R. Izurieta, David A DeLacure, A. Izurieta, Ismael Hoare, M. Ortiz
{"title":"Mayaro virus: the jungle flu","authors":"R. Izurieta, David A DeLacure, A. Izurieta, Ismael Hoare, M. Ortiz","doi":"10.2147/VAAT.S128711","DOIUrl":"https://doi.org/10.2147/VAAT.S128711","url":null,"abstract":"php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). Virus Adaptation and Treatment 2018:10 9–17 Virus Adaptation and Treatment Dovepress","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"23 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121355169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Management strategies of enterovirus D68 outbreaks: current perspectives","authors":"N. Milhano, K. S. Borge, K. Bragstad, S. Dudman","doi":"10.2147/VAAT.S140376","DOIUrl":"https://doi.org/10.2147/VAAT.S140376","url":null,"abstract":": Following its discovery in California in 1962, enterovirus D68 (EV-D68) was reported only sporadically around the world. In August 2014, a marked increase of EV-D68 cases in young children with severe respiratory infections was reported in the USA and Canada and later in Europe and Asia. Some of these cases were also found to be associated with acute flaccid paralysis, which exacerbated public health concern, and has since triggered international efforts to strengthen both EV-D68 and acute flaccid paralysis surveillance systems. This review summarizes the current knowledge on EV-D68, offering an overview of EV-D68 epidemiology, clinical presentations, diagnostic methodologies, and treatment strategies, as well as surveillance and outbreak management.","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116085862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Lujo virus: current concepts","authors":"N. Sewlall, J. Pawęska","doi":"10.2147/vaat.s113593","DOIUrl":"https://doi.org/10.2147/vaat.s113593","url":null,"abstract":": Lujo virus (LUJV), a novel Old World arenavirus, was found to cause a fulminant viral hemorrhagic fever syndrome in an outbreak in 2008. The primary patient was from Lusaka, Zambia, and subsequent nosocomial transmission occurred to four other patients in Johannesburg, South Africa, hence the name Lujo virus. Like all arenaviruses, LUJV is a segmented, single-stranded, negative-sense RNA virus. Genomic sequencing confirmed that LUJV G1 glycoprotein was novel, diverse and genetically equidistant from other arenaviruses. A clinical syndrome resembling severe, fulminant Lassa virus infection was responsible for a high case fatality rate of 80% (4/5 cases). This review describes briefly the clinical course of the disease, laboratory findings and diagnosis. Recent studies address the current aspects of epidemiology, and treatments, specifically comparing with Lassa virus.","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"5 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129053796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Usutu virus: current knowledge and future perspectives","authors":"J. Saiz, A. Blázquez","doi":"10.2147/VAAT.S123619","DOIUrl":"https://doi.org/10.2147/VAAT.S123619","url":null,"abstract":": The Flavivirus genus (Flaviviridae family) contains important pathogens such as yellow fever virus, Japanese encephalitis virus, St Louis encephalitis virus, West Nile virus, Usutu virus (USUV), Zika virus, and dengue virus, many of which constitute a worrisome threat to global human and animal health. USUV is transmitted by mosquitoes and, as any other flavivirus, is an enveloped plus-strand RNA virus. The virus was first isolated from Culex neavei mosquitoes in South Africa in 1959 near the Usutu River, from where it takes its name. Since then, the virus was confined to Africa until its first detection in Austria in 2001, although it was probably present in Europe since 1996 or even earlier. After that, USUV has spread throughout Europe, causing a considerable mortality among birds and a few neurologic cases in humans. The main USUV natural hosts are birds, but infection has also been reported in other vertebrate species, including humans. The fast spread of the virus through the continent, the relatively high mortality caused in birds, and the recent neuroinvasive human cases related to USUV infection reported in Europe have raised serious concerns about its possible consequences for public health. Here, an updated review of current knowledge about this emerging pathogen is presented.","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"34 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116664844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Juliarena, Clarisa Natalia Barrios, C. Lützelschwab, E. Esteban, S. Gutiérrez
