Key result
CypA depletion in Huh7 cells reduced equine arteritis virus yields by ~3-log and MERS-CoV titers by 3-fold, while human coronavirus 229E replication remained unchanged.
The replication of different nidoviruses varies strikingly in its dependence on cellular Cyclophilin A.
Cyclophilin A (CypA) is an important host factor in the replication of a variety of RNA viruses. Also the replication of several nidoviruses was reported to depend on CypA, although possibly not to the same extent. These prior studies are difficult to compare, since different nidoviruses, cell lines and experimental set-ups were used. Here, we investigated the CypA dependence of three distantly related nidoviruses that can all replicate in Huh7 cells: the arterivirus equine arteritis virus (EAV), the alphacoronavirus human coronavirus 229E (HCoV-229E), and the betacoronavirus Middle East respiratory syndrome coronavirus (MERS-CoV). The replication of these viruses was compared in the same parental Huh7 cells and in CypA-knockout Huh7 cells generated using CRISPR/Cas9-technology. CypA depletion reduced EAV yields by ~ 3-log, whereas MERS-CoV progeny titers were modestly reduced (3-fold) and HCoV-229E replication was unchanged. This study reveals that the replication of nidoviruses can differ strikingly in its dependence on cellular CypA.
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Wilde et al. (2017) studied Nidovirus replication (EAV, HCoV-229E, MERS-CoV). CypA depletion via CRISPR/Cas9 knockout vs. Parental Huh7 cells was evaluated on Viral replication yields. CypA depletion in Huh7 cells reduced equine arteritis virus yields by ~3-log and MERS-CoV titers by 3-fold, while human coronavirus 229E replication remained unchanged.
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