Abstract
Egyptian rousette bats (Rousettus aegyptiacus) are natural reservoir hosts of Marburg virus (MARV), and Ravn virus (RAVV; collectively called marburgviruses) and have been linked to human cases of Marburg virus disease (MVD). We investigated the clinical and pathologic effects of experimental MARV infection in Egyptian rousettes through a serial euthanasia study and found clear evidence of mild but transient disease. Three groups of nine, captive-born, juvenile male bats were inoculated subcutaneously with 10,000 TCID50 of Marburg virus strain Uganda 371Bat2007, a minimally passaged virus originally isolated from a wild Egyptian rousette. Control bats (n = 3) were mock-inoculated. Three animals per day were euthanized at 3, 5–10, 12 and 28 days post-inoculation (DPI); controls were euthanized at 28 DPI. Blood chemistry analyses showed a mild, statistically significant elevation in alanine aminotransferase (ALT) at 3, 6 and 7 DPI. Lymphocyte and monocyte counts were mildly elevated in inoculated bats after 9 DPI. Liver histology revealed small foci of inflammatory infiltrate in infected bats, similar to lesions previously described in wild, naturally-infected bats. Liver lesion severity scores peaked at 7 DPI, and were correlated with both ALT and hepatic viral RNA levels. Immunohistochemical staining detected infrequent viral antigen in liver (3–8 DPI, n = 8), spleen (3–7 DPI, n = 8), skin (inoculation site; 3–12 DPI, n = 20), lymph nodes (3–10 DPI, n = 6), and oral submucosa (8–9 DPI, n = 2). Viral antigen was present in histiocytes, hepatocytes and mesenchymal cells, and in the liver, antigen staining co-localized with inflammatory foci. These results show the first clear evidence of very mild disease caused by a filovirus in a reservoir bat host and provide support for our experimental model of this virus-reservoir host system.
Highlights
The Marburgviruses are non-segmented, negative-sense, single-stranded RNA viruses that cause sporadic outbreaks of severe hemorrhagic fever in humans.Marburg virus disease (MVD) is characterized by rapid onset, person-to-person transmission and a high case fatality rate
Our goal was to characterize the response of a reservoir host to experimental Marburg virus infection, which is a first step in understanding the mechanisms by which Egyptian rousettes might control virus infection
Body weights tended to increase over the course of the study, and there was no statistical difference in daily percent weight change between experimental groups or between infected and mock-infected animals
Summary
The Marburgviruses (family Filoviridae; genus Marburgvirus) are non-segmented, negative-sense, single-stranded RNA viruses that cause sporadic outbreaks of severe hemorrhagic fever in humans.Marburg virus disease (MVD) is characterized by rapid onset, person-to-person transmission and a high case fatality rate. In humans and non-human primates, the clinical features and pathology of MVD are highly similar to Ebola virus disease (EVD), which is caused by several closely-related filoviruses in the genus Ebolavirus (Ebola virus, Zaire ebolavirus; Sudan virus, Sudan ebolavirus; Bundibugyo virus, Bundibugyo ebolavirus; and, Taï Forest virus, Taï Forest ebolavirus) [1,2,3]. Gross and histologic pathology of EVD and MVD in humans and non-human primates is characterized by widely disseminated lesions including focal to widespread hepatocellular necrosis, often without inflammatory infiltrate; lymphoid depletion with lymphocyte apoptosis and accumulation of necrotic debris; acute renal tubular necrosis; and variably severe necrosis or apoptosis in the gastrointestinal tract, bone marrow, and other sites. Intracytoplasmic inclusion bodies are present in hepatocytes, macrophages, and other cells, though these are more consistently identified in cases of EVD than MVD [1,3]
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