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SARS-CoV-2 spike proteins interact with the human angiotensin-converting enzyme 2 (ACE2) receptor, together with accessory molecules that facilitate viral entry, through its spike receptor-binding domain (RBD). Although ACE2 is the primary receptor required for viral replication, its expression patterns do not fully correlate with viral distribution or tissue pathology. Moreover, SARS-CoV-2 has been shown to infect cells and tissues lacking detectable ACE2 expression. Viral entry via ACE2-independent pathways may also confer resistance to some monoclonal antibodies (Abs) targeting the spike RBD that block ACE2-mediated binding. These observations highlight the potential significance of ACE2-independent entry factors in SARS-CoV-2 infection, particularly in vaccinated individuals with Abs directed against ACE2-dependent viral entry. In this review, we discuss the emerging roles of ACE2-independent entry factors in SARS-CoV-2 infection and the immune responses. These factors include CD147, AXL, CD169\/Siglec-1, CD209L, CD209, CLEC4G, ASGR1, LDLRAD3, TMEM30A, TMEM106B, transferrin receptor 1, GPR78, integrin \u03b15\u03b21, KREMEN1, LFA-1, and CD4. While ACE2 remains central to viral replication, ACE2-independent entry appears sufficient to elicit immune responses. Therefore, future investigations are warranted to elucidate the roles of ACE2-independent mechanisms in immune-mediated pathology and viral evolution, independent of immune pressure targeting ACE2-mediated entry in previously infected or vaccinated individuals.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.01897-24","type":"journal-article","created":{"date-parts":[[2025,12,22]],"date-time":"2025-12-22T14:00:32Z","timestamp":1766412032000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":3,"title":["ACE2-independent entry factors for SARS-CoV-2 infection and immune activation"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0009-0005-5467-8655","authenticated-orcid":false,"given":"Yiyu","family":"Sun","sequence":"first","affiliation":[{"name":"Rutgers School of Graduate Studies","place":["Newark, USA"]},{"name":"Public Health Research Institute","place":["Newark, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0727-8289","authenticated-orcid":true,"given":"Lok-Yin Roy","family":"Wong","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/014ye1258","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers New Jersey Medical School","place":["Newark, USA"]},{"id":[{"id":"https:\/\/ror.org\/014ye1258","id-type":"ROR","asserted-by":"publisher"}],"name":"Center for Virus-Host Innate Immunity, Rutgers New Jersey Medical School","place":["Newark, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0696-9755","authenticated-orcid":true,"given":"Theresa L.","family":"Chang","sequence":"additional","affiliation":[{"name":"Public Health Research Institute","place":["Newark, USA"]},{"id":[{"id":"https:\/\/ror.org\/014ye1258","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers New Jersey Medical School","place":["Newark, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/d41586-023-00014-3"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(23)00050-8"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.3389\/fpubh.2020.00241"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-022-05325-5"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S2666-7568(21)00253-1"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1080\/22221751.2022.2052358"},{"key":"e_1_3_2_8_2","unstructured":"World Health Organization. 2025. 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