Assessment of resistances to multiple pathogens in experimental sweet pepper hybrids

The aim of this study was to assess resistance to some of the major sweet pepper pathogens [Phytophthora capsici, Pepper yellow mosaic virus (PepYMV) and Meloidogyne incognita] in a group of experimental hybrids and their respective parental lines, and to identify hybrids possibly resistant to all three pathogens. Ten parental breeding lines, thirty experimental hybrids and seven commercial controls (Konan-R, Magali-R, Martha-R, Stephany, Mallorca, Magnata Super and Criollo de Morelos-334) were used. Each experiment was set up in a randomized complete block design with three replications and plots consisting of 16 plants. For assessment of resistance to P. capsici and PepYMV, the percent of asymptomatic plants was considered. In evaluating reactions to M. incognita, both the nematode reproduction index and the nematode reproduction factor were calculated. Five hybrids were found with resistance to all three pathogens. For all three pathogens, there was evidence that hybrids with two resistant parental lines showed slightly higher levels of pathogen resistance than those with only one resistant parental line. © 2017, Sociedade de Olericultura do Brasil. All rights reserved

The eukaryotic translation initiation factor 3 subunit L protein interacts with Flavivirus NS5 and may modulate yellow fever virus replication

Background: Yellow fever virus (YFV) belongs to the Flavivirus genus and causes an important disease. An alarming resurgence of viral circulation and the expansion of YFV-endemic zones have been detected in Africa and South America in recent years. NS5 is a viral protein that contains methyltransferase and RNA-dependent RNA polymerase (RdRp) domains, which are essential for viral replication, and the interactions between NS5 and cellular proteins have been studied to better understand viral replication. The aim of this study was to characterize the interaction of the NS5 protein with eukaryotic translation initiation factor 3 subunit L (eIF3L) and to evaluate the role of eIF3L in yellow fever replication. Methods. To identify interactions of YFV NS5 with cellular proteins, we performed a two-hybrid screen using the YFV NS5 RdRp domain as bait with a human cDNA library, and RNApol deletion mutants were generated and analyzed using the two-hybrid system for mapping the interactions. The RNApol region involved was segmented into three fragments and analyzed using an eIF3L-expressing yeast strain. To map the NS5 residues that are critical for the interactions, we performed site-direct mutagenesis in segment 3 of the interaction domain (ID) and confirmed the interaction using in vitro assays and in vivo coimmunoprecipitation. The significance of eIF3L for YFV replication was investigated using eIF3L overexpression and RNA interference. Results: In this work, we describe and characterize the interaction of NS5 with the translation factor eIF3L. The interaction between NS5 and eIF3L was confirmed using in vitro binding and in vivo coimmunoprecipitation assays. This interaction occurs at a region (the interaction domain of the RNApol domain) that is conserved in several flaviviruses and that is, therefore, likely to be relevant to the genus. eIF3L overexpression and plaque reduction assays showed a slight effect on YFV replication, indicating that the interaction of eIF3L with YFV NS5 may play a role in YFV replication. Conclusions: Although the precise function of eIF3L on interactions with viral proteins is not entirely understood, these results indicate an interaction of eIF3L with YF NS5 and that eIF3L overexpression facilitates translation, which has potential implications for virus replication. © 2013 Morais et al.; licensee BioMed Central Ltd

The small nuclear ribonucleoprotein U1A interacts with NS5 from yellow fever virus

The flavivirus NS5 protein is one of the most important proteins of the replication complex, and cellular proteins can interact with it. This study shows for the first time that the yellow fever virus (YFV) NS5 protein is able to interact with U1A, a protein involved in splicing and polyadenylation. We confirmed this interaction by GST-pulldown assay and by co-immunoprecipitation in YFV-infected cells. A region between amino acids 368 and 448 was identified as the site of interaction of the NS5 protein with U1A. This region was conserved among some flaviviruses of medical importance. The implications of this interaction for flavivirus replication are discussed.FAPESP[04/11098]Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)FAPESP[05/03260-7]CNPq[473613/2007-7]Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)CNPq[566289/2008-3]Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq

Impact of preexisting dengue immunity on Zika virus emergence in a dengue endemic region

