What is it about?
The highly pathogenic Ebola virus (EBOV) can enter into virtually all target cells except lymphocytes and several cellular factors required for entry are known. However, it is largely unknown whether low endogenous expression of these factors can limit viral entry into certain cells. This study shows that the lung derived cell line Calu-3 is largely resistant to entry driven by the glycoprotein of EBOV and several other filoviruses. Entry could be restored upon directed expression of the cysteine protease cathepsin L, which primes the viral glycoprotein for entry and is known to be expressed at low levels in Calu-3 cells, or of the C-type lectin DC-SIGN, which is know to boost EBOV entry into cells.
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Why is it important?
The study demonstrates that EBOV glycoprotein-driven entry into target cells can be limited at the stages of attachment and glycoprotein priming.
Perspectives
Calu-3 cells might be a useful tool to investigate EBOV interactions with entry factors. Moreover, the observation that either directed expression of DC-SIGN or cathepsin L was sufficient to restore Calu-3 cell entry suggests that attachment and priming might be interconnected and it will be interesting to explore this connection.
Professor Stefan Pöhlmann
German Primate Center
Read the Original
This page is a summary of: Calu-3 cells are largely resistant to entry driven by filovirus glycoproteins and the entry defect can be rescued by directed expression of DC-SIGN or cathepsin L, Virology, June 2019, Elsevier,
DOI: 10.1016/j.virol.2019.03.020.
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