Journal
VETERINARY SCIENCES
Volume 8, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/vetsci8110272
Keywords
PCV2; Cap; MLS; subcellular localization
Categories
Funding
- Changde Research Center for Agricultural Biomacromolecule [2020AB02, 2020AB03]
- Postgraduate Research and Innovation Project of Hunan Agricultural University
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The mitochondrial localization signal (MLS) in the PCV2 Cap is critical for Cap-induced apoptosis and essential for PCV2 replication, as deletion of the MLS is lethal for virus rescue.
Porcine circovirus 2 (PCV2), considered one of the most globally important porcine pathogens, causes postweaning multisystemic wasting syndrome (PMWS). This virus is localized in the mitochondria in pigs with PMWS. Here, we identified, for the first time, a mitochondrial localization signal (MLS) in the PCV2 capsid protein (Cap) at the N-terminus. PK-15 cells showed colocalization of the MLS-EGFP fusion protein with mitochondria. Since the PCV2 Cap also contained a nuclear localization signal (NLS) that mediated entry into the nucleus, we inferred that the subcellular localization of the PCV2 Cap is inherently complex and dependent on the viral life cycle. Furthermore, we also determined that deletion of the MLS attenuated Cap-induced apoptosis. More importantly, the MLS was essential for PCV2 replication, as absence of the MLS resulted in failure of virus rescue from cells infected with infectious clone DNA. In conclusion, the MLS of the PCV2 Cap plays critical roles in Cap-induced apoptosis, and MLS deletion of Cap is lethal for virus rescue.
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