg bw/day), or the combination of both, were administered orally to animals during 28 days. No deaths, decrease in feed consumption or change in the body weight of animals were observed in any group. In the OTA-treated group a decrease in locomotion as well as increased DNA damage in blood, kidney and bone marrow cells were observed. ChlA alone was not genotoxic for animals. The combination of OTA+ChlA decreased the DNA damage by 37% in blood cells, by 55% in kidney cells and by 80% in bone marrow cells compared to OTA-treated group. In conclusion, oral treatment with ChlA showed a good protective effect on genotoxicity produced by OTA in rats during 28 days exposure.El ácido clorogénico (ChlA) mostró efectos protectores a corto plazo contra los efectos citogenotóxicos de ocratoxina A (OTA). En el presente estudio se evaluó si este polifenol mantiene su efecto protector mediante la administración oral en ratas Wistar machos expuestas a OTA. OTA (0,4 mg/kg/día), ChlA (5 mg/kg/día), o la combinación de ambos, fueron administrados a los animales por vía oral durante 28 días. No se observaron muertes, ni disminución en el consumo de alimento, ni cambios en el peso corporal en ningún grupo de animales. En el grupo tratado con OTA se observó disminución en la locomoción, así como daño en el ADN en las células de sangre, riñón y médula ósea. En los animales que solo recibieron ChlA no se observaron efectos genotóxicos. La combinación de OTA + ChlA disminuyó el daño del ADN en un 37% en las células sanguíneas, en un 55% en las células renales y en un 80% en las células de la médula ósea con respecto al grupo tratado con OTA. En conclusión, el tratamiento oral con ChlA mostró buen efecto protector sobre la genotoxicidad producida por OTA en ratas durante 28 días de exposición

Rol protector del ácido clorogénico sobre el daño del ADN causado por la exposición a ocratoxina A

Chlorogenic acid (ChlA) has shown short-term protective effects against the cytogenotoxic effects of ochratoxin A (OTA). The present study evaluated the effect of oral administration of ChlA in male Wistar rats exposed to OTA. OTA (0.4 mg/kg bw/ day), ChlA (5 mg/kg bw/day), or the combination of both, were administered orally to animals during 28 days. No deaths, decrease in feed consumption or change in the body weight of animals were observed in any group. In the OTA-treated group a decrease in locomotion as well as increased DNA damage in blood, kidney and bone marrow cells were observed. ChlA alone was not genotoxic for animals. The combination of OTA +ChlA decreased the DNA damage by 37% in blood cells, by 55% in kidney cells and by 80% in bone marrow cells compared to OTA-treated group. In conclusion, oral treatment with ChlA showed a good protective effect on genotoxicity produced by OTA in rats during 28 days exposure.El ácido clorogénico (ChlA) mostró efectos protectores a corto plazo contra los efectos citogenotóxicos de ocratoxina A (OTA). En el presente estudio se evaluó si este polifenol mantiene su efecto protector mediante la administración oral en ratas Wistar machos expuestas a OTA. OTA (0,4 mg/kg/día), ChlA (5 mg/kg/día), o la combinación de ambos, fueron administrados a los animales por vía oral durante 28 días. No se observaron muertes, ni disminución en el consumo de alimento, ni cambios en el peso corporal en ningún grupo de animales. En el grupo tratado con OTA se observó disminución en la locomoción, así como daño en el ADN en las células de sangre, riñón y médula ósea. En los animales que solo recibieron ChlA no se observaron efectos genotóxicos. La combinación de OTA + ChlA disminuyó el daño del ADN en un 37%en las células sanguíneas, en un 55% en las células renales y en un 80% en las células de la médula ósea con respecto al grupo tratado con OTA. En conclusión, el tratamiento oral con ChlA mostró buen efecto protector sobre la genotoxicidad producida por OTA en ratas durante 28 días de exposición.Facultad de Ciencias Veterinaria

Host-Toxoplasma gondii Coadaptation Leads to Fine Tuning of the Immune Response

Toxoplasma gondii has successfully developed strategies to evade host’s immune response and reach immune privileged sites, which remains in a controlled environment inside quiescent tissue cysts. In this review, we will approach several known mechanisms used by the parasite to modulate mainly the murine immune system at its favor. In what follows, we review recent findings revealing interference of host’s cell autonomous immunity and cell signaling, gene expression, apoptosis, and production of microbicide molecules such as nitric oxide and oxygen reactive species during parasite infection. Modulation of host’s metalloproteinases of extracellular matrix is also discussed. These immune evasion strategies are determinant to parasite dissemination throughout the host taking advantage of cells from the immune system to reach brain and retina, crossing crucial hosts’ barriers

Cellular Stress and Senescence Induction during <i>Trypanosoma cruzi</i> Infection

Chagas disease (CD) is a neglected tropical disease caused by Trypanosoma cruzi infection that, despite being discovered over a century ago, remains a public health problem, mainly in developing countries. Since T. cruzi can infect a wide range of mammalian host cells, parasite–host interactions may be critical to infection outcome. The intense immune stimulation that helps the control of the parasite’s replication and dissemination may also be linked with the pathogenesis and symptomatology worsening. Here, we discuss the findings that support the notion that excessive immune system stimulation driven by parasite persistence might elicit a progressive loss and collapse of immune functions. In this context, cellular stress and inflammatory responses elicited by T. cruzi induce fibroblast and other immune cell senescence phenotypes that may compromise the host’s capacity to control the magnitude of T. cruzi-induced inflammation, contributing to parasite persistence and CD progression. A better understanding of the steps involved in the induction of this chronic inflammatory status, which disables host defense capacity, providing an extra advantage to the parasite and predisposing infected hosts prematurely to immunosenescence, may provide insights to designing and developing novel therapeutic approaches to prevent and treat Chagas disease

