Conjunctival epithelial cells resist productive SARS-CoV-2 infection

Author:

Jackson Robert M,Hatton Catherine F,Spegarova Jarmila Stremenova,Georgiou Maria,Collin Joseph,Stephenson Emily,Verdon Bernard,Haq Iram J,Hussain Rafiqul,Coxhead Jonathan MORCID,Mudhar Hardeep-Singh,Wagner BartORCID,Hasoon Megan,Davey Tracey,Rooney Paul,Anjam Khan C.M.,Ward ChrisORCID,Brodlie Malcolm,Haniffa Muzlifah,Hambleton Sophie,Armstrong Lyle,Figueiredo Francisco,Queen Rachel,Duncan Christopher J A,Lako MajlindaORCID

Abstract

AbstractAlthough tropism of SARS-CoV-2 for respiratory tract epithelial cells is well established, an open question is whether the conjunctival epithelium is also a target for SARS-CoV-2. Conjunctival epithelial cells, which express viral entry receptors ACE2 and TMPRSS2, constitute the largest exposed epithelium of the ocular surface tissue, and may represent a relevant viral entry route. To address this question, we generated an organotypic air-liquid-interface model of conjunctival epithelium, composed of progenitor, basal and superficial epithelial cells and fibroblasts, which could be maintained successfully up to day 75 of differentiation. Using single-cell RNA Seq, with complementary imaging and virological assays, we observed that while all conjunctival cell types were permissive to SARS-CoV-2 genome expression, a productive infection did not ensue. The early innate immune response to SARS-CoV-2 infection in conjunctival cells was characterised by a robust autocrine and paracrine NF-Kβ activity, without activation of antiviral interferon signalling. Collectively, these data enrich our understanding of SARS-CoV-2 infection at the human ocular surface, with potential implications for the design of preventive strategies and conjunctival transplants.

Publisher

Cold Spring Harbor Laboratory

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