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Stray dogs and cats pose significant challenges for public health and animal welfare due to their potential involvement in zoonotic disease transmission, accidents, and aggressions. Large urban centers exacerbated challenges due to the presence of these animals in public areas with high human density. Ethical Population Management Programs (EPMP), rooted in the One Health approach, are crucial for addressing this issue comprehensively. This study aimed to demonstrate the approach on cats and dogs EPMP and evaluate the perceptions of academic community regarding EPMP implementation on a campus situated in urban territory. The study was conducted at the Pampulha campus of UFMG in Belo Horizonte, Brazil. In response to issues of animal abandonment and conflicts, the Permanent Commission for Animal Policies (CPPA-UFMG) was established in 2019 to manage the campus’s dog, cat, and wildlife populations. The commission implemented the Trap-Neuter-Return (TNR) method, along with health assessments and vaccinations for animals. Interviews were conducted with campus staff to gauge their perception of animal management strategies. Retrospective and prospective analyses of the commission’s actions were carried out to assess implementation processes and challenges. The animal population survey conducted on campus between July 2018 and September 2021 revealed a total of 266 animals recorded. Among these animals, 195 were cats (73.3%) and 71 were dogs (26.7%), with the majority being adults. Subsequent surveys in 2019 and 2021 showed a slight increase in the animal population, with measures such as sterilization contributing to population control. Perception analysis among campus users indicated strategies such as TNR were widely endorsed for population control. The employees perception questionnaire was applied to 115 individuals, representing 42  units/departments and five gates. Associations were found between these beliefs and support for institutional actions. The majority favored sterilization (92.17%) and agreed that TNR is an appropriate approach to population control. Overall, the study reflects a community concerned about animal welfare and supportive of measures to address population management and cruelty prevention. The continuous efforts of the university’s CPPA have led to stability in the resident animal population, indicating success in achieving population control objectives. [ABSTRACT FROM AUTHOR]

Background: Herpes simplex virus type 1 (HSV-1) cause not only mild symptoms but also blindness and encephalitis. It was previously shown that the immune response against HSV-1 occurs mainly in the trigeminal ganglia (TG) and that Toll-like receptors 2 and 9 (TLR2/9) are important in mediating this response. It was also demonstrated that iNOS (nitric oxide synthase) and interleukin 1 beta (IL-1β) play an essential role in the defense against HSV-1 infection. Importantly, the present work aimed to identify the primary cells responsible for iNOS and IL-1β production and search for other important molecules and cells that might or might not depend on TLR2/9 receptors to mediate the immune response against HSV-1. Methods: C57BL/6 (wild type, WT) and TLR2/9-/- mice were infected by the intranasal route with HSV-1 (1 × 106 p.f.u.). Cells were obtained from the TG and spleen tissues and the profile of immune cells was determined by flow cytometry in infected and mock infected WT and knockout mice. The percentage of cells producing iNOS, IL-1β, granzyme B and perforin was also determined by flow cytometry. Chemokine monocyte chemoattractant protein-1 (MCP1) was measured by Cytometric Bead Array (CBA) in the TG, spleen and lung. Expression of type I interferons (IFNs), interleukins (IL) 5 and 10, IL-1β and granzyme B were quantified by real time PCR. Results: The results indicate that dendritic cells (DCs) and monocytes/macrophages (Mo/Mϕ) were the main sources of IL-1β and iNOS, respectively, which, together with type I IFNs, were essential for the immune response against HSV-1. Additionally, we showed that granzyme B produced by CD8+ T and NK lymphocytes and MCP-1 were also important for this immune response. Moreover, our data indicate that the robust production of MCP-1 and granzyme B is either TLR-independent or down regulated by TLRs and occurs in the TG of TLR2/9-/- infected mice. Conclusion: Taken together, our data provide strong evidence that the responses mediated by DCs, Mo/Mϕ, NK and CD8+ T lymphocytes through IL-1β, iNOS and granzyme B production, respectively, together with the production of type I IFN early in the infection, are crucial to host defense against HSV-1. [ABSTRACT FROM AUTHOR]

