Ebola virus mediated infectivity is restricted in canine and feline cells

•Cells of canine and feline origin are susceptible to Ebola GP-mediated entry.•However, Ebola GP-mediated infectivity of canine and feline cells is restricted.•The NPC1-mediated mechanism of Ebola entry is conserved in canine and feline cells. Ebolaviruses and marburgviruses belong to the Filovirida...

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Bibliographic Details
Published in:Veterinary microbiology 2016-01, Vol.182, p.102-107
Main Authors: Han, Ziying, Bart, Stephen M., Ruthel, Gordon, Vande Burgt, Nathan H., Haines, Kathleen M., Volk, Susan W., Vite, Charles H., Freedman, Bruce D., Bates, Paul, Harty, Ronald N.
Format: Article
Language:English
Subjects:
Animals
Canine
Carrier Proteins - genetics
Carrier Proteins - metabolism
Cats
Cells, Cultured
Dogs
Ebola virus
Ebolavirus - classification
Ebolavirus - physiology
Entry
Feline
Fibroblasts - metabolism
Fibroblasts - virology
Filovirus
Gene Deletion
Gene Expression Regulation
Infectivity
Pseudotypes
Species Specificity
Susceptibility
Viral Fusion Proteins
Virus Internalization
VSV recombinant
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Summary:•Cells of canine and feline origin are susceptible to Ebola GP-mediated entry.•However, Ebola GP-mediated infectivity of canine and feline cells is restricted.•The NPC1-mediated mechanism of Ebola entry is conserved in canine and feline cells. Ebolaviruses and marburgviruses belong to the Filoviridae family and often cause severe, fatal hemorrhagic fever in humans and non-human primates. The magnitude of the 2014 outbreak in West Africa and the unprecedented emergence of Ebola virus disease (EVD) in the United States underscore the urgency to better understand the dynamics of Ebola virus infection, transmission and spread. To date, the susceptibility and possible role of domestic animals and pets in the transmission cycle and spread of EVD remains unclear. We utilized infectious VSV recombinants and lentivirus pseudotypes expressing the EBOV surface glycoprotein (GP) to assess the permissiveness of canine and feline cells to EBOV GP-mediated entry. We observed a general restriction in EBOV-mediated infection of primary canine and feline cells. To address the entry mechanism, we used cells deficient in NPC1, a host protein implicated in EBOV entry, and a pharmacological blockade of cholesterol transport, to show that an NPC1-dependent mechanism of EBOV entry is conserved in canine and feline cells. These data demonstrate that cells of canine and feline origin are susceptible to EBOV GP mediated infection; however, infectivity of these cells is reduced significantly compared to controls. Moreover, these data provide new insights into the mechanism of EBOV GP mediated entry into cells of canine and feline origin.
ISSN:0378-1135
1873-2542
DOI:10.1016/j.vetmic.2015.11.011