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Schroeder, D. C.

Publications and source records attributed to Schroeder, D. C..

2 recordsLinked to original sources

Sacbrood viruses and select Lake Sinai virus variants dominated Apis mellifera colonies symptomatic for European foulbrood

European foulbrood (EFB) is a prevalent disease of the European honey bee (Apis mellifera) in the US, which can lead to colony decline and collapse. The bacterial components of EFB are well studied, but the diversity of viral infections within infected colonies has not been explored. Here we use meta-transcriptomics sequencing of 12 honey bee hives, symptomatic (+) and asymptomatic (-) for EFB to explore viral infection associated with the disease. We identified 41 viral genomes, belonging to two families, with a predominant occurrence of 34 genomes observed in colonies with severe EFB. This is in contrast to fewer, and a complete absence of Dicistroviridae genomes, recovered from healthy colonies (7 genomes). Identified viruses included multiple lineages previously reported in honey bees, namely Lake Sinai virus, Deformed wing virus, Sacbrood virus, Black queen cell virus, and Israeli acute paralysis virus. We observed specific Lake Sinai virus clades associated exclusively with EFB+ or EFB-colonies, in addition to EFB-afflicted colonies that exhibited an increase in relative abundance of sacbrood viruses. Multivariant analyses highlighted that a combination of site and EFB disease status influenced RNA virome composition, while EFB status alone didnt significantly impact it, presenting a challenge for comparisons between colonies kept in different yards. These findings contribute to the understanding of viral dynamics in honey bee colonies compromised by EFB and underscore the need for future investigations to consider viral composition when investigating EFB. ImportanceThis study on the viromes of honey bee colonies affected by European foulbrood (EFB) sheds light on the dynamics of viral populations in bee colonies in the context of a prevalent bacterial brood disease. The identification of distinct Lake Sinai virus and Sacbrood virus clades associated with colonies with severe EFB suggests a potential connection between viral composition and disease status, emphasizing the need for further investigation into the role of viruses during EFB infection. The observed increase in sacbrood viruses during EFB infection implies a possible viral dysbiosis, with potential implications for honey bee brood health. These findings contribute valuable insights for apicultural practices, offering a foundation for future research aimed at understanding and mitigating the impact of bacterial and viral infection in commercial honey bee operations and the management of EFB.

molecular biology↗

Structure and replication cycle of a virus infecting climate-modulating alga Emiliania huxleyi

The globally distributed marine alga Emiliania huxleyi produces reflective calcite disks (coccoliths) that increase the albedo of ocean water and thus reduce the heat absorption in the ocean, which cools the Earths climate. The population density of E. huxleyi is restricted by nucleocytoplasmic large DNA viruses, including E. huxleyi virus 201 (EhV-201). Despite the impact of E. huxleyi viruses on the climate, there is limited information about their structure and replication. Here we show that the dsDNA genome inside the EhV-201 virion is protected by an inner membrane, capsid, and outer membrane decorated with numerous transmembrane proteins. The virions are prone to deformation, and parts of their capsids deviate from the icosahedral arrangement. EhV-201 virions infect E. huxleyi by using their fivefold vertex to bind to a host cell and fuse the viruss inner membrane with the plasma membrane. Whereas the replication of EhV-201 probably occurs in the nucleus, virions assemble in the cytoplasm at the surface of endoplasmic reticulum-derived membrane segments. Genome packaging initiates synchronously with the capsid assembly and completes through an aperture in the forming capsid. Upon the completion of genome packaging, the capsids change conformation, which enables them to acquire an outer membrane by budding into intracellular vesicles. EhV-201 infection induces a loss of surface protective layers from E. huxleyi cells, which allows the continuous release of virions by exocytosis. Our results provide insight into how EhVs bypass the surface protective layers of E. huxleyi and exploit the organelles of an infected cell for progeny assembly.

molecular biology↗