scholarly journals Natural selection in the evolution of SARS-CoV-2 in bats created a generalist virus and highly capable human pathogen

PLoS Biology ◽  
2021 ◽  
Vol 19 (3) ◽  
pp. e3001115 ◽  
Author(s):  
Oscar A. MacLean ◽  
Spyros Lytras ◽  
Steven Weaver ◽  
Joshua B. Singer ◽  
Maciej F. Boni ◽  
...  
Keyword(s):  
Natural Selection ◽  
Evolutionary History ◽  
Purifying Selection ◽  
Human Pathogen ◽  
Intermediate Species ◽  
New Host ◽  
Host Shifts ◽  
Bat Virus ◽  
Horseshoe Bats ◽  
New Host Species

Virus host shifts are generally associated with novel adaptations to exploit the cells of the new host species optimally. Surprisingly, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has apparently required little to no significant adaptation to humans since the start of the Coronavirus Disease 2019 (COVID-19) pandemic and to October 2020. Here we assess the types of natural selection taking place in Sarbecoviruses in horseshoe bats versus the early SARS-CoV-2 evolution in humans. While there is moderate evidence of diversifying positive selection in SARS-CoV-2 in humans, it is limited to the early phase of the pandemic, and purifying selection is much weaker in SARS-CoV-2 than in related bat Sarbecoviruses. In contrast, our analysis detects evidence for significant positive episodic diversifying selection acting at the base of the bat virus lineage SARS-CoV-2 emerged from, accompanied by an adaptive depletion in CpG composition presumed to be linked to the action of antiviral mechanisms in these ancestral bat hosts. The closest bat virus to SARS-CoV-2, RmYN02 (sharing an ancestor about 1976), is a recombinant with a structure that includes differential CpG content in Spike; clear evidence of coinfection and evolution in bats without involvement of other species. While an undiscovered “facilitating” intermediate species cannot be discounted, collectively, our results support the progenitor of SARS-CoV-2 being capable of efficient human–human transmission as a consequence of its adaptive evolutionary history in bats, not humans, which created a relatively generalist virus.

scholarly journals Natural selection in the evolution of SARS-CoV-2 in bats, not humans, created a highly capable human pathogen

2020 ◽  
Author(s):  
Oscar A. MacLean ◽  
Spyros Lytras ◽  
Steven Weaver ◽  
Joshua B. Singer ◽  
Maciej F. Boni ◽  
...  
Keyword(s):  
Natural Selection ◽  
Host Species ◽  
Early Phase ◽  
Evolutionary History ◽  
Rna Viruses ◽  
Purifying Selection ◽  
Selective Sweeps ◽  
Human Pathogen ◽  
Bat Virus ◽  
Horseshoe Bats

AbstractRNA viruses are proficient at switching host species, and evolving adaptations to exploit the new host’s cells efficiently. Surprisingly, SARS-CoV-2 has apparently required no significant adaptation to humans since the start of the COVID-19 pandemic, with no observed selective sweeps since genome sampling began. Here we assess the types of natural selection taking place in Sarbecoviruses in horseshoe bats versus SARS-CoV-2 evolution in humans. While there is moderate evidence of diversifying positive selection in SARS-CoV-2 in humans, it is limited to the early phase of the pandemic, and purifying selection is much weaker in SARS-CoV-2 than in related bat Sarbecoviruses. In contrast, our analysis detects significant positive episodic diversifying selection acting on the bat virus lineage SARS-CoV-2 emerged from, accompanied by an adaptive depletion in CpG composition presumed to be linked to the action of antiviral mechanisms in ancestral hosts. The closest bat virus to SARS-CoV-2, RmYN02 (sharing an ancestor ∼1976), is a recombinant with a structure that includes differential CpG content in Spike; clear evidence of coinfection and evolution in bats without involvement of other species. Collectively our results demonstrate the progenitor of SARS-CoV-2 was capable of near immediate human-human transmission as a consequence of its adaptive evolutionary history in bats, not humans.

scholarly journals SARS-CoV-2 genome evolution exposes early human adaptations

2020 ◽  
Author(s):  
Erik S. Wright ◽  
Seema S. Lakdawala ◽  
Vaughn S. Cooper
Keyword(s):  
Purifying Selection ◽  
Dominant Mode ◽  
Neutral Evolution ◽  
Nucleotide Substitutions ◽  
New Host ◽  
Fitness Advantage ◽  
Essential Components ◽  
Frequent Mutations ◽  
Repeated Evolution ◽  
New Host Species

