91 research outputs found
Virus ontogeny:How zoonotic viruses interact with their reservoir hosts
No full textEmerging infectious viral diseases in humans frequently arise from their changing contacts with animals. By studying these virus infections in their original animal host species, we can also gain insights into the pathogeneses of these virus infections in humans
Virus ontogeny:How zoonotic viruses interact with their reservoir hosts
No full textEmerging infectious viral diseases in humans frequently arise from their changing contacts with animals. By studying these virus infections in their original animal host species, we can also gain insights into the pathogeneses of these virus infections in humans
Comparative pathogenesis of rabies in bats and carnivores, and implications for spillover to humans
No full textBat-acquired rabies is becoming increasingly common, and its diagnosis could be missed partly because its clinical presentation differs from that of dog-acquired rabies. We reviewed the scientific literature to compare the pathogenesis of rabies in bats and carnivores—including dogs—and related this pathogenesis to differences in the clinical presentation of bat-acquired and dog-acquired rabies in human beings. For bat-acquired rabies, we found that the histological site of exposure is usually limited to the skin, the anatomical site of exposure is more commonly the face, and the virus might be more adapted for entry via the skin than for dog-acquired rabies. These factors could help to explain several differences in clinical presentation between individuals with bat-acquired and those with dog-acquired rabies. A better understanding of these differences should improve the recording of a patient's history, enable drawing up of a more sophisticated list of clinical characteristics, and therefore obtain an earlier diagnosis of rabies after contact with a bat or carnivore that has rabies.
Corrections:
Begeman L, GeurtsvanKessel C, Finke S, et al. Comparative pathogenesis of rabies in bats and carnivores, and implications for spillover to humans. Lancet Infect Dis 2017; published online Oct 31. http://dx.doi.org/S1473-3099(17)30574-1. The affiliation for L Begeman, C GeurtsvanKessel, Prof M Koopmans, and Prof T Kuiken should have been “Department of Viroscience, Postgraduate School Molecular Medicine, Erasmus University Medical Centre, Rotterdam, Netherlands”. This correction has been made to the online version as of Nov 29, 2017 and will be made to the printed Review
Modeling Infection and Tropism of Human Parainfluenza Virus Type 3 in Ferrets
No full textHuman parainfluenza virus type 3 (HPIV-3) is a significant cause of lower respiratory tract infections, with the most severe disease in young infants, immunocompromised individuals, and the elderly. HPIV-3 infections are currently untreatable with licensed therapeutics, and prophylactic and therapeutic options are needed for patients at risk. To complement existing human airway models of HPIV-3 infection and develop an animal model to assess novel intervention strategies, we evaluated infection and transmission of HPIV-3 in ferrets. A well-characterized human clinical isolate (CI) of HPIV-3 engineered to express enhanced green fluorescent protein (rHPIV-3 CI-1-EGFP) was passaged on primary human airway epithelial cells (HAE) or airway organoids (AO) to avoid tissue culture adaptations. rHPIV3 CI-1-EGFP infection was assessed in vitro in ferret AO and in ferrets in vivo. Undifferentiated and differentiated ferret AO cultures supported rHPIV-3 CI-1-EGFP replication, but the ferret primary airway cells from AO were less susceptible and permissive than HAE. In vivo rHPIV-3 CI-1-EGFP replicated in the upper and lower airways of ferrets and targeted respiratory epithelial cells, olfactory epithelial cells, type I pneumocytes, and type II pneumocytes. The infection efficiently induced specific antibody responses. Taken together, ferrets are naturally susceptible to HPIV-3 infection; however, limited replication was observed that led to neither overt clinical signs nor ferret-to-ferret transmission. However, in combination with ferret AO, the ferret model of HPIV-3 infection, tissue tropism, and neutralizing antibodies complements human ex vivo lung models and can be used as a platform for prevention and treatment studies for this important respiratory pathogen. IMPORTANCE HPIV-3 is an important cause of pediatric disease and significantly impacts the elderly. Increasing numbers of immunocompromised patients suffer from HPIV-3 infections, often related to problems with viral clearance. There is a need to model HPIV-3 infections in vitro and in vivo to evaluate novel prophylaxis and treatment options. Currently existing animal models lack the potential for studying animal-to-animal transmission or the effect of immunosuppressive therapy. Here, we describe the use of the ferret model in combination with authentic clinical viruses to further complement human ex vivo models, providing a platform to study approaches to prevent and treat HPIV-3 infection. Although we did not detect ferret-to-ferret transmission in our studies, these studies lay the groundwork for further refinement of the ferret model to immunocompromised ferrets, allowing for studies of severe HPIV-3-associated disease. Such models for preclinical evaluation of prophylaxis and antivirals can contribute to reducing the global health burden of HPIV-3
Data_Sheet_1_The pathogenesis of zoonotic viral infections: Lessons learned by studying reservoir hosts.docx
No full textZoonotic viral infections that cause severe disease or even death in some people may be asymptomatic or mild in reservoir hosts. Comparison of the pathogenesis of these two host categories may potentially explain the difference in disease. However, infections in reservoir hosts are often neglected. Therefore, we compared the pathogenesis of rabies virus, macacine alphaherpesvirus, West Nile virus, Puumala orthohantavirus, monkeypox virus, Lassa mammarenavirus, H5N1 highly pathogenic avian influenza, Marburg virus, Nipah virus, Middle East respiratory syndrome, and simian/human immunodeficiency viruses in both humans and reservoir hosts. We showed that most aspects of the pathogeneses were remarkably similar. The remaining differences lead to the identification of tipping points in the pathogeneses that are important for explaining the disease outcome in severe human cases. Further elucidating these tipping points by studying zoonotic viral infections in their reservoir hosts may teach us how to reduce the severity of zoonotic viral diseases in humans.</p
A record of twin fetuses in a harbor porpoise (Phocoena phocoena) stranded on the Dutch coast
No full textPresence of coronaviruses in the common pipistrelle (P. pipistrellus) and Nathusius´ pipistrelle (P. nathusii) in relation to landscape composition
No full textA Suspected Scavenging Event by Red Foxes (Vulpes vulpes) on a Live, Stranded Harbour Porpoise (Phocoena phocoena)
No full textA Suspected Scavenging Event by Red Foxes (Vulpes vulpes) on a Live, Stranded Harbour Porpoise (Phocoena phocoena)
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