Abstract
Mojiang virus (MojV) is the first henipavirus identified in a rodent and known only by sequence data, whereas all other henipaviruses have been isolated from bats (Hendra virus, Nipah virus, Cedar virus) or discovered by sequence data from material of bat origin (Ghana virus). Ephrin-B2 and -B3 are entry receptors for Hendra and Nipah viruses, but Cedar virus can utilize human ephrin-B1, -B2, -A2 and -A5 and mouse ephrin-A1. However, the entry receptor for MojV remains unknown, and its species tropism is not well characterized. Here, we utilized recombinant full-length and soluble forms of the MojV fusion (F) and attachment (G) glycoproteins in membrane fusion and receptor tropism studies. MojV F and G were functionally competent and mediated cell–cell fusion in primate and rattine cells, albeit with low levels and slow fusion kinetics. Although a relative instability of the pre-fusion conformation of a soluble form of MojV F was observed, MojV F displayed significantly greater fusion activity when heterotypically paired with Ghana virus G. An exhaustive investigation of A- and B-class ephrins indicated that none serve as a primary receptor for MojV. The MojV cell fusion phenotype is therefore likely the result of receptor restriction rather than functional defects in recombinant MojV F and G glycoproteins.
Highlights
Henipaviruses are unique members of the Paramyxoviridae family [1]
These findings suggest that if A-class if A-class ephrin ligands play a role in Mojiang virus (MojV) F and G-mediated cell fusion, they most likely ephrin ligands play a role in MojV F and G-mediated cell fusion, they most likely do not do not act as primary functional receptor(s) for MojV
We demonstrated that, functional, MojV F and G-mediated cell fusion possessed a low and slow cell fusion phenotype when compared to Hendra virus (HeV) and Cedar virus (CedV), which was in agreement with observations reported (Figure 8D) [39]
Summary
Henipaviruses are unique members of the Paramyxoviridae family [1]. The prototypical henipavirus species, Hendra virus (HeV) and Nipah virus (NiV), are highly pathogenic. Biological Safety Level-4 (BSL-4) select agents that emerged in the 1990s in Australia and peninsular Malaysia, respectively [2] They possess a broad host range spanning six mammalian orders [3,4,5] and cause infections that can result in severe respiratory illnesses and/or encephalitis with associated high fatality rates in humans (40–100%) [6,7] and other mammals, such as horses and pigs [3,4,5]. These data indicate that the MojV cell fusion phenotype is likely the result of host cell receptor restrictions rather than inherent functional defects in recombinant MojV F and G
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