Abstract
Reptarenaviruses cause Boid Inclusion Body Disease (BIBD), and co-infections by several reptarenaviruses are common in affected snakes. Reptarenaviruses have only been found in captive snakes, and their reservoir hosts remain unknown. In affected animals, reptarenaviruses appear to replicate in most cell types, but their complete host range, as well as tissue and cell tropism are unknown. As with other enveloped viruses, the glycoproteins (GPs) present on the virion’s surface mediate reptarenavirus cell entry, and therefore, the GPs play a critical role in the virus cell and tissue tropism. Herein, we employed single cycle replication, GP deficient, recombinant vesicular stomatitis virus (VSV) expressing the enhanced green fluorescent protein (scrVSV∆G-eGFP) pseudotyped with different reptarenavirus GPs to study the virus cell tropism. We found that scrVSV∆G-eGFPs pseudotyped with reptarenavirus GPs readily entered mammalian cell lines, and some mammalian cell lines exhibited higher, compared to snake cell lines, susceptibility to reptarenavirus GP-mediated infection. Mammarenavirus GPs used as controls also mediated efficient entry into several snake cell lines. Our results confirm an important role of the virus surface GP in reptarenavirus cell tropism and that mamma-and reptarenaviruses exhibit high cross-species transmission potential.
Highlights
Viral zoonoses can have severe consequences on human health as illustrated by viral hemorrhagic fevers (VHFs) caused by filo, flavi, hanta, nairo, and arenaviruses [1–7]
We think that our results are indicative of receptor abundance in the tested cell lines, and provide preliminary data for further studies of receptor usage and cell tropism with isolated viruses
The observed differences in the “GP-driven” tropism need to be revisited using isolated reptarena- and hartmaniviruses, since factors other than entry significantly contribute to the tissue and cell tropism
Summary
Viral zoonoses can have severe consequences on human health as illustrated by viral hemorrhagic fevers (VHFs) caused by filo-, flavi-, hanta-, nairo-, and arenaviruses [1–7]. These viruses cause long-term, usually subclinical, chronic infections in their natural host reservoirs [8]. Upon zoonotic transmission, these viruses can cause severe disease in humans via different mechanisms [4,9,10]. Boid Inclusion Body Disease (BIBD), initially recognized in the 1970s, affects mainly captive boas and pythons [11]. BIBD is characterized by the formation of electron dense intracytoplasmic inclusion bodies (IB) [12] in various cell types (including blood cells) and tissues [13–15]. Clinical manifestations of BIBD are variable and include central nervous system (CNS)
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