tetano
Editor, Senior Moderator
Pathogens
. 2022 Dec 14;11(12):1535.
doi: 10.3390/pathogens11121535.
SARS-CoV-2 Exploits Non-Canonical Autophagic Processes to Replicate, Mature, and Egress the Infected Vero E6 Cells
Juraj Koči[SUP] 1 [/SUP], Marta Novotová[SUP] 2 [/SUP], Monika Sláviková[SUP] 1 [/SUP], Boris Klempa[SUP] 1 3 [/SUP], Ivan Zahradník[SUP] 2 [/SUP]
Affiliations
Abstract
The coronavirus transforms the cytoplasm of susceptible cells to support virus replication. It also activates autophagy-like processes, the role of which is not well understood. Here, we studied SARS-CoV-2-infected Vero E6 cells using transmission electron microscopy and autophagy PCR array. After 6-24 h post-infection (hpi), the cytoplasm of infected cells only contained double-membrane vesicles, phagophores, and phagosomes engulfing virus particles and cytoplasmic debris, including damaged mitochondria. The phagosomes interacted with the viral nucleoprotein complex, virus particles, mitochondria, and lipid droplets. The phagosomes transformed into egress vacuoles, which broke through the plasmalemma and discharged the virus particles. The Vero E6 cells exhibited pronounced virus replication at 6 hpi, which stabilized at 18-24 hpi at a high level. The autophagy PCR array tests revealed a significant upregulation of 10 and downregulation of 8 autophagic gene markers out of 84. Altogether, these results underline the importance of autophagy-like processes for SARS-CoV-2 maturation and egress, and point to deviations from a canonical autophagy response.
Keywords: SARS-CoV-2; autophagy; gene regulation; mitophagy; virus egress; virus maturation.
. 2022 Dec 14;11(12):1535.
doi: 10.3390/pathogens11121535.
SARS-CoV-2 Exploits Non-Canonical Autophagic Processes to Replicate, Mature, and Egress the Infected Vero E6 Cells
Juraj Koči[SUP] 1 [/SUP], Marta Novotová[SUP] 2 [/SUP], Monika Sláviková[SUP] 1 [/SUP], Boris Klempa[SUP] 1 3 [/SUP], Ivan Zahradník[SUP] 2 [/SUP]
Affiliations
- PMID: 36558869
- DOI: 10.3390/pathogens11121535
Abstract
The coronavirus transforms the cytoplasm of susceptible cells to support virus replication. It also activates autophagy-like processes, the role of which is not well understood. Here, we studied SARS-CoV-2-infected Vero E6 cells using transmission electron microscopy and autophagy PCR array. After 6-24 h post-infection (hpi), the cytoplasm of infected cells only contained double-membrane vesicles, phagophores, and phagosomes engulfing virus particles and cytoplasmic debris, including damaged mitochondria. The phagosomes interacted with the viral nucleoprotein complex, virus particles, mitochondria, and lipid droplets. The phagosomes transformed into egress vacuoles, which broke through the plasmalemma and discharged the virus particles. The Vero E6 cells exhibited pronounced virus replication at 6 hpi, which stabilized at 18-24 hpi at a high level. The autophagy PCR array tests revealed a significant upregulation of 10 and downregulation of 8 autophagic gene markers out of 84. Altogether, these results underline the importance of autophagy-like processes for SARS-CoV-2 maturation and egress, and point to deviations from a canonical autophagy response.
Keywords: SARS-CoV-2; autophagy; gene regulation; mitophagy; virus egress; virus maturation.