Background Herpes simplex 1 (HSV-1) causes various human clinical manifestations, ranging from simple cold sores to encephalitis. Innate immune cells recognize pathogens through Toll-like receptors (TLRs), thus initiating the immune response. Previously, we demonstrated that the immune response against HSV-1 is dependent on TLR2 and TLR9 expression and on IFN gamma production in the trigeminal ganglia (TG) of infected mice. In this work, we further investigated the cells, molecules, and mechanisms of HSV-1 infection control, especially those that are TLR-dependent. Methods C57BL/6 wild-type (WT), TLR2-/-, TLR9-/-, and TLR2/9-/- mice were intranasally infected with HSV-1. On the viral peak day, the TG and brains were collected from mice and TLR expression was measured in the TG and brain and inducible nitric oxide synthase (iNOS) expression was measured in the TG by real-time PCR. Immunofluorescence assays were performed in mice TG to detect iNOS production by F4/80+ cells. Intraperitoneal macrophages nitric oxide (NO) production was evaluated by the Griess assay. WT, CD8, RAG-/-, and iNOS-/- mice were intranasally infected in a survival assay, and their cytokine expression was measured in the TG by real-time PCR. Results Infected WT mice exhibited significantly increased TLR expression, compared with their respective controls, in the TG but not in the brain. TLR-deficient mice had moderately increased TLR expression in the TG and brain in compare with the non-infected animals. iNOS expression in the WT infected mice TG was higher than in the other groups with increased production by macrophages in the WT infected mice, which did not occur in the TLR2/9-/- mice. Additionally, the intraperitoneal macrophages of the WT mice had a higher production of NO compared with those of the TLR-deficient mice. The CD8-/-, RAG-/-, and iNOS-/- mice had 100% mortality after the HSV-1 infection compared with 10% of the WT mice. Cytokines were overexpressed in the iNOS-/- infected mice, while the RAG-/- mice were nearly unresponsive to the virus. Conclusion TLRs efficiently orchestrate the innate immune cells, eliciting macrophage response (with NO production by the macrophages), thereby controlling the HSV-1 infection through the immune response in the TG of mice. [ABSTRACT FROM AUTHOR]

Background: The neuroinflammatory response aimed at clearance of herpes simplex virus-1 (HSV-1) plays a key role in the pathogenesis of neuroaxonal damage in herpetic encephalitis. Leukocytes activated in an adaptive immune response access brain tissue by passing through the blood-brain barrier. The chemokine CCL5/RANTES is involved in recruitment of these cells to the brain acting via the receptors CCR1, CCR3 and mainly CCR5. Here, we evaluated the role of CCR5 on traffic of leukocytes in the brain microvasculature, cellular and cytokines profile in a severe form of herpetic encephalitis. Results: Wild type and mice lacking CCR5 (CCR5-/-) were inoculated intracerebrally with 104 PFU of neurotropic HSV-1. We evaluated the traffic of leukocytes in the brain microvasculature using intravital microscopy and the profile of cytokines by Enzyme-Linked Immunosorbent Assay at 1 day post infection. Flow cytometry and histopathological analyses were also carried out in brain tissue. Absence of CCR5 leads to lower viral load and an increased leukocyte adhesion in brain microvasculature, predominantly of neutrophils (CD11+ Ly6G+ cells). Moreover, there was a significant increase in the levels of MIP-1/CCL2, RANTES/CCL5, KC/CXCL1 and MIG/CXCL9 in the brain of infected CCR5-/- mice. Conclusions: These results suggest that the absence of CCR5 may boost the immune response with a high neutrophil recruitment which most likely helps in viral clearance. Nonetheless, the elevated immune response may be detrimental to the host. [ABSTRACT FROM AUTHOR]

