Restrictions on roaming Until the past century or so, the movement of wild animals was relatively unrestricted, and their travels contributed substantially to ecological processes. As humans have increasingly altered natural habitats, natural animal movements have been restricted. Tucker et al. examined GPS locations for more than 50 species. In general, animal movements were shorter in areas with high human impact, likely owing to changed behaviors and physical limitations. Besides affecting the species themselves, such changes could have wider effects by limiting the movement of nutrients and altering ecological interactions. Science , this issue p. 466
Viruses are involved in various interactions both within and between infected cells. Social evolution theory offers a conceptual framework for how virus-virus interactions, ranging from conflict to cooperation, have evolved. A critical examination of these interactions could expand our understanding of viruses and be exploited for epidemiological and medical interventions.
Infection of more than one virus in a host, coinfection, is common across taxa and environments. Viral coinfection can enable genetic exchange, alter the dynamics of infections, and change the course of viral evolution. Yet, a systematic test of the factors explaining variation in viral coinfection across different taxa and environments awaits completion. Here I employ three microbial data sets of virus–host interactions covering cross-infectivity, culture coinfection, and single-cell coinfection (total: 6,564 microbial hosts, 13,103 viruses) to provide a broad, comprehensive picture of the ecological and biological factors shaping viral coinfection. I found evidence that ecology and virus–virus interactions are recurrent factors shaping coinfection patterns. Host ecology was a consistent and strong predictor of coinfection across all three data sets: cross-infectivity, culture coinfection, and single-cell coinfection. Host phylogeny or taxonomy was a less consistent predictor, being weak or absent in the cross-infectivity and single-cell coinfection models, yet it was the strongest predictor in the culture coinfection model. Virus–virus interactions strongly affected coinfection. In the largest test of superinfection exclusion to date, prophage sequences reduced culture coinfection by other prophages, with a weaker effect on extrachromosomal virus coinfection. At the single-cell level, prophage sequences eliminated coinfection. Virus–virus interactions also increased culture coinfection with ssDNA–dsDNA coinfections >2× more likely than ssDNA-only coinfections. The presence of CRISPR spacers was associated with a ∼50% reduction in single-cell coinfection in a marine bacteria, despite the absence of exact spacer matches in any active infection. Collectively, these results suggest the environment bacteria inhabit and the interactions among surrounding viruses are two factors consistently shaping viral coinfection patterns. These findings highlight the role of virus–virus interactions in coinfection with implications for phage therapy, microbiome dynamics, and viral infection treatments.
The canonical lytic–lysogenic binary has been challenged in recent years, as more evidence has emerged on alternative bacteriophage infection strategies. These infection modes are little studied, and yet they appear to be more abundant and ubiquitous in nature than previously recognized, and can play a significant role in the ecology and evolution of their bacterial hosts. In this review, we discuss the extent, causes and consequences of alternative phage lifestyles, and clarify conceptual and terminological confusion to facilitate research progress. We propose distinct definitions for the terms ‘pseudolysogeny’ and ‘productive or non-productive chronic infection’, and distinguish them from the carrier state life cycle, which describes a population-level phenomenon. Our review also finds that phages may change their infection modes in response to environmental conditions or the physiological state of the host cell. We outline known molecular mechanisms underlying the alternative phage–host interactions, including specific genetic pathways and their considerable biotechnological potential. Moreover, we discuss potential implications of the alternative phage lifestyles for microbial biology and ecosystem functioning, as well as applied topics such as phage therapy.
Rationale There is little doubt that aerosols play a major role in the transmission of SARS-CoV-2. The significance of the presence and infectivity of this virus on environmental surfaces, especially in a hospital setting, remains less clear. Objectives We aimed to analyze surface swabs for SARS-CoV-2 RNA and infectivity, and to determine their suitability for sequence analysis. Methods Samples were collected during two waves of COVID-19 at the University of California, Davis Medical Center, in COVID-19 patient serving and staff congregation areas. qRT-PCR positive samples were investigated in Vero cell cultures for cytopathic effects and phylogenetically assessed by whole genome sequencing. Measurements and main results Improved cleaning and patient management practices between April and August 2020 were associated with a substantial reduction of SARS-CoV-2 qRT-PCR positivity (from 11% to 2%) in hospital surface samples. Even though we recovered near-complete genome sequences in some, none of the positive samples (11 of 224 total) caused cytopathic effects in cultured cells suggesting this nucleic acid was either not associated with intact virions, or they were present in insufficient numbers for infectivity. Phylogenetic analysis suggested that the SARS-CoV-2 genomes of the positive samples were derived from hospitalized patients. Genomic sequences isolated from qRT-PCR negative samples indicate a superior sensitivity of viral detection by sequencing. Conclusions This study confirms the low likelihood that SARS-CoV-2 contamination on hospital surfaces contains infectious virus, disputing the importance of fomites in COVID-19 transmission. Ours is the first report on recovering near-complete SARS-CoV-2 genome sequences directly from environmental surface swabs.
In this Community Page, we learn how a scientific community leverages social networking tools to connect a group of dispersed scientific researchers in Ciencia Puerto Rico; this effort fosters innovative research and educational collaborations and changes the way scientists interact with the public.
Wild birds of the Anseriformes and Charadriiformes order represent a natural and asymptomatic reservoir for avian influenza viruses (AIv) that infect domestic, captive and wild free-ranging bird species (Pantin-Jackwood & Swayne, 2009). Due to the presence of influenza A viruses in waterfowl which can be excreted from faecal/oral routes into the environment (Ronnqvist, Ziegler, von Bonsdorff, & Maunula, 2012),
13Infection of more than one virus in a host, coinfection, is common across taxa and environments. 14 Viral coinfection can enable genetic exchange, alter the dynamics of infections, and change the 15 course of viral evolution. Yet, the factors influencing the frequency and extent of viral 16 coinfection remain largely unexplored. Here, employing three microbial data sets of virus-host 17 interactions covering cross-infectivity, culture coinfection, and single-cell coinfection (total: 18 6,564 microbial hosts, 13,103 viruses), I found evidence that ecology and virus-virus interactions 19 are recurrent factors shaping coinfection patterns. Host ecology was a consistent and strong 20predictor of coinfection across all three datasets: potential, culture, and single-cell coinfection. 21Host phylogeny or taxonomy was a less consistent predictor, being weak or absent in potential 22 and single-cell coinfection models, yet it was the strongest predictor in the culture coinfection 23 model. Virus-virus interactions strongly affected coinfection. In the largest test of superinfection 24 exclusion to date, prophage infection reduced culture coinfection by other prophages, with a 25 weaker effect on extrachromosomal virus coinfection. At the single-cell level, prophages 26 eliminated coinfection. Virus-virus interactions also increased culture coinfection with ssDNA-27 dsDNA coinfections >2x more likely than ssDNA-only coinfections. Bacterial defense limited 28 single-cell coinfection in marine bacteria CRISPR spacers reduced coinfections by ~50%, 29 2 despite the absence of spacer matches in any active infection. Collectively, these results suggest 30 the environment bacteria inhabit and the interactions among surrounding viruses are two factors 31 consistently shaping viral coinfection patterns. These findings highlight the role of virus-virus 32 interactions in coinfection with implications for phage therapy, microbiome dynamics, and viral 33 infection treatments.34
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