{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T15:38:00Z","timestamp":1791214680901,"version":"4.1.0"},"reference-count":37,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2016,4,15]],"date-time":"2016-04-15T00:00:00Z","timestamp":1460678400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100000925","name":"Department of Health | National Health and Medical Research Council","doi-asserted-by":"publisher","award":["399700"],"award-info":[{"award-number":["399700"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"Department of Health | National Health and Medical Research Council","doi-asserted-by":"publisher","award":["1047252"],"award-info":[{"award-number":["1047252"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"Department of Health | National Health and Medical Research Council","doi-asserted-by":"publisher","award":["1059167"],"award-info":[{"award-number":["1059167"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001862","name":"Svenska Forskningsr\u00e5det Formas","doi-asserted-by":"publisher","award":["621-2014-4718"],"award-info":[{"award-number":["621-2014-4718"]}],"id":[{"id":"10.13039\/501100001862","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2016,4,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The alphaviral\n            <jats:italic>6k<\/jats:italic>\n            gene region encodes the two structural proteins 6K protein and, due to a ribosomal frameshift event, the transframe protein (TF). Here, we characterized the role of the\n            <jats:italic>6k<\/jats:italic>\n            proteins in the arthritogenic alphavirus Ross River virus (RRV) in infected cells and in mice, using a novel\n            <jats:italic>6k<\/jats:italic>\n            in-frame deletion mutant. Comprehensive microscopic analysis revealed that the\n            <jats:italic>6k<\/jats:italic>\n            proteins were predominantly localized at the endoplasmic reticulum of RRV-infected cells. RRV virions that lack the\n            <jats:italic>6k<\/jats:italic>\n            proteins 6K and TF [RRV-(\u03946K)] were more vulnerable to changes in pH, and the corresponding virus had increased sensitivity to a higher temperature. While the\n            <jats:italic>6k<\/jats:italic>\n            deletion did not reduce RRV particle production in BHK-21 cells, it affected virion release from the host cell. Subsequent\n            <jats:italic>in vivo<\/jats:italic>\n            studies demonstrated that RRV-(\u03946K) caused a milder disease than wild-type virus, with viral titers being reduced in infected mice. Immunization of mice with RRV-(\u03946K) resulted in a reduced viral load and accelerated viral elimination upon secondary infection with wild-type RRV or another alphavirus, chikungunya virus (CHIKV). Our results show that the\n            <jats:italic>6k<\/jats:italic>\n            proteins may contribute to alphaviral disease manifestations and suggest that manipulation of the\n            <jats:italic>6k<\/jats:italic>\n            gene may be a potential strategy to facilitate viral vaccine development.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            Arthritogenic alphaviruses, such as chikungunya virus (CHIKV) and Ross River virus (RRV), cause epidemics of debilitating rheumatic disease in areas where they are endemic and can emerge in new regions worldwide. RRV is of considerable medical significance in Australia, where it is the leading cause of arboviral disease. The mechanisms by which alphaviruses persist and cause disease in the host are ill defined. This paper describes the phenotypic properties of an RRV\n            <jats:italic>6k<\/jats:italic>\n            deletion mutant. The absence of the\n            <jats:italic>6k<\/jats:italic>\n            gene reduced virion release from infected cells and also reduced the severity of disease and viral titers in infected mice. Immunization with the mutant virus protected mice against viremia not only upon exposure to RRV but also upon challenge with CHIKV. These findings could lead to the development of safer and more immunogenic alphavirus vectors for vaccine delivery.\n          <\/jats:p>","DOI":"10.1128\/jvi.03192-15","type":"journal-article","created":{"date-parts":[[2016,2,11]],"date-time":"2016-02-11T20:32:31Z","timestamp":1455222751000},"page":"4150-4159","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":46,"title":["Effects of an In-Frame Deletion of the\n            <i>6k<\/i>\n            Gene Locus from the Genome of Ross River Virus"],"prefix":"10.1128","volume":"90","author":[{"given":"Adam","family":"Taylor","sequence":"first","affiliation":[{"name":"Emerging Viruses and Inflammation Research Group, Institute for Glycomics, Griffith University, Gold Coast, QLD, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julian V.","family":"Melton","sequence":"additional","affiliation":[{"name":"Division of Molecular Biosciences, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5661-9828","authenticated-orcid":false,"given":"Lara J.","family":"Herrero","sequence":"additional","affiliation":[{"name":"Emerging Viruses and Inflammation Research Group, Institute for Glycomics, Griffith University, Gold Coast, QLD, Australia"},{"name":"Virus and Inflammation Research Group, Faculty of Applied Science, University of Canberra, Canberra, ACT, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bastian","family":"Thaa","sequence":"additional","affiliation":[{"name":"Karolinska Institutet, Department of Microbiology, Tumor, and Cell Biology (MTC), Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liis","family":"Karo-Astover","sequence":"additional","affiliation":[{"name":"Institute of Technology, University of Tartu, Tartu, Estonia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter W.","family":"Gage","sequence":"additional","affiliation":[{"name":"Division of Molecular Biosciences, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle A.","family":"Nelson","sequence":"additional","affiliation":[{"name":"Virus and Inflammation Research Group, Faculty of Applied Science, University of Canberra, Canberra, ACT, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kuo-Ching","family":"Sheng","sequence":"additional","affiliation":[{"name":"Emerging Viruses and Inflammation Research Group, Institute for Glycomics, Griffith University, Gold Coast, QLD, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brett A.","family":"Lidbury","sequence":"additional","affiliation":[{"name":"Department of Genome Biology, The John Curtin 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