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How hosts restore organelle homeostasis and how these responses influence viral replication remain elusive. Using beet black scorch virus (BBSV), a (+)RNA virus that replicates on the endoplasmic-reticulum (ER) and induces severe deformation of ER membranes, as a model in Nicotiana benthamiana, we demonstrated that BBSV induces ER-phagy, primarily mediated by its auxiliary replication protein p23. p23 interacts with the ER-phagy receptor NbSec62, with phenylalanine at position 48 being critical for this interaction and ER-phagy induction. Upon BBSV infection, the unfolded protein response (UPR) is triggered to promote viral replication. However, the activation of the UPR also induces NbSec62-mediated ER-phagy to suppress BBSV replication. Furthermore, NbSec62 restricts other ER-replicating (+)RNA viruses, including tobacco mosaic virus and turnip mosaic virus. Our findings reveal NbSec62 as a restriction factor that interacts with BBSV VROs to regulate the balance of viral replication and ER homeostasis, providing insights into the UPR-ER-phagy signaling network in virus\u2013host interactions.<\/jats:p>","DOI":"10.1093\/plcell\/koag014","type":"journal-article","created":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T12:39:27Z","timestamp":1769171967000},"source":"Crossref","is-referenced-by-count":6,"title":["Sec62 restricts ER-replicating positive-strand RNA virus infections via UPR-dependent ER-phagy"],"prefix":"10.1093","volume":"38","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-1153-8289","authenticated-orcid":false,"given":"Ruiqi","family":"Wang","sequence":"first","affiliation":[{"name":"State Key Laboratory of Plant Environmental Resilience, College of Biological Sciences, China Agricultural University , Beijing 100193 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