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However, these and likely other DNA virus families have evolved host species-specific counter-defenses that are equally potent and serve to protect viral DNA from restriction. Although high-risk human papillomavirus (HPV) infection triggers A3B upregulation, potentially as part of an antiviral response, the impact of this restriction factor on papillomavirus replication and pathogenesis has yet to be assessed. To study human A3B antiviral function in the absence of a species-specific counter-defense, here, we ask whether human A3B is capable of restricting\n                      <jats:italic toggle=\"yes\">Mus musculus<\/jats:italic>\n                      papillomavirus (MmuPV1)\n                      <jats:italic toggle=\"yes\">in cellulo<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      . First, we created human A3B and catalytic mutant A3B-E255A expressing FVB\/N mice. Second, MmuPV1 gene expression and replication were quantified in primary keratinocytes from these animals and, surprisingly, enzymatically active human A3B caused no measurable impairment in viral transcript or DNA accumulation. Third, A3B, catalytic mutant A3B-E255A, and nontransgenic FVB\/N animals were infected with MmuPV1, and similar pathologies were found, regardless of the A3B functionality. Thus, despite likely never being exposed to human A3B during evolution, MmuPV1 appears to be unaffected by this potent, primate-specific antiviral factor. These results suggest that MmuPV1 and perhaps papillomaviruses more broadly possess a conserved mechanism to efficiently escape restriction by human A3B and related DNA deaminases.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Human papillomaviruses (HPVs) are nearly ubiquitous, and persistent infection with high-risk types causes approximately 5% of cancers worldwide. Although HPV vaccination is effective for preventing infection, insufficient global coverage and a rising incidence of HPV-associated malignancies, such as oropharyngeal carcinoma, highlight the need to understand innate virus clearance mechanisms. APOBEC3 enzymes are a central component of the mammalian innate immune system and are hypothesized to restrict papillomavirus infection, particularly between species. Here, we establish mice that express the human antiviral enzyme APOBEC3B (A3B). Surprisingly, we find that human A3B is incapable of blocking the replication of a murine papillomavirus (\n                        <jats:italic toggle=\"yes\">Mus musculus<\/jats:italic>\n                        papillomavirus 1, MmuPV1) in relevant primary cells from these animals or in infected tissues\n                        <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                        . These findings highlight the complexity of teasing apart host-pathogen interactions and suggest that papillomaviruses may have a general mechanism for escaping restriction by antiviral enzymes, such as A3B.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/jvi.01922-25","type":"journal-article","created":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T14:00:46Z","timestamp":1770818446000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["<i>Mus musculus<\/i>\n                    papillomavirus MmuPV1 resists restriction by human APOBEC3B"],"prefix":"10.1128","volume":"100","author":[{"given":"Xingyu","family":"Liu","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01kd65564","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biochemistry and Structural Biology, University of Texas at San 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