Bacteria Facilitate Enteric Virus Co-infection of Mammalian Cells and Promote Genetic Recombination

Erickson, Andrea K.; Jesudhasan, Palmy R.; Mayer, Melinda J.; Narbad, Arjan; Winter, Sebastian; Pfeiffer, Julie K.

doi:10.1016/j.chom.2017.11.007

Cited by 159 publications

(182 citation statements)

References 45 publications

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“…The binding of poliovirus to bacteria enhances coinfection by promoting the delivery of multiple virions to a single cell [3]. Coinfection results in enhanced rates of recombination, which can increase fitness of the viral progeny.…”

Section: Microbial Effects On Coinfection and Tropismmentioning

confidence: 99%

Virus interactions with bacteria: Partners in the infectious dance

Neu

Mainou

2020

PLoS Pathog

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The outcome of viral infection depends on the interplay between host factors and the environment. Host factors, like the expression of viral receptors, convey permissiveness to infection, define tropism, regulate antiviral immune responses, determine viral clearance, and spread. The host microbiota, the constellation of microbes inhabiting an organism, also plays a key role in the outcome of infection. Microbes and microbial products can directly interact with viral particles. Our understanding of how the microbiota impacts virus infection is largely limited to the bacterial component of the microbiota. Although bacteria do not support eukaryotic virus infection, they can promote viral fitness by enhancing virion stability, promoting infection of eukaryotic cells, and increasing coinfection rates. Virus binding of bacteria can also impact bacterial biology, including bacterial adherence to eukaryotic cells. These interactions can also indirectly affect the host response to viral infection. In this Pearl, we focus on how direct and indirect interactions between viruses and bacteria impact viral biology and touch on recent findings that illustrate how bacterial biology can also be impacted by interactions with eukaryotic viruses (Fig 1).

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Section: Microbial Effects On Coinfection and Tropismmentioning

confidence: 99%

Virus interactions with bacteria: Partners in the infectious dance

Neu

Mainou

2020

PLoS Pathog

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“…Such enveloped forms of typically non-enveloped viruses display an increased infection efficiency compared with non-enveloped viral particles [185] and use alternative entry receptors. Another recent discovery challenging previous dogmas is that enteric viruses rely on other microbes for stability/survival and potentially also for attachment to and entry into target cells [186]. As described above, future research should also consider that even soluble host molecules (such as blood factors and lactoferrin) can affect attachment and entry mechanisms.…”

Section: Perspectives: Current Challenges and Future Directionsmentioning

confidence: 99%

Glycomics and Proteomics Approaches to Investigate Early Adenovirus–Host Cell Interactions

Laßwitz

Chandra

Arnberg

2018

Journal of Molecular Biology

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Adenoviruses as most viruses rely on glycan and protein interactions to attach to and enter susceptible host cells. The Adenoviridae family comprises more than 80 human types and they differ in their attachment factor and receptor usage, which likely contributes to the diverse tropism of the different types. In the past years, methods to systematically identify glycan and protein interactions have advanced. In particular sensitivity, speed and coverage of mass spectrometric analyses allow for high-throughput identification of glycans and peptides separated by liquid chromatography. Also, developments in glycan microarray technologies have led to targeted, high-throughput screening and identification of glycan-based receptors. The mapping of cell surface interactions of the diverse adenovirus types has implications for cell, tissue, and species tropism as well as drug development. Here we review known adenovirus interactions with glycan- and protein-based receptors, as well as glycomics and proteomics strategies to identify yet elusive virus receptors and attachment factors. We finally discuss challenges, bottlenecks, and future research directions in the field of non-enveloped virus entry into host cells.

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“…The implications of multiple infection in these diverse systems are still being explored. In a number of cases, however, collective delivery was demonstrated to increase the efficiency of infection relative to free virus particles 4, 5 , or to increase the rate of genetic exchange through recombination 6 .…”

Section: Introductionmentioning

confidence: 99%

Collective interactions augment influenza A virus replication in a host-dependent manner

Phipps

Ganti

Jacobs

et al. 2019

Preprint

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22implicated the PA gene segment as a major driver of this phenotype and quantification of viral 33RNA synthesis indicated that both replication and transcription were affected. These findings 34 indicate that multiple distinct mechanisms underlie IAV reliance on multiple infection and 35 underscore the importance of virus-virus interactions in IAV infection, evolution and emergence. 36Importantly, multiple infection with identical viral genomes can also alter infection 58 outcomes. Such cooperation was documented for VSV and HIV, where rates of transcription and 59 replication were enhanced with increasing multiplicity of infection (MOI) 23,24 . Similarly, faster 60 kinetics of virus production were seen at high MOI for poliovirus and IAV 19,25 . In these instances, 61 it is thought that increased copy number of infecting viral genomes provides a kinetic benefit 62 important in the race to establish infection before innate antiviral responses take hold. Indeed, it 63 has been suggested that multiple infection may be particularly relevant for facilitating viral growth 64 under adverse conditions, such as antiviral drug treatment 3,26 . 65For IAV, an important adverse condition to consider is that of a novel host environment. 66IAVs occupy a broad host range, including multiple species of wild waterfowl, poultry, swine, 67 humans and other mammals 27,28 . Host barriers to infection typically confine a given lineage to 68 circulation in one species or a small number of related species 29,30 . Spillovers occur occasionally, 69 however, and can seed novel lineages. When a novel IAV lineage is established in humans, the 70 result is a pandemic of major public health consequence 31,32 . The likelihood of successful cross-71 species transfer of IAV is determined largely by the presence, absence, and compatibility of host 72 factors on which the virus relies to complete its life cycle, and on the viruses' ability to overcome 73 antiviral defenses in the novel host [33][34][35] . 74Our objective herein was to assess the degree to which IAV relies on the delivery of 75 multiple viral genomes to a cell to ensure production of progeny. In particular, we sought to 76 determine whether this phenotype varies with host species. We therefore examined the 77 multiplicity dependence of one human and a panel of avian-origin viruses in multiple host systems. 78Results from all virus/cell combinations tested confirm prior reports that cells multiply-infected with 79 IAV produce more viral progeny than singly-infected cells. Importantly, however, the extent to 80 which viral progeny production is concentrated within the multiply-infected fraction of a cell 81 population varies greatly with virus-host context. Two poultry-adapted H9N2 viruses (A/guinea 82 fowl/HK/WF10/99 (GFHK99) and A/quail/HK/A28945/88 (QaHK88)) exhibit an acute dependence 83 on multiple infection in mammalian systems that is greatly diminished in natural host systems. 84This strong dependence on multiple infection is not seen for the human strain, influenza 85 ...

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Bacteria Facilitate Enteric Virus Co-infection of Mammalian Cells and Promote Genetic Recombination

Cited by 159 publications

References 45 publications

Virus interactions with bacteria: Partners in the infectious dance

Virus interactions with bacteria: Partners in the infectious dance

Glycomics and Proteomics Approaches to Investigate Early Adenovirus–Host Cell Interactions

Collective interactions augment influenza A virus replication in a host-dependent manner

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