Hepatitis E virus (HEV) is a common etiology of acute viral hepatitis worldwide. Recombinant HEV vaccines have been developed, but only one is commercially available and licensed in China since 2011. Epidemiological studies have identified genotype 3 as the major cause of chronic infection in immunocompromised individuals. Ribavirin has been shown to be effective as a monotherapy to induce HEV clearance in chronic patients who have undergone solid organ transplant (SOT) under immunosuppressive therapy. Efforts and improvements in prevention and control have been made to reduce the instances of acute and chronic hepatitis E in endemic and nonendemic countries. However, this review shows that further studies are required to demonstrate the importance of preventive vaccination and treatment worldwide, with emphasis on hepatitis E infection in the public health system.
Laboratory animals are essential mainly for experiments aiming to study pathogenesis and evaluate antivirals and vaccines against emerging human infectious diseases. Preclinical studies of coronavirus disease 19 (COVID-19) pathogenesis have used several animal species as models: transgenic human ACE2 mice (K18 mice), inbred BALB/c or C57BL/6N mice, ferrets, minks, domestic cats and dogs, hamsters, and macaques. However, the choice of an animal model relies on several limitations. Besides the host susceptibility, the researcher's experience with animal model management and the correct interpretation of clinical and laboratory records are crucial to succeed in preclinical translational research. Here, we summarise pathological and clinical findings correlated with virological data and immunological changes observed from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) experimental infections using different well-established SARS-CoV-2 animal model species. This essay aims to critically evaluate the current state of animal model translation to clinical data, as described in the human SARS-CoV-2 infection.
Introduction:The Herpesviridae family harbors a large number of viruses that infect a variety of animal types, including humans and non-human primates.The transmission of humans to non-human primates can occur through contact scratches with lesions, infected saliva and mainly through food offered contaminated to monkeys.The close relationship between humans and non-human primates allows this transmission between different species.Therefore, cross-infection can lead to severe illness or even death for both the animal and man.In 2017, during the outbreak of yellow fever in Brazil, mainly in the state of Rio de Janeiro, most of the non-human primates Sapajus sp, Leontopithecus sp, Alouatta sp and Callithrix sp., obtained a negative result for the ongoing infection, the cause of death of these animals until then was not identified. Objective:The present project aims to investigate and detect the possible circulation of herpesvirus in the population of non-human primates that were negative for the infection of yellow fever. Methodology:The dead monkeys were found in several regions and municipalities and were referred by the Health Surveillance services to LACEN / RIO, while in turn sent to FIOCRUZ.Liver tissue samples were extracted in ambient and safety NB3 by Flavivirus laboratory.Negative samples were tested for herpesvirus detection by the Pan-PCR technique, which amplifies the conserved region of the polymerase (DPOL) and allows the simultaneous detection of viruses of the family Herpesviridae.To confirm the presence of Human alphaherpesvirus 1, PCR was performed based on the amplification of the conserved region of glycoprotein G virus and construction of the phylogenetic tree through the PCR region UL 23. Results:From the total of primates negative for yellow fever 283 samples were tested with a prevalence of 34.6% (98/283) for herpesvirus, Callitrichine gamaherpesvirus 3 (CalHV-3) was detected in 30.22% (81/283), Epstein-Barr homologous virus in human.CalHV-3 can cause lymphoproliferative disease presenting B-cell lymphomas and can be fatal.In 83 individuals the prevalence of Human alfaherpesvirus 1 was 29.3% (83/283), a human virus lethal to the monkeys of the New World and no sample showed mutation of resistance to acyclovir.In addition, CalHV-1 / HHV-1 co-infection was observed in 11.6% (33/283). Conclusion:The results of this work contributed to surveillance and data can be used to raise public awareness of management and close contact with non-human primates in public spaces and forests.There were no limitations to elaborate the project, since all inputs are part of the routine laboratory practice.
O câncer colorretal (CCR) corresponde ao terceiro câncer mais incidente no mundo e o segundo mais mortal, com uma maior taxa de incidencia em paises desenvolvidos. O sistema de sinalizacao purinergico abrange enzimas e receptores celulares nos quais os nucleotideos e nucleosideos (ATP, ADP e Adenosina) atuam como sinalizadores de diversos mecanismos patofisiologicos importantes para o desenvolvimento tumoral como: estimular ou inibir a apoptose, estimular a proliferacao, migracao e diferenciacao celular, induzir a secrecao de fatores de crescimento e mediadores de inflamacao.
Abstract The immune response is crucial for coronavirus disease 19 (COVID‐19) progression, with the participation of proinflammatory cells and cytokines, inducing lung injury and loss of respiratory function. CLEC5A expression on monocytes can be triggered by viral and bacterial infections, leading to poor outcomes. Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is able to induce neutrophil activation by CLEC5A and Toll‐like receptor 2, leading to an aggressive inflammatory cascade, but little is known about the molecular interactions between CLEC5A and SARS‐CoV‐2 proteins. Here, we aimed to explore how CLEC5A expression could be affected by SARS‐CoV‐2 infection using immunological tools with in vitro, in vivo, and in silico assays. The findings revealed that high levels of CLEC5A expression were found in monocytes from severe COVID‐19 patients in comparison with mild COVID‐19 and unexposed subjects, but not in vaccinated subjects who developed mild COVID‐19. In hamsters, we detected CLEC5A gene expression during 3–15 days of Omicron strain viral challenge. Our results also showed that CLEC5A can interact with SARS‐CoV‐2, promoting inflammatory cytokine production, probably through an interaction with the receptor‐binding domain in the N‐acetylglucosamine binding site (NAG‐601). The high expression of CLEC5A and high levels of proinflammatory cytokine production were reduced in vitro by a human CLEC5A monoclonal antibody. Finally, CLEC5A was triggered by spike glycoprotein, suggesting its involvement in COVID‐19 progression; therapy with a monoclonal antibody could be a good strategy for COVID‐19 treatment, but vaccines are still the best option to avoid hospitalization/deaths.
Human Parvovirus B19 (B19V) is a common pathogen worldwide. After primary infection, B19V-DNA may permanently persist in non-erythroid tissues, including the liver of patients with acute liver failure (ALF).To validate a real-time PCR (qPCR) for the quantification of B19V-DNA, in order to establish a differential diagnosis for B19V infection in ALF patients.The qPCR techniques were based on Sybr Green® and TaqMan® methodologies. To evaluate the quality parameters of both methods, samples from patients with or without B19V infection were tested. The diagnostic utility of qPCR in the detection B19V-DNA in patients with ALF was evaluated by testing archived serum and hepatic tissue explants from 10 patients.The Sybr Green® methodology showed 97% efficiency, the limits of detection and quantification were 62.6 and 53,200 copies/mL, respectively. The TaqMan® methodology showed 95% efficiency, the limits of detection and quantification were 4.48 and 310 copies/mL, respectively. A false positive result was found only with the Sybr Green® methodology. Among ALF patients without defined etiology, three (30%) were positive for B19V DNA in serum and liver.The qPCR methods validated here were effective in clarifying uncommon cases of B19V-related ALF and are fit for differential diagnosis of ALF causes.