How the COVID-19 pandemics inspired the development of analogical games: database review and game development

COVID-19 pandemics impacted everyone's lives. Risk of infection by the SARS-CoV-2 virus imposed severe restrictive measures, submitting the population to home isolation, daily use of face masks and restringing social encounters. In this work we present the results of a research on analogical game databases where we searched for COVID-19-themed  tabletop games, discussing which health concepts were presented on these games and what kind of structure and mechanics were used. Subsequently, we present the development of a serious board game, thought to call attention of the prevention measures to reduce the risk of infection by SARS-CoV-2 and other respiratory viruses. We discuss the rationale for the selection of game mechanics and how do they fit on the health concepts that we wanted to reinforce. The product is a print and play serious game that will be available as an open educational resource

Tissue Tropism and Target Cells of NSs-Deleted Rift Valley Fever Virus in Live Immunodeficient Mice

Rift Valley fever, caused by a member of the Bunyaviridae family, has spread during recent years to most sub-Saharan African countries, in Egypt and in the Arabian peninsula. The virus can be transmitted by insect vectors or by direct contacts with infectious tissues. The analysis of virus replication and dissemination in laboratory animals has been hampered by the need to euthanize sufficient numbers of animals and to assay appropriate organs at various time points after infection to evaluate the viral replication. By following the bioluminescence and fluorescence of Rift Valley fever viruses expressing light reporters, we were able to track the real-time dissemination of the viruses in live immunodeficient mice. We showed that the first infected organs were the thymus, spleen and liver, but the liver rapidly became the main location of viral replication. Phagocytes also appeared as important targets, and their systemic depletion by use of clodronate liposomes decreased the number of viruses in the blood, delayed the viral dissemination and prolonged the survival of the infected mice

Leishmania amazonensis resistance in murine macrophages: Analysis of possible mechanisms.

Leishmaniasis encompass a group of infectious parasitic diseases occurring in 97 endemic countries where over one billion people live in areas at risk of infection. It is in the World Health Organization list of neglected diseases and it is considered a serious public health problem, with more than 20,000 deaths a year and high morbidity. Infection by protozoa from the genus Leishmania can cause several forms of the disease, which may vary from a self-healing ulcer to fatal visceral infection. Leishmania species, as well as host immune response and genetics can modulate the course of the disease. Leishmania sp are obligatory intracellular parasites that have macrophages as their main host cell. Depending on the activation phenotype, these cells may have distinct roles in disease development, acting in parasite control or proliferation. Therefore, the purpose of this work was to analyze Leishmania amazonensis infection in primary macrophage cells obtained from mice with two distinct genetic backgrounds, ie. different susceptibility to the infection; evaluating the cause for that difference. After infection, peritoneal macrophages from the resistant C3H/He strain presented lower parasite load when compared to susceptible BALB/c macrophages. The same was also true when cells received a Th2 stimulus after infection, but the difference was abrogated under Th1 stimulus. Nitric oxide production and arginase activity was different between the strains under Th1 or Th2 stimulus, respectively, but iNOS inhibition was unable to suppress C3H/He resistance. Hydrogen peroxide production was also higher in C3H/He than BALB/c under Th1 stimulus, but it could not account for differences in susceptibility. These results led us to conclude that, although they have an important role in parasite control, neither NO nor H2O2 production can explain C3H/He resistance to infection. Other studies are needed to uncover different mechanisms of resistance/susceptibility to L. amazonensis

How Do Mouse Strains and Inoculation Routes Influence the Course of Experimental <em>Trypanosoma cruzi</em> Infection?