{"title":"Bovine leukemia virus: current perspectives","authors":"M. Juliarena, Clarisa Natalia Barrios, C. Lützelschwab, E. Esteban, S. Gutiérrez","doi":"10.2147/VAAT.S113947","DOIUrl":"https://doi.org/10.2147/VAAT.S113947","url":null,"abstract":"Fil: Juliarena, Marcela Alicia. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Conicet - Tandil. Centro de Investigacion Veterinaria de Tandil. Universidad Nacional del Centro de la Provincia de Buenos Aires. Centro de Investigacion Veterinaria de Tandil. Provincia de Buenos Aires. Gobernacion. Comision de Investigaciones Cientificas. Centro de Investigacion Veterinaria de Tandil; Argentina","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123547393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Guillain–Barrè peptide signatures: from Zika virus to Campylobacter, and beyond","authors":"G. Lucchese, D. Kanduc","doi":"10.2147/VAAT.S124535","DOIUrl":"https://doi.org/10.2147/VAAT.S124535","url":null,"abstract":"","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"22 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116535767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Phosphorylation of the viral coat protein regulates RNA virus infection","authors":"Haley Hoover, C. Kao","doi":"10.2147/VAAT.S118440","DOIUrl":"https://doi.org/10.2147/VAAT.S118440","url":null,"abstract":"php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). Virus Adaptation and Treatment 2016:8 13–20 Virus Adaptation and Treatment Dovepress","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"65 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122642582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Porcine epidemic diarrhea virus: current insights","authors":"C. Lv, Yan Xiao, Xiangdong Li, K. Tian","doi":"10.2147/VAAT.S107275","DOIUrl":"https://doi.org/10.2147/VAAT.S107275","url":null,"abstract":"and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). Virus Adaptation and Treatment","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"67 3","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2016-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132531909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Recent advances in host–virus interactomics during entry and infection","authors":"S. Bhattacharjee","doi":"10.2147/VAAT.S60265","DOIUrl":"https://doi.org/10.2147/VAAT.S60265","url":null,"abstract":"Viral infections and pandemics result in millions of deaths worldwide each year. Viruses exploit host cellular processes, not only to gain entry and to deliver their genetic cargo, but also to counteract and use host immune defenses. To this end, a variety of ingenious strategies have evolved in viruses that involve fusion between virus and host membranes, channel formation through the host plasma membranes, disruption of the membrane vesicles, or a combination of these events. The entry and infection pathways of virus are thus largely defined by the inter - actions between virus particles and their cell surface and cytoplasmic receptors. A thorough analysis of virus-host interactomes may reveal novel mechanisms in virus entry, virus infection, and pathogenic strategies to modulate host metabolic pathways. The study of viral entry, infec- tion, and pathogenesis has evolved over a long period. A host of next-generation technological advancements in this field has been discussed in this review.","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125805270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Impact and differential clinical utility of cobicistat-boosted darunavir in HIV/AIDS","authors":"M. Cossu, N. Astuti, A. Capetti, G. Rizzardini","doi":"10.2147/VAAT.S83680","DOIUrl":"https://doi.org/10.2147/VAAT.S83680","url":null,"abstract":": Cobicistat (Cobi) is a pharmacoenhancer, without anti-HIV activity, that optimizes systemic exposures of protease inhibitors (PIs) such as atazanavir (ATV) and darunavir (DRV). In particular, Cobi is a potent inhibitor of cytochrome P450 (CYP) 3A enzymes, the main metabolizing pathway of this class of antiretrovirals. Due to its more selective inhibition of CYP3A, Cobi has a lower potential for off-target drug interactions than the standard boosting agent ritonavir (RTV), and lower likelihood for enzymatic induction. In pharmacokinetic studies of healthy volunteers, DRV boosted with Cobi attains plasma concentrations that are comparable to those achieved with 100 mg RTV as booster. In Phase III clinical trials, conducted in naïve subjects, the coformulation yielded high rates of suppression of viral replication, on average 82%–83% of treated patients reaching undetectable viremia after 48 weeks of therapy. The selection of resistance associated with mutations was a rare event and no phenotypic resistance to DRV emerged in viral failures. Generally, Cobi was well tolerated; however, it has been shown to decrease estimated creatinine clearance (ClCr) due to inhibition of tubular secretion of creatinine. Cobi, therefore, should not be initiated in patients with ClCr less than 70 mL/min, if any coadministered agent (eg, emtricitabine, lamivudine, tenofovir disoproxil fumarate, or adefovir) requires dose adjustment based on ClCr.DRV/Cobi fixed-dose combination is part of an important evolution of antiretroviral therapy toward simpler yet potent formulations. In this setting, it is important to combine potency, simplicity, safety, and high genetic barrier, as in this case.","PeriodicalId":337688,"journal":{"name":"Virus Adaptation and Treatment","volume":"21 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2015-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121518342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}