Submitted by Paulo Silva ([email protected]) on 2019-10-03T17:21:43Z No. of bitstreams: 1 Impact of preexisting dengue immunity on Zika virus emergence in a dengue endemic region..pdf: 2371298 bytes, checksum: 0c1708bd2e3740e95d72a2499b753a21 (MD5)Approved for entry into archive by Paulo Silva ([email protected]) on 2019-10-03T18:27:03Z (GMT) No. of bitstreams: 1 Impact of preexisting dengue immunity on Zika virus emergence in a dengue endemic region..pdf: 2371298 bytes, checksum: 0c1708bd2e3740e95d72a2499b753a21 (MD5)Made available in DSpace on 2019-10-03T18:27:03Z (GMT). No. of bitstreams: 1 Impact of preexisting dengue immunity on Zika virus emergence in a dengue endemic region..pdf: 2371298 bytes, checksum: 0c1708bd2e3740e95d72a2499b753a21 (MD5) Previous issue date: 2019University of California. Department of Medicine. San Francisco, CA, USA.Universidade Federal da Bahia. Instituto da Saúde Coletiva. Salvador, BA, Brasil / Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / Yale School of Public Health. Department of Epidemiology of Microbial Diseases. New Haven, CT, USA.University of Pittsburgh. Department of Infectious Disease and Microbiology. Pittsburgh, PA, USA.Universidade Federal da Bahia. Instituto da Saúde Coletiva. Salvador, BA, Brasil / Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil.Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil / Universidade de Pernambuco. Faculdade de Ciências Médicas. Recife, PE, Brasil.Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil.Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil.Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil.Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil.Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / Yale School of Public Health. Department of Epidemiology of Microbial Diseases. New Haven, CT, USA.Yale School of Public Health. Department of Epidemiology of Microbial Diseases. New Haven, CT, USA.Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / Yale School of Public Health. Department of Epidemiology of Microbial Diseases. New Haven, CT, USA.Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil / Universidade Federal de Pernambuco. Departamento de Química Fundamental. Recife, PE, Brasil.University of Texas Medical Branch. Institute for Translational Science. Galveston, TX, USA.University of Texas Medical Branch. Department of Microbiology and Immunology. Galveston, TX, USA.University of Texas Medical Branch. Department of Pathology. Galveston, TX, USA.University of Texas Medical Branch. Department of Microbiology and Immunology. Galveston, TX, USA.Universidade Federal da Bahia. Instituto da Saúde Coletiva. Salvador, BA, Brasil / Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / Universidade Federal da Bahia. Faculdade de Medicina. Salvador, BA, Brasil.Sustainable Sciences Institute. Managua, Nicaragua / Ministry of Health. Centro Nacional de Diagnóstico y Referencia. Laboratorio Nacional de Virología. Managua, Nicaragua.University of California. School of Public Health. Division of Infectious Diseases and Vaccinology. Berkeley, CA, USA.Faculdade de Medicina de São José do Rio Preto. São Jose do Rio Preto, SP, Brasil.Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / Yale School of Public Health. Department of Epidemiology of Microbial Diseases. New Haven, CT, USA / Universidade Federal da Bahia. Faculdade de Medicina. Salvador, BA, Brasil.University of Pittsburgh. Department of Infectious Disease and Microbiology. Pittsburgh, PA, USA / Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil / University of Pittsburgh. Graduate School of Public Health. Pittsburgh, PA, USA.University of Florida. Department of Biology. Gainesville, FL, USA / University of Florida. Emerging Pathogens Institute. Gainesville, FL, USA.Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / Yale School of Public Health. Department of Epidemiology of Microbial Diseases. New Haven, CT, USA.The clinical outcomes associated with Zika virus (ZIKV) in the Americas have been well documented, but other aspects of the pandemic, such as attack rates and risk factors, are poorly understood. We prospectively followed a cohort of 1453 urban residents in Salvador, Brazil, and, using an assay that measured immunoglobulin G3 (IgG3) responses against ZIKV NS1 antigen, we estimated that 73% of individuals were infected during the 2015 outbreak. Attack rates were spatially heterogeneous, varying by a factor of 3 within a community spanning 0.17 square kilometers. Preexisting high antibody titers to dengue virus were associated with reduced risk of ZIKV infection and symptoms. The landscape of ZIKV immunity that now exists may affect the risk for future transmission