ABSTRACTThe set of mutations observed at the outset of the SARS-CoV-2 pandemic may illuminate how the virus will adapt to humans as it continues to spread. Viruses are expected to quickly acquire beneficial mutations upon jumping to a new host species. Advantageous nucleotide substitutions can be identified by their parallel occurrence in multiple independent lineages and are likely to result in changes to protein sequences. Here we show that SARS-CoV-2 is acquiring mutations more slowly than expected for neutral evolution, suggesting purifying selection is the dominant mode of evolution during the initial phase of the pandemic. However, several parallel mutations arose in multiple independent lineages and may provide a fitness advantage over the ancestral genome. We propose plausible reasons for several of the most frequent mutations. The absence of mutations in other genome regions suggests essential components of SARS-CoV-2 that could be the target of drug development. Overall this study provides genomic insights into how SARS-CoV-2 has adapted and will continue to adapt to humans.SUMMARYIn this study we sought signals of evolution to identify how the SARS-CoV-2 genome has adapted at the outset of the COVID-19 pandemic. We find that the genome is largely undergoing purifying selection that maintains its ancestral sequence. However, we identified multiple positions on the genome that appear to confer an adaptive advantage based on their repeated evolution in independent lineages. This information indicates how SARS-CoV-2 will evolve as it diversifies in an increasing number of hosts.

scholarly journals Computational and Functional Analysis of the Virus-Receptor Interface Reveals Host Range Trade-Offs in New World Arenaviruses

2015 ◽  
Vol 89 (22) ◽  
pp. 11643-11653 ◽  
Author(s):  
Scott A. Kerr ◽  
Eleisha L. Jackson ◽  
Oana I. Lungu ◽  
Austin G. Meyer ◽  
Ann Demogines ◽  
...  
Keyword(s):  
Natural Selection ◽  
New World ◽  
New Host ◽  
Virus Receptor ◽  
Computational Docking ◽  
Trade Offs ◽  
Animal Populations ◽  
Machupo Virus ◽  
Selection For ◽  
New Host Species

ABSTRACTAnimal viruses frequently cause zoonotic disease in humans. As these viruses are highly diverse, evaluating the threat that they pose remains a major challenge, and efficient approaches are needed to rapidly predict virus-host compatibility. Here, we develop a combined computational and experimental approach to assess the compatibility of New World arenaviruses, endemic in rodents, with the host TfR1 entry receptors of different potential new host species. Using signatures of positive selection, we identify a small motif on rodent TfR1 that conveys species specificity to the entry of viruses into cells. However, we show that mutations in this region affect the entry of each arenavirus differently. For example, a human single nucleotide polymorphism (SNP) in this region, L212V, makes human TfR1 a weaker receptor for one arenavirus, Machupo virus, but a stronger receptor for two other arenaviruses, Junin and Sabia viruses. Collectively, these findings set the stage for potential evolutionary trade-offs, where natural selection for resistance to one virus may make humans or rodents susceptible to other arenavirus species. Given the complexity of this host-virus interplay, we propose a computational method to predict these interactions, based on homology modeling and computational docking of the virus-receptor protein-protein interaction. We demonstrate the utility of this model for Machupo virus, for which a suitable cocrystal structural template exists. Our model effectively predicts whether the TfR1 receptors of different species will be functional receptors for Machupo virus entry. Approaches such at this could provide a first step toward computationally predicting the “host jumping” potential of a virus into a new host species.IMPORTANCEWe demonstrate how evolutionary trade-offs may exist in the dynamic evolutionary interplay between viruses and their hosts, where natural selection for resistance to one virus could make humans or rodents susceptible to other virus species. We present an algorithm that predicts which species have cell surface receptors that make them susceptible to Machupo virus, based on computational docking of protein structures. Few molecular models exist for predicting the risk of spillover of a particular animal virus into humans or new animal populations. Our results suggest that a combination of evolutionary analysis, structural modeling, and experimental verification may provide an efficient approach for screening and assessing the potential spillover risks of viruses circulating in animal populations.

scholarly journals Intra- and Cross-Species Transmission of Astroviruses

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1127
Author(s):  
Shanley N. Roach ◽  
Ryan A. Langlois
Keyword(s):  
Rna Viruses ◽  
Neurological Complications ◽  
Avian Species ◽  
Future Research ◽  
Zoonotic Potential ◽  
Extensive Disease ◽  
New Host ◽  
Viral Spread ◽  
Common Causes ◽  
New Host Species

Astroviruses are non-enveloped, single-stranded RNA viruses that infect mammalian and avian species. In humans, astrovirus infections are one of the most common causes of gastroenteritis in children. Infection has also been linked to serious neurological complications, especially in immunocompromised individuals. More extensive disease has also been characterized in non-human mammalian and avian species. To date, astroviruses have been detected in over 80 different avian and mammalian hosts. As the number of hosts continues to rise, the need to understand how astroviruses transmit within a given species as well as to new host species becomes increasingly important. Here, we review the current understanding of astrovirus transmission, the factors that influence viral spread, and the potential for cross-species transmission. Additionally, we highlight the current gaps in knowledge and areas of future research that will be key to understanding astrovirus transmission and zoonotic potential.

