{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T13:13:26Z","timestamp":1792588406172,"version":"4.5.0"},"reference-count":39,"publisher":"American Society for Microbiology","issue":"20","license":[{"start":{"date-parts":[[2006,10,15]],"date-time":"2006-10-15T00:00:00Z","timestamp":1160870400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2006,10,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Lack\nof an appropriate animal model for dengue virus (DEN), which causes\ndengue fever and dengue hemorrhagic fever\/dengue shock syndrome\n(DHF\/DSS), has impeded characterization of the mechanisms underlying\nthe disease pathogenesis. The cardinal feature of DHF\/DSS, the severe\nform of DEN infection, is increased vascular permeability. To develop a\nmurine model that is more relevant to DHF\/DSS, a novel DEN strain,\nD2S10, was generated by alternately passaging a non-mouse-adapted DEN\nstrain between mosquito cells and mice, thereby mimicking the natural\ntransmission cycle of the virus between mosquitoes and humans. After\ninfection with D2S10, mice lacking interferon receptors died early\nwithout manifesting signs of paralysis, carried infectious virus in\nboth non-neuronal and neuronal tissues, and exhibited signs of\nincreased vascular permeability. In contrast, mice infected with the\nparental DEN strain developed paralysis at late times after infection,\ncontained detectable levels of virus only in the central nervous\nsystem, and displayed normal vascular permeability. In the mice\ninfected with D2S10, but not the parental DEN strain, significant\nlevels of serum tumor necrosis factor alpha (TNF-\u03b1) were\nproduced, and the neutralization of TNF-\u03b1 activity prevented\nearly death of D2S10-infected mice. Sequence analysis comparing D2S10\nto its parental strain implicated a conserved region of amino acid\nresidues in the envelope protein as a possible source for the D2S10\nphenotype. These results demonstrate that D2S10 causes a more relevant\ndisease in mice and that TNF-\u03b1 may be one of several key\nmediators of severe DEN-induced disease in mice. This report represents\na significant advance in animal models for severe DEN disease, and it\nbegins to provide mechanistic insights into DEN-induced disease in\nvivo.<\/jats:p>","DOI":"10.1128\/jvi.00062-06","type":"journal-article","created":{"date-parts":[[2006,9,27]],"date-time":"2006-09-27T18:19:39Z","timestamp":1159381179000},"page":"10208-10217","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":318,"title":["Murine Model for Dengue Virus-Induced Lethal Disease with IncreasedVascular Permeability"],"prefix":"10.1128","volume":"80","author":[{"given":"Sujan","family":"Shresta","sequence":"first","affiliation":[{"name":"La Jolla Institute for\rAllergy and Immunology, 10355 Science Center Drive, San Diego,\rCalifornia 92121"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristin L.","family":"Sharar","sequence":"additional","affiliation":[{"name":"La Jolla Institute for\rAllergy and Immunology, 10355 Science Center Drive, San Diego,\rCalifornia 92121"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniil M.","family":"Prigozhin","sequence":"additional","affiliation":[{"name":"La Jolla Institute for\rAllergy and Immunology, 10355 Science Center Drive, San Diego,\rCalifornia 92121"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. Robert","family":"Beatty","sequence":"additional","affiliation":[{"name":"Division\rof Infectious Diseases, School of Public Health, 140 Warren Hall,\rUniversity of California at Berkeley, Berkeley, California\r94720-7360"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eva","family":"Harris","sequence":"additional","affiliation":[{"name":"Division\rof Infectious Diseases, School of Public Health, 140 Warren Hall,\rUniversity of California at Berkeley, Berkeley, California\r94720-7360"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.virol.2005.06.009"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1006\/viro.1999.9887"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-695X.2003.tb00646.x"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.21.13797-13799.2005"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.36.3.1036-1041.1982"},{"key":"e_1_3_2_7_2","first-page":"1043","volume":"1","year":"2001","unstructured":"Burke, D. 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Harris. 2005. Inhibition of dengue virus translation and RNA synthesis by a morpholino oligomer targeted to the top of the terminal 3\u2032 stem-loop structure. 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