Chagas’ disease outcomes depend on several factors including parasite and host genetics, immune response, and route of infection. In this study, we investigate the influence of inoculation route and host genetic background on the establishment and development of Chagas disease in mice, using an isolate of Trypanosoma cruzi SC2005 strain (TcII), which was obtained from an oral Chagas’ disease outbreak in Santa Catarina, Brazil. Comparative analysis of the immunopathological, histopathological, and hematological profiles of mice was performed demonstrating the influence of the route of infection in disease severity. In outbred mice, intraperitoneal (IP) infection led to higher infection and mortality rates and more severe parasitaemia, when compared with intragastric (IG) infection. Nevertheless, tissue colonization was similar, showing severe damage in the heart, with intense lymphocytic inflammatory infiltrates, regardless of the route of infection. On the other hand, in mice IG-infected, the host genetic background influences the start timing of immune response against Trypanosoma cruzi. The susceptible BALB/c inbred mouse strain presented an earlier development of a cytotoxic cellular profile, when compared with A mice. We hypothesize that the cytotoxic response mounted before the parasitaemia increase allowed for a milder manifestation of Chagas’ disease in intragastrically infected mice

MBT/Pas mouse: a relevant model for the evaluation of Rift Valley fever vaccines.

International audienceCurrently, there are no worldwide licensed vaccines for Rift Valley fever (RVF) that are both safe and effective. Development and evaluation of vaccines, diagnostics and treatments depend on the availability of appropriate animal models. Animal models are also necessary to understand the basic pathobiology of infection. Here, we report the use of an inbred MBT/Pas mouse model that consistently reproduces RVF disease and serves our purpose for testing the efficacy of vaccine candidates; an attenuated Rift Valley fever virus (RVFV) and a recombinant RVFV-capripoxvirus. We show that this model is relevant for vaccine testing

A new mouse model reveals a critical role for host innate immunity in resistance to Rift Valley fever.

Rift Valley fever (RVF) is an arthropod-borne viral disease repeatedly reported in many African countries and, more recently, in Saudi Arabia and Yemen. RVF virus (RVFV) primarily infects domesticated ruminants, resulting in miscarriage in pregnant females and death for newborns and young animals. It also has the ability to infect humans, causing a feverish syndrome, meningoencephalitis, or hemorrhagic fever. The various outcomes of RVFV infection in animals and humans argue for the existence of host genetic determinants controlling the disease. We investigated the susceptibility of inbred mouse strains to infection with the virulent RVFV ZH548 strain. Compared with classical BALB/cByJ mice, wild-derived Mus m. musculus MBT/Pas mice exhibited earlier and greater viremia and died sooner, a result in sharp contrast with their resistance to infection with West Nile virus and influenza A. Infection of mouse embryonic fibroblasts (MEFs) from MBT/Pas mice with RVFV also resulted in higher viral production. Microarray and quantitative RT-PCR experiments showed that BALB/cByJ MEFs displayed a significant activation of the type I IFN pathway. In contrast, MBT/Pas MEFs elicited a delayed and partial type I IFN response to RVFV infection. RNA interference-mediated inhibition of genes that were not induced by RVFV in MBT/Pas MEFs increased viral production in BALB/cByJ MEFs, thus demonstrating their functional importance in limiting viral replication. We conclude that the failure of MBT/Pas murine strain to induce, in due course, a complete innate immune response is instrumental in the selective susceptibility to RVF

Can P-glycoprotein and β-tubulin polymorphisms be used as genetic markers of resistance in Dirofilaria immitis from Rio de Janeiro, Brazil?

