Abstract
While increasing evidence points to a key role of monocytes in amphibian host defenses, monocytes are also thought to be important in the dissemination and persistent infection caused by ranavirus. However, little is known about the fate of infected macrophages or if ranavirus exploits immune privileged organs, such as the brain, in order to establish a reservoir. The amphibian Xenopus laevis and Frog Virus 3 (FV3) were established as an experimental platform for investigating in vivo whether ranavirus could disseminate to the brain. Our data show that the FV3 infection alters the BBB integrity, possibly mediated by an inflammatory response, which leads to viral dissemination into the central nervous system in X. laevis tadpole but not adult. Furthermore, our data suggest that the macrophages play a major role in viral dissemination by carrying the virus into the neural tissues.
Highlights
The alarming increase in host range and amphibian mortality caused by ranaviruses (Iridoviridae) worldwide raises practical concerns about biodiversity and aquaculture, and poses fundamental issues related to the evolution of host/pathogen interactions[1,2,3,4,5]
Frog virus 3 (FV3) infections are associated with inflammation that may cause tissue damage in tadpoles irrespective of viral load[16], and such inflammation may compromise the blood brain barrier (BBB), which protects the brain from the rest of the body
Increasing evidence points to a central role of monocytes in amphibian host defense as well as in the dissemination and persistence of ranavirus[15,24,32]
Summary
3-phosphate dehydrogenase) were used as an endogenous control, and the expression of these genes were normalized to GAPDH. In three independent experiments involving a total of 10 tadpole recipients for each group, large numbers of adoptively transferred PLs were found to infiltrate neural tissues in infected tadpole recipients as compared with their uninfected counterparts (Fig. 7A). It did not reach statistical significance because of individual variability, there was a trend toward increased infiltration of non-infected PLs in the brain of infected tadpoles consistent with the detection of large number of HAM56-positive cells found in infected tadpoles (Fig. 2). The data suggest that the PLs, possibly macrophages, harboring FV3 mediate viral entry into the tadpole brain by crossing the BBB and that the inflammation associated with FV3 infection may potentiate this phenomenon
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