Modulation of cell sialoglycophenotype: a stylish mechanism adopted by Trypanosoma cruzi to ensure its persistence in the infected host

Trypanosoma cruzi, the etiological agent of Chagas disease exhibits multiple mechanisms to guarantee its establishment and persistence in the infected host. It has been well demonstrated that T. cruzi is not able to synthesize sialic acids (Sia). To acquire the monosaccharide, the parasite makes use of a multifunctional enzyme called trans-sialidase (Tc-TS). Since this enzyme has no analogous in the vertebrate host, it has been used as a target in drug therapy development. Tc-TS preferentially catalyzes the transfer of Sia from the host glycoconjugates to the terminal β-galactopyranosyl residues of mucin-like molecules present on the parasite's cell surface. Alternatively, the enzyme can sialylate/re-sialylate glycoconjugates expressed on the surface of host cells. Since its discovery, several studies have shown that T. cruzi employs the Tc-TS activity to modulate the host cell sialoglycophenotype, thus favoring its perpetuation in the infected vertebrate. In this review, we summarize the dynamic of host/parasite sialylglycophenotype modulation, highlighting its role in the subversion of host immune response in order to promote the establishment of persistent chronic infection

Immune Responses in Leishmaniasis: An Overview

Leishmaniasis is a parasitic, widespread, and neglected disease that affects more than 90 countries in the world. More than 20 Leishmania species cause different forms of leishmaniasis that range in severity from cutaneous lesions to systemic infection. The diversity of leishmaniasis forms is due to the species of parasite, vector, environmental and social factors, genetic background, nutritional status, as well as immunocompetence of the host. Here, we discuss the role of the immune system, its molecules, and responses in the establishment, development, and outcome of Leishmaniasis, focusing on innate immune cells and Leishmania major interactions

Immunomodulatory Role of Capsular Polysaccharides Constituents of Cryptococcus neoformans

Submitted by Sandra Infurna ([email protected]) on 2020-03-19T15:25:32Z No. of bitstreams: 1 MariseNunes_AlexandreMorrot_etal_IOC_2019.pdf: 281134 bytes, checksum: 889971e7c48db82f9ec1e4b6c01ce3c7 (MD5)Approved for entry into archive by Sandra Infurna ([email protected]) on 2020-03-19T15:41:09Z (GMT) No. of bitstreams: 1 MariseNunes_AlexandreMorrot_etal_IOC_2019.pdf: 281134 bytes, checksum: 889971e7c48db82f9ec1e4b6c01ce3c7 (MD5)Made available in DSpace on 2020-03-19T15:41:09Z (GMT). No. of bitstreams: 1 MariseNunes_AlexandreMorrot_etal_IOC_2019.pdf: 281134 bytes, checksum: 889971e7c48db82f9ec1e4b6c01ce3c7 (MD5) Previous issue date: 2019Universidade Federal Rural do Rio de Janeiro. Instituto de Veterinária. Seropédica, RJ, Brasil.Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.Universidade Federal Rural do Rio de Janeiro. Instituto de Veterinária. Seropédica, RJ, Brasil / Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunoparasitologia. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunoparasitologia. Rio de Janeiro, RJ, Brasil / Universidade Federal do Rio de Janeiro. Faculdade de Medicina. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.Cryptococcosis is a systemic fungal infection caused by Cryptococcus neoformans. In immunocompetent patients, cryptococcal infection is often confined to the lungs. In immunocompromised individuals, C. neoformans may cause life-threatening illness, either from novel exposure or through reactivation of a previously acquired latent infection. For example, cryptococcal meningitis is a severe clinical disease that can manifest in people that are immunocompromised due to AIDS. The major constituents of the Cryptococcus polysaccharide capsule, glucuronoxylomannan (GXM), and galactoxylomannan (GalXM), also known as glucuronoxylomanogalactan (GXMGal), are considered the primary virulence factors of Cryptococcus. Despite the predominance of GXM in the polysaccharide capsule, GalXM has more robust immunomodulatory effects on host cellular immunity. This review summarizes current knowledge regarding host-Crytococcus neoformans interactions and the role of capsular polysaccharides in host immunomodulation. Future studies will likely facilitate a better understanding of the mechanisms involved in antigenic recognition and host immune response to C. neoformans and lead to the development of new therapeutic pathways for cryptococcal infection

COVID-19 Infection and Neuropathological Features

The pathology associated with COVID-19 infection is progressively being revealed. Recent postmortem assessments have revealed acute airway inflammation as well as diffuse alveolar damage, which bears resemblance to severe acute respiratory syndromes induced by both SARS-CoV and MERS-CoV infections. Although recent papers have highlighted some neuropathologies associated with COVID-19 infection, little is known about this topic of great importance in the area of public health. Here, we discuss how neuroinflammation related to COVID-19 could be triggered by direct viral neuroinvasion and/or cytokine release over the course of the infection