Abstract
Bats are reservoir hosts of several high-impact viruses that cause significant human diseases, including Nipah virus, Marburg virus and rabies virus. They also harbor many other viruses that are thought to have caused disease in humans after spillover into intermediate hosts, including SARS and MERS coronaviruses. As is usual with reservoir hosts, these viruses apparently cause little or no pathology in bats. Despite the importance of bats as reservoir hosts of zoonotic and potentially zoonotic agents, virtually nothing is known about the host/virus relationships; principally because few colonies of bats are available for experimental infections, a lack of reagents, methods and expertise for studying bat antiviral responses and immunology, and the difficulty of conducting meaningful field work. These challenges can be addressed, in part, with new technologies that are species-independent that can provide insight into the interactions of bats and viruses, which should clarify how the viruses persist in nature, and what risk factors might facilitate transmission to humans and livestock.
Highlights
Bats belong to Chiroptera, the second-most species-rich order of mammals with more than 1100 species [1]
Infection of any organism has an inherent cost to the host and infectious agent, and a balance of host response and virus replication is essential for establishment of a reservoir host/virus relationship
Experimental infection of A. literatus with H. capsulatum resulted in fatal histoplasmosis in some bats but chronic systemic infection in others, suggesting this species can act as a reservoir and develop disease [20], similar to what is observed in rabies virus infections of bats
Summary
Bats belong to Chiroptera, the second-most species-rich order of mammals with more than 1100 species [1]. Many microbial agents, viruses, have evolved immune-evasion strategies that manipulate the host response in a manner favorable to the virus [39,40,41,42] These immune evasion molecules, most of which are virally-encoded accessory proteins, affect other species, such as humans, after spillover events. Experimental expression of viral proteins in mammalian cells often uses viral genes cloned into mammalian expression vectors that produce abundant viral protein that is probably not reflective of the levels found in cells infected with virus [42,43,44,45] This presents another interpretation difficulty because host responses of reservoirs can be fine-tuned by evolution and subtle quantitative changes in gene expression can dramatically impact infectious outcomes [46]. Experiments examining the functions of these proteins should use vectors that have controllable promotors, such as those mediated by tetracycline, so that quantitative effects can be measured and compared between primary bat cells and cells from humans to identify differences in cellular responses that might account for pathology
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