Regressive evolution of an effector following a host jump in the Irish Potato Famine Pathogen Lineage

2021 ◽  
Author(s):  
Erin K. Zess ◽  
Yasin F. Dagdas ◽  
Esme Peers ◽  
Abbas Maqbool ◽  
Mark J. Banfield ◽  
...  
Keyword(s):  
Host Species ◽  
Irish Potato ◽  
Sequence Motif ◽  
New Host ◽  
Regressive Evolution ◽  
Host Environment ◽  
Host Jump ◽  
Potato Famine ◽  
Irish Potato Famine ◽  
New Host Species

AbstractIn order to infect a new host species, the pathogen must evolve to enhance infection and transmission in the novel environment. Although we often think of evolution as a process of accumulation, it is also a process of loss. Here, we document an example of regressive evolution in the Irish potato famine pathogen (Phytophthora infestans) lineage, providing evidence that a key sequence motif in the effector PexRD54 has degenerated following a host jump. We began by looking at PexRD54 and PexRD54-like sequences from across Phytophthora species. We found that PexRD54 emerged in the common ancestor of Phytophthora clade 1b and 1c species, and further sequence analysis showed that a key functional motif, the C-terminal ATG8-interacting motif (AIM), was also acquired at this point in the lineage. A closer analysis showed that the P. mirabilis PexRD54 (PmPexRD54) AIM appeared unusual, the otherwise-conserved central residue mutated from a glutamate to a lysine. We aimed to determine whether this PmPexRD54 AIM polymorphism represented an adaptation to the Mirabilis jalapa host environment. We began by characterizing the M. jalapa ATG8 family, finding that they have a unique evolutionary history compared to previously characterized ATG8s. Then, using co-immunoprecipitation and isothermal titration calorimetry assays, we showed that both full-length PmPexRD54 and the PmPexRD54 AIM peptide bind very weakly to the M. jalapa ATG8s. Through a combination of binding assays and structural modelling, we showed that the identity of the residue at the position of the PmPexRD54 AIM polymorphism can underpin high-affinity binding to plant ATG8s. Finally, we conclude that the functionality of the PexRD54 AIM was lost in the P. mirabilis lineage, perhaps owing to as-yet-unknown pressure on this effector in the new host environment.Author SummaryPathogens evolve in concert with their hosts. When a pathogen begins to infect a new host species, known as a “host jump,” the pathogen must evolve to enhance infection and transmission. These evolutionary processes can involve both the gain and loss of genes, as well as dynamic changes in protein function. Here, we describe an example of a pathogen protein that lost a key functional domain following a host jump, a salient example of “regressive evolution.” Specifically, we show that an effector protein from the plant pathogen Phytopthora mirabilis, a host-specific lineage closely related to the Irish potato famine pathogen Phytopthora infestans, has a derived amino acid polymorphism that results in a loss of interaction with certain host machinery.

scholarly journals The AntCardiocondyla elegansas Host of the Enigmatic Endoparasitic FungusMyrmicinosporidium durum

2015 ◽  
Vol 2015 ◽  
pp. 1-4
Author(s):  
Julia Giehr ◽  
Jürgen Heinze ◽  
Alexandra Schrempf
Keyword(s):  
Host Species ◽  
Sampling Methods ◽  
Infection Rates ◽  
New Host ◽  
High Infection ◽  
New Host Species

Data on host species and the distribution of the endoparasitic fungusMyrmicinosporidium durumincreased continuously in recent decades. Here, we add the antCardiocondyla elegansas new host species. Colonies of the monogynous species were found infested in the region of Languedoc-Roussillon (South France). Samples from the nest indicate high infection rates. All castes and sexes were infected by the spores. Variations of infection rates between sampling methods and species are discussed.

scholarly journals SARS-Like Coronaviruses in Horseshoe Bats (Rhinolophus spp.) in Russia, 2020

Viruses ◽  
2022 ◽  
Vol 14 (1) ◽  
pp. 113
Author(s):  
Sergey Alkhovsky ◽  
Sergey Lenshin ◽  
Alexey Romashin ◽  
Tatyana Vishnevskaya ◽  
Oleg Vyshemirsky ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Evolutionary History ◽  
Structural Proteins ◽  
Rt Pcr ◽  
Phylogenetic Lineage ◽  
History Of ◽  
Horseshoe Bats ◽  
Regions Of Russia ◽  
Nonstructural Genes

