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bioRxiv · 10.1101/466094

Susceptibility of Spotted Doves (Streptopelia chinensis) to Experimental Infection with the SFTS Phlebovirus

Abstract

BackgroundSevere fever with thrombocytopenia syndrome virus (SFTSV), an emerging human pathogen naturally transmitted by ticks, has spread widely during the last few years. Although SFTSV has been detected in wild birds, the natural reservoir and amplifying hosts for the virus have not been well-studied.\n\nMethodology/Principle FindingsHere we report an experimental infection of spotted doves (Streptopelia chinensis) with two strains of SFTSV, JS2010-14 (hereafter JS2010), a Chinese lineage strain and JS2014-16 (JS2014) from a Japanese lineage, which represent the main viral genotypes currently circulating in East Asia. We determined that spotted doves were susceptible to SFTSV and the severity of the viremia was dose-dependent. When challenged with 107 and 105 PFU, all doves developed viremia which peaked 3-5 days post-infection (dpi). A subset (25-62.5%) of the birds challenged at 103 PFU, developed viremia. Virulence of SFTSV in spotted doves appeared to be strain-dependent. Infection with the strain of JS2014 led to a death rate of 12.5% and higher viremia titers in experimentally inoculated birds. The doves inoculated with the JS2010 strain survived infection with relatively lower virus titers in the blood.\n\nConclusions/SignificanceOur results suggest that spotted doves, one of the most abundant bird species in China, could be a competent amplifying host of SFTSV, the strain of the Japanese lineage in particular, with higher viremia titers and play an important role in the transmission of SFTSV. Our observations shed light on the ecology of SFTSV which could benefit the implementation of future surveillance and control programs.\n\nAuthor SummarySevere fever with thrombocytopenia syndrome virus (SFTSV), an emerging human pathogen naturally transmitted by ticks. Our recent study have showed that some species of migratory birds, such as swan geese and spotted doves, could be parasitized by H. longicornis, and antibodies against the virus could also be determined in these birds, which showed that migratory birds could be infected by SFTSV naturally. Other studies have reported that migratory bird routes and the distribution of H. longicornis in East Asia overlap with the geographic distribution of SFTSV. Migratory birds are known to be carriers and transmitters of infectious agents, like the causative agents of influenza, West Nile encephalitis, and Lyme disease. Wild birds often travel long distances carrying various parasites, including ticks, which may be infected with viruses and bacteria. It is therefore reasonable to hypothesize that migratory birds may have played an important role in dispersing H. longicornis-borne SFTSV in both scenarios, either the birds are infected directly with the virus or the birds are carriers of parasitic ticks that are infected with the virus. Here we report an experimental infection of spotted doves (Streptopelia chinensis) with two strains of SFTSV, JS2010-14 (hereafter JS2010), a Chinese lineage strain and JS2014-16 (JS2014) from a Japanese lineage, which represent the main viral genotypes currently circulating in East Asia. We determined that spotted doves were susceptible to SFTSV and the severity of the viremia was dose-dependent.\n\nInterestingly, virulence of SFTSV in spotted doves appeared to be strain-dependent. Infection with the strain of JS2014 led to a death rate of 12.5% and higher viremia titers in experimentally inoculated birds. The doves inoculated with the JS2010 strain survived infection with relatively lower virus titers in the blood. These findings provide novel insights for understanding the rapid spread of the virus in a short time span, especially the SFTSV strains from the Japanese lineage (genotype E), which presented cross ocean transmission.

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Li, Z., Bao, C., Hu, J., Gao, C., Zhang, N., Huo, X., Cardona, C. J., Xing, Z.. 2018-11-08. Susceptibility of Spotted Doves (Streptopelia chinensis) to Experimental Infection with the SFTS Phlebovirus. https://doi.org/10.1101/466094

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