{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T13:28:54Z","timestamp":1787059734585,"version":"build-2736575974"},"reference-count":36,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:00:00Z","timestamp":1787011200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:00:00Z","timestamp":1787011200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100005992","name":"Ministry of Education, Science, and Culture","doi-asserted-by":"crossref","award":["20H3164"],"award-info":[{"award-number":["20H3164"]}],"id":[{"id":"10.13039\/501100005992","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100009619","name":"Japan Agency for Medical Research and Development","doi-asserted-by":"publisher","award":["JP253fa827017, 26fk0310544s0302, 25fk0108911h0001"],"award-info":[{"award-number":["JP253fa827017, 26fk0310544s0302, 25fk0108911h0001"]}],"id":[{"id":"10.13039\/100009619","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2026,8,18]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Foot-and-mouth disease virus (FMDV) and classical swine fever virus (CSFV) both exploit host factors for internal ribosomal entry site (IRES)-mediated translation when they infect hosts. We previously identified polycystic kidney disease 1-like 3 (PKD1L3) and ubiquitin-specific peptidase 31 (USP31) as host factors for IRES-mediated translation, common to both viruses\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      . To further investigate these host factor roles in IRES activity and viral replication\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      , we established\n                      <jats:italic toggle=\"yes\">Pkd1l3<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ,\n                      <jats:italic toggle=\"yes\">\n                        Usp31\n                        <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      <\/jats:italic>\n                      , and\n                      <jats:italic toggle=\"yes\">\n                        Pkd1l3\n                        <jats:sup>\u2212\/\u2212<\/jats:sup>\n                        Usp31\n                        <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      <\/jats:italic>\n                      (double-knockout [DKO]) mice. These knockout mice were viable through 1 year after birth. FMDV and encephalomyocarditis virus (EMCV) IRES activities were significantly suppressed in\n                      <jats:italic toggle=\"yes\">\n                        Pkd1l3\n                        <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      <\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">\n                        Usp31\n                        <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      <\/jats:italic>\n                      , and DKO mouse liver tissue. CSFV IRES activity was decreased, but non-significantly, in single-knockout and DKO mouse liver tissue. CSFV replicon replication was significantly decreased in the livers of USP31\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      and DKO mice. Mice were further infected with porcine EMCV (an FMDV surrogate), and\n                      <jats:italic toggle=\"yes\">Pkd1l3<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ,\n                      <jats:italic toggle=\"yes\">Usp<\/jats:italic>\n                      31\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      , and DKO mice showed slightly less neuronal ischemic necrosis in the cerebral cortex than wild-type (WT) mice. Extramedullary hematopoiesis in the spleen was observed only in WT cases. Viral titer and\/or RNA level was significantly decreased in the lung in all KO mice, and in the brain in DKO mice. In the heart, a major target for this virus, copy number levels decreased in the order of WT,\n                      <jats:italic toggle=\"yes\">\n                        Pkd1l3\n                        <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      <\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">\n                        Usp31\n                        <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      <\/jats:italic>\n                      , and DKO, albeit without showing significant differences. Accordingly, this study provides useful evidence on PKD1L3 and USP31 host-factor deletion, as a step to developing FMDV- and CSFV-resistant livestock through the prevention of IRES-mediated translation.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Foot-and-mouth disease virus (FMDV) and classical swine fever virus (CSFV) are highly infectious to livestock, and novel mitigation strategies are required. Establishment of FMDV- and CSFV-resistant animals has the potential to prevent FMD and CSF infection. This study provides useful evidence for the development of such resistant livestock, through an\n                        <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                        evaluation of host factors for internal ribosomal entry site (IRES)-mediated translation.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/jvi.00905-26","type":"journal-article","created":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T13:02:06Z","timestamp":1784725326000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Analysis of host factors for internal ribosomal entry site-mediated translation of foot and mouth disease virus and classical swine fever virus: an\n                    <i>in vivo<\/i>\n                    evaluation in single- and double-knockout 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