{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T03:35:57Z","timestamp":1792035357966,"version":"4.4.0"},"reference-count":54,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2007,3,1]],"date-time":"2007-03-01T00:00:00Z","timestamp":1172707200000},"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":[[2007,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Alphaviruses\nare widely distributed throughout the world. During the last few\nthousand years, the New World viruses, including Venezuelan equine\nencephalitis virus (VEEV) and eastern equine encephalitis virus (EEEV),\nevolved separately from those of the Old World, i.e., Sindbis virus\n(SINV) and Semliki Forest virus (SFV). Nevertheless, the results of our\nstudy indicate that both groups have developed the same characteristic:\ntheir replication efficiently interferes with cellular transcription\nand the cell response to virus replication. Transcriptional shutoff\ncaused by at least two of the Old World alphaviruses, SINV and SFV,\nwhich belong to different serological complexes, depends on nsP2, but\nnot on the capsid protein, functioning. Our data suggest that the New\nWorld alphaviruses VEEV and EEEV developed an alternative mechanism of\ntranscription inhibition that is mainly determined by their capsid\nprotein, but not by the nsP2. The ability of the VEEV capsid to inhibit\ncellular transcription appears to be controlled by the amino-terminal\nfragment of the protein, but not by its protease activity or by the\npositively charged RNA-binding domain. These data provide new insights\ninto alphavirus evolution and present a plausible explanation for the\nparticular recombination events that led to the formation of western\nequine encephalitis virus (WEEV) from SINV- and EEEV-like ancestors.\nThe recombination allowed WEEV to acquire capsid protein functioning in\ntranscription inhibition from EEEV-like virus. Identification of the\nnew functions in the New World alphavirus-derived capsids opens an\nopportunity for developing new, safer alphavirus-based gene expression\nsystems and designing new types of attenuated vaccine strains of VEEV\nand\nEEEV.<\/jats:p>","DOI":"10.1128\/jvi.02073-06","type":"journal-article","created":{"date-parts":[[2006,11,15]],"date-time":"2006-11-15T23:23:45Z","timestamp":1163633025000},"page":"2472-2484","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":264,"title":["The Old World and New World Alphaviruses Use Different Virus-Specific Proteins for Induction of Transcriptional Shutoff"],"prefix":"10.1128","volume":"81","author":[{"given":"Natalia","family":"Garmashova","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas 77555-1019"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rodion","family":"Gorchakov","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas 77555-1019"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eugenia","family":"Volkova","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas 77555-1019"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Slobodan","family":"Paessler","sequence":"additional","affiliation":[{"name":"Department of\rPathology, University of Texas Medical Branch, Galveston, Texas\r77555-0609"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Frolova","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas 77555-1019"},{"name":"Department of Biochemistry\rand Molecular Biology, University of Texas Medical Branch, Galveston,\rTexas 77555-1072"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ilya","family":"Frolov","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas 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