Abstract
Since the largest 2014–2016 Ebola virus disease outbreak in West Africa, understanding of Ebola virus infection has improved, notably the involvement of innate immune mediators. Amongst them, collectins are important players in the antiviral innate immune defense. A screening of Ebola glycoprotein (GP)-collectins interactions revealed the specific interaction of human surfactant protein D (hSP-D), a lectin expressed in lung and liver, two compartments where Ebola was found in vivo. Further analyses have demonstrated an involvement of hSP-D in the enhancement of virus infection in several in vitro models. Similar effects were observed for porcine SP-D (pSP-D). In addition, both hSP-D and pSP-D interacted with Reston virus (RESTV) GP and enhanced pseudoviral infection in pulmonary cells. Thus, our study reveals a novel partner of Ebola GP that may participate to enhance viral spread.
Highlights
The Ebolavirus genus is composed of five species, Zaire ebolavirus, Sudan ebolavirus, Tai Forest ebolavirus, Bundibugyo ebolavirus, and Reston ebolavirus
Our study shows for the first time that SP-D interaction with a viral glycoprotein can enhance virus infection in mammalian cells
The interaction between purified EBOV and Reston GP and human surfactant protein D (hSP-D) and porcine SP-D (pSP-D) was characterized using Surface plasmon resonance (SPR) analyses. Both hSP-D and pSP-D bound to GP with a high affinity and the interaction involved calcium-dependent binding of the lectin carbohydrate recognition domain (CRD) domain to GP glycans
Summary
The Ebolavirus genus is composed of five species, Zaire ebolavirus (type virus, EBOV), Sudan ebolavirus (type virus, SUDV), Tai Forest ebolavirus (type virus, TAFV), Bundibugyo ebolavirus (type virus, BDBV), and Reston ebolavirus (type virus, RESTV). Viruses 2019, 11, 15 and lungs, and evidence has emerged that EBOV was able to persist in immune-privileged sites in the body for over several months after its clearance [3,4,5,6]. These findings increased the concerns with regard to control and containment of possible future outbreaks, including the 2018 outbreak in Congo [7,8]. The mechanisms by which the virus causes disease in humans remain insufficiently understood, notably the mechanism leading to tissue invasion by the virus
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