Submitted by Sandra Infurna ([email protected]) on 2018-08-30T17:01:44Z No. of bitstreams: 1 norma_LABARTHE_ETAL_ioc_2018.PDF: 1026902 bytes, checksum: 557a4e9a1ac3873af86f4f7889b1112d (MD5)Approved for entry into archive by Sandra Infurna ([email protected]) on 2018-08-30T17:12:22Z (GMT) No. of bitstreams: 1 norma_LABARTHE_ETAL_ioc_2018.PDF: 1026902 bytes, checksum: 557a4e9a1ac3873af86f4f7889b1112d (MD5)Made available in DSpace on 2018-08-30T17:12:22Z (GMT). No. of bitstreams: 1 norma_LABARTHE_ETAL_ioc_2018.PDF: 1026902 bytes, checksum: 557a4e9a1ac3873af86f4f7889b1112d (MD5) Previous issue date: 2018Universidade Federal Fluminense. Faculdade de Veterinária. Programa de Pós‑Graduação em Medicina Veterinária – Clínica e Reprodução Animal. Niterói, RJ, Brasil / Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunomodulação e Protozoologia. Rio de Janeiro, RJ, Brasil.Universidade Federal Fluminense. Faculdade de Veterinária. Programa de Pós‑Graduação em Medicina Veterinária – Clínica e Reprodução Animal. Niterói, RJ, Brasil / Fundação Oswaldo Cruz. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunomodulação e Protozoologia. Rio de Janeiro, RJ, Brasil.Universidade Federal Rural do Rio de Janeiro. Instituto de Veterinária. Departamento de Medicina e Cirurgia Veterinária. Seropédica, RJ, Brasil.Médica Veterinária, Vet Ypiranga. Rio de Janeiro, RJ, Brasil.Universidade Federal Fluminense. Faculdade de Veterinária. Programa de Pós‑Graduação em Medicina Veterinária – Clínica e Reprodução Animal. Niterói, RJ, Brasil.Universidade Federal Fluminense. Faculdade de Veterinária. Programa de Pós‑Graduação em Medicina Veterinária – Clínica e Reprodução Animal. Niterói, RJ, BrasilDirofilaria immitis, the causative agent of , is worldwide the most important filarid to affect domestic dogs. Prevention of this infection is done by macrocyclic lactones, but some reports on the lack of efficacy have been published. Although the actual cause of resistance is unknown, single nucleotide polymorphisms (SNPs) on a P-glycoprotein ABC transporter and β-tubulin genes have been pointed out as candidates for genetic markers of resistance. We conducted a survey to verify the presence of these suggested genetic markers in microfilariae from 30 naturally infected dogs under macrocyclic lactones treatment living in an endemic area in the state of Rio de Janeiro

MOESM1 of Can P-glycoprotein and β-tubulin polymorphisms be used as genetic markers of resistance in Dirofilaria immitis from Rio de Janeiro, Brazil?

Additional file 1. Sequencing data. Chromatograms obtained by sequencing the samples of microfilariae pools of Dirofilaria immitis. Each figure shows all chromatograms for a given position of either Pgp or Tub gene

Genetic dissection of Rift Valley fever pathogenesis: Rvfs2 locus on mouse chromosome 11 enables survival to early-onset hepatitis

International audienceInfection of mice with Rift Valley fever virus (RVFV) reproduces major pathological features of severe human disease, notably the early-onset hepatitis and delayed-onset encephalitis. We previously reported that the Rvfs2 locus from the susceptible MBT/Pas strain reduces survival time after RVFV infection. Here, we used BALB/cByJ (BALB) mice congenic for Rvfs2 (C.MBT-Rvfs2) to investigate the pathophysiological mechanisms impacted by Rvfs2. Clinical, biochemical and histopathological features indicated similar liver damage in BALB and C.MBT-Rvfs2 mice until day 5 after infection. However, while C.MBT-Rvfs2 mice succumbed from acute liver injury, most BALB mice recovered and died later of encephalitis. Hepatocytes of BALB infected liver proliferated actively on day 6, promoting organ regeneration and recovery from liver damage. By comparison with C.MBT-Rvfs2, BALB mice had up to 100-fold lower production of infectious virions in the peripheral blood and liver, strongly decreased RVFV protein in liver and reduced viral replication in primary cultured hepatocytes, suggesting that the BALB Rvfs2 haplotype limits RVFV pathogenicity through decreased virus replication. Moreover, bone marrow chimera experiments showed that both hematopoietic and non-hematopoietic cells are required for the protective effect of the BALB Rvfs2 haplotype. Altogether, these results indicate that Rvfs2 controls critical events which allow survival to RVFV-induced hepatitis