Richard Suu-Ire1,2,3,4‡, Lineke Begeman5‡, Ashley C. Banyard6, Andrew C. Breed6, Christian Drosten7, Elisa Eggerbauer8, Conrad M. Freuling8, Louise Gibson1, Hooman Goharriz6, Daniel L. Horton9, Daisy Jennings6, Ivan V. Kuzmin10, Denise Marston6, Yaa Ntiamoa-Baidu2, Silke Riesle Sbarbaro1,11, David Selden6, Emma L. Wise6, Thijs Kuiken5, Anthony R. Fooks6, Thomas Mu¨ller8, James L. N. Wood11, Andre A. Cunningham1*
1 Institute of Zoology, Zoological Society of London, London, United Kingdom,
2 Department of Animal Biology and Conservation Science, University of Ghana, Accra, Ghana,
3 Veterinary Services Department Ministry of Food and Agriculture, Accra, Ghana,
4 Wildlife Division of the Forestry Commission, Accra, Ghana,
5 Department of Viroscience, Erasmus University Medical Centre, Rotterdam, The Netherlands,
6 Wildlife Zoonoses and Vector Borne Disease Research Group, Animal and Plant Health Agency, Addlestone, United Kingdom,
7 Institute of Virology, Medical University of Berlin, Berlin, Germany,
8 Institute of Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Greifswald, Island of Riems, Germany,
9 School of Veterinary Medicine, University of Surrey,
Guildford, United Kingdom,
10 Department of Pathology, University of Texas Medical Branch, Galveston, Texas, United States of America,
11 Department of Veterinary Medicine, University of Cambridge, Cambridge, United Kingdom
Rabies is a fatal neurologic disease caused by lyssavirus infection. People are infected through contact with infected animals. The relative increase of human rabies acquired from bats calls for a better understanding of lyssavirus infections in their natural hosts. So far, there is no experimental model that mimics natural lyssavirus infection in the reservoir bat species. Lagos bat virus is a lyssavirus that is endemic in straw-colored fruit bats (Eidolon helvum) in Africa. Here we compared the susceptibility of these bats to three strains of Lagos bat virus (from Senegal, Nigeria, and Ghana) by intracranial inoculation. To allow comparison between strains, we ensured the same titer of virus was inoculated in the same location of the brain of each bat. All bats (n = 3 per strain) were infected, and developed neurological signs, and fatal meningoencephalitis with lyssavirus antigen expression in neurons. There were three main differences among the groups. First, time to death was substantially shorter in the Senegal and Ghana groups (4 to 6 days) than in the Nigeria group (8 days). Second, each virus strain produced a distinct clinical syndrome. Third, the spread of virus to peripheral tissues, tested by hemi-nested reverse transcriptase PCR, was frequent (3 of 3 bats) and widespread (8 to 10 tissues positive of 11 tissues examined) in the Ghana group, was frequent and less widespread in the Senegal group (3/3 bats, 3 to 6 tissues positive), and was rare and restricted in the Nigeria group (1/3 bats, 2 tissues positive).
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