{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,27]],"date-time":"2026-05-27T19:34:22Z","timestamp":1779910462297,"version":"3.53.1"},"reference-count":137,"publisher":"MDPI AG","issue":"6","license":[{"start":{"date-parts":[[2024,6,4]],"date-time":"2024-06-04T00:00:00Z","timestamp":1717459200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Viruses"],"abstract":"<jats:p>A proteomics analysis of purified rabies virus (RABV) revealed 47 entrapped host proteins within the viral particles. Out of these, 11 proteins were highly disordered. Our study was particularly focused on five of the RABV-entrapped mouse proteins with the highest levels of disorder: Neuromodulin, Chmp4b, DnaJB6, Vps37B, and Wasl. We extensively utilized bioinformatics tools, such as FuzDrop, D2P2, UniProt, RIDAO, STRING, AlphaFold, and ELM, for a comprehensive analysis of the intrinsic disorder propensity of these proteins. Our analysis suggested that these disordered host proteins might play a significant role in facilitating the rabies virus pathogenicity, immune system evasion, and the development of antiviral drug resistance. Our study highlighted the complex interaction of the virus with its host, with a focus on how the intrinsic disorder can play a crucial role in virus pathogenic processes, and suggested that these intrinsically disordered proteins (IDPs) and disorder-related host interactions can also be a potential target for therapeutic strategies.<\/jats:p>","DOI":"10.3390\/v16060916","type":"journal-article","created":{"date-parts":[[2024,6,5]],"date-time":"2024-06-05T03:49:28Z","timestamp":1717559368000},"page":"916","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Intrinsic Disorder in the Host Proteins Entrapped in Rabies Virus Particles"],"prefix":"10.3390","volume":"16","author":[{"given":"Hafiza Nimra","family":"Ashraf","sequence":"first","affiliation":[{"name":"Department of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4037-5857","authenticated-orcid":false,"given":"Vladimir N.","family":"Uversky","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA"},{"name":"USF Health Byrd Alzheimer\u2019s Research Institute, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,6,4]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"101","DOI":"10.1016\/S1474-4422(02)00041-8","article-title":"Human rabies: A disease of complex neuropathogenetic mechanisms and diagnostic challenges","volume":"1","author":"Hemachudha","year":"2002","journal-title":"Lancet Neurol."},{"key":"ref_2","unstructured":"Greenlee, J.E. 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