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Abstract: Herpes simplex virus-1 (HSV-1) is a pathogen for humans that may cause severe encephalitis. Tumor necrosis factor α (TNF-α) plays a role in several viral diseases of the central nervous system (CNS). The classic proinflammatory activities of TNF-α are mediated mainly through activation of the receptor 1 for TNF-α (TNFR1). However, when HSV-1 is inoculated in the periphery, TNF-α seems to protect C57Bl/6 mice against encephalitis by a mechanism independent of TNFR1. This study aims to investigate the role of TNFR1 in HSV-1 encephalitis induced by the inoculation of the virus into the brain. Wild-type C57BL/6 (WT) and TNFR1−/− were inoculated with 102 plaque-forming units of HSV-1 by the intracranial route. Infection with HSV-1 was lethal in TNFR1−/− mice in early times after infection. TNFR1−/− mice had reduced expression of the chemokines CCL3 and CCL5, and decreased leukocyte adhesion in the brain vasculature compared to WT mice 4 days post-infection (dpi). At this time point TNFR1−/− infected mice also had higher HSV-1 viral replication and more injuries in the brain, especially in the hippocampus. In conclusion, TNFR1 seems to play a relevant role in the control of viral replication in the CNS when HSV-1 is inoculated by intracranial route. [Copyright &y& Elsevier]

In order to detect and identify Campylobacter spp. in broiler chicken carcasses, and to compare detection methods, 43 chilled and 43 frozen carcasses were collected and analyzed. Three methodologies were evaluated: an automated Enzyme Linked Fluorescent Assay (ELFA) VIDAS®30, Polymerase Chain Reaction (PCR) and real-time PCR. Only four chilled carcasses (4.6%) were considered positive for Campylobacter spp. by VIDAS®30 and no sample was positive when the conventional PCR technique was used. However, real-time PCR showed a higher incidence of contamination by Campylobacter spp. in broiler carcasses, with 45 (52.3%) positive samples. C. jejuni was the species most frequently reported in the samples (88.8%). No differences in the frequencies of Campylobacter spp. were observed between the chilled and frozen broiler carcasses. In conclusion, real-time PCR was the most sensitive method for the detection of Campylobacter spp. in chilled or frozen broiler carcasses, which were mainly contaminated by C. jejuni. [ABSTRACT FROM AUTHOR]

The most severe manifestation of Herpes Simplex Type 1 virus (HSV-1) infection is encephalitis characterized by arousal impairment and seizures that can evolve to coma and death. Previous studies reported the involvement of suppressor of cytokine signaling (SOCS) proteins, specifically SOCS1 and SOCS3, in HSV-1 infection, suggesting that other members of this family could be involved in the immune response against HSV-1. No previous study has reported the role of SOCS2 in HSV-1 infection. In the current study, C57BL/6 wild-type mice (WT) and mice deficient in SOCS2 gene (SOCS2 −/− ) were subjected to intracranial inoculation with 10 2 plaque forming units (PFU) of HSV-1. Survival curve, neuroinflammatory parameters and neuropathology were evaluated. Infected SOCS2 −/− mice had increased survival in comparison with infected WT animals. This better outcome was associated with reduced leukocyte infiltration, concentration of cytokines, and structural changes in the brain. SOCS2 seems to play a detrimental role in HSV-1 encephalitis. Moreover, the control of neuroinflammatory response in HSV-1 infection was of paramount importance to clinical outcome. [ABSTRACT FROM AUTHOR]

The aims of this study were to address the protective immune response induced by S19 vaccination ( n = 10) and RB51 revaccination, in pregnant ( n = 9) and non-pregnant ( n = 10) S19 calfhood-vaccinated cattle as follows: evaluate the in vitro CD4 + and CD8 + T-lymphocytes specific proliferation, and in vitro expression of IFN-γ by CD4 + and CD8 + T-cells and IL-4 by CD4 + , CD8 + and CD21 + lymphocytes subset. Upon in vitro stimulation with γ-irradiated Brucella abortus 2308, blood mononuclear cells from S19 vaccinated and RB51 revaccinated cows exhibited significantly higher proliferation of CD4 + and CD8 + T-lymphocytes and CD4 + IFN-γ + T-cells compared to non-vaccinated animals. RB51 revaccination, regardless of the pregnancy status, did not enhance the proliferation of CD4 + or CD8 + T-cells nor IFN-γ or IL-4 production. Data from the present study suggest that cattle's cellular immune response induced after brucellosis vaccination and revaccination is due to CD4 + and CD8 + T-lymphocytes, being CD4 + T-cells the main source of IFN-γ. [ABSTRACT FROM AUTHOR]