We found and genetically described two novel SARS-like coronaviruses in feces and oral swabs of the greater (R. ferrumequinum) and the lesser (R. hipposideros) horseshoe bats in southern regions of Russia. The viruses, named Khosta-1 and Khosta-2, together with related viruses from Bulgaria and Kenya, form a separate phylogenetic lineage. We found evidence of recombination events in the evolutionary history of Khosta-1, which involved the acquisition of the structural proteins S, E, and M, as well as the nonstructural genes ORF3, ORF6, ORF7a, and ORF7b, from a virus that is related to the Kenyan isolate BtKY72. The examination of bats by RT-PCR revealed that 62.5% of the greater horseshoe bats in one of the caves were positive for Khosta-1 virus, while its overall prevalence was 14%. The prevalence of Khosta-2 was 1.75%. Our results show that SARS-like coronaviruses circulate in horseshoe bats in the region, and we provide new data on their genetic diversity.

scholarly journals Rapid divergence in independent aspects of the compatibility phenotype in the Spiroplasma/Drosophila interaction

2021 ◽  
Author(s):  
Joanne S. Griffin ◽  
Michael Gerth ◽  
Gregory D. D. Hurst
Keyword(s):  
Vertical Transmission ◽  
Host Species ◽  
High Efficiency ◽  
Host Shift ◽  
Direct Selection ◽  
New Host ◽  
Host Shifts ◽  
Species Pairs ◽  
Novel Host ◽  
Rapid Divergence

AbstractHeritable symbionts represent important components of host biology, both as antagonistic reproductive parasites and as beneficial protective partners. An important component of heritable microbes’ biology is their ability to establish in new host species, a process equivalent to a host shift for an infectiously transmitted parasite or pathogen. For a host shift to occur, the symbiont must be compatible with the host: it must not cause excess pathology, must have good vertical transmission, and possess a drive phenotype that enables spread. Classically, compatibility has been considered a declining function of genetic distance between novel and ancestral host species. Here we investigate the evolutionary lability of compatibility to heritable microbes by comparing the capacity for a symbiont to establish in two novel host species equally related to the ancestral host. Compatibility of the protective Spiroplasma from D. hydei with D. simulans and D. melanogaster was tested. The Spiroplasma had contrasting compatibility in these two host species. The transinfection showed pathology and low vertical transmission in D. melanogaster but was asymptomatic and transmitted with high efficiency in D. simulans. These results were not affected by the presence/absence of Wolbachia in either of the two species. The pattern of protection was not congruent with that for pathology/transmission, with protection being weaker in the D. simulans, the host in which Spiroplasma was asymptomatic and transmitted well. Further work indicated pathological interactions occurred in D. sechellia and D. yakuba, indicating that D. simulans was unusual in being able to carry the symbiont without damage. The differing compatibility of the symbiont with these closely related host species emphasises first the rapidity with which host-symbiont compatibility evolves despite compatibility itself not being subject to direct selection, and second the independence of the different components of compatibility (pathology, transmission, protection). This requirement to fit three different independently evolving aspects of compatibility, if commonly observed, is likely to be a major feature limiting the rate of host shifts. Moving forward, the variation between sibling species pairs observed above provides an opportunity to identify the mechanisms behind variable compatibility between closely related host species, which will drive hypotheses as to the evolutionary drivers of compatibility variation.

scholarly journals A Role for Tetracycline Selection in Recent Evolution of Agriculture-Associated Clostridium difficile PCR Ribotype 078

mBio ◽  
2019 ◽  
Vol 10 (2) ◽  
Author(s):  
Kate E. Dingle ◽  
Xavier Didelot ◽  
T. Phuong Quan ◽  
David W. Eyre ◽  
Nicole Stoesser ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Evolutionary History ◽  
Selective Pressure ◽  
Tetracycline Resistance ◽  
Clonal Expansion ◽  
Human Pathogen ◽  
Content Type ◽  
Resistance Determinants ◽  
Ribotype 078 ◽  
Human Infections

ABSTRACT The increasing clinical importance of human infections (frequently severe) caused by Clostridium difficile PCR ribotype 078 (RT078) was first reported in 2008. The severity of symptoms (mortality of ≤30%) and the higher proportion of infections among community and younger patients raised concerns. Farm animals, especially pigs, have been identified as RT078 reservoirs. We aimed to understand the recent changes in RT078 epidemiology by investigating a possible role for antimicrobial selection in its recent evolutionary history. Phylogenetic analysis of international RT078 genomes (isolates from 2006 to 2014, n = 400), using time-scaled, recombination-corrected, maximum likelihood phylogenies, revealed several recent clonal expansions. A common ancestor of each expansion had independently acquired a different allele of the tetracycline resistance gene tetM. Consequently, an unusually high proportion (76.5%) of RT078 genomes were tetM positive. Multiple additional tetracycline resistance determinants were also identified (including efflux pump tet40), frequently sharing a high level of nucleotide sequence identity (up to 100%) with sequences found in the pig pathogen Streptococcus suis and in other zoonotic pathogens such as Campylobacter jejuni and Campylobacter coli. Each RT078 tetM clonal expansion lacked geographic structure, indicating rapid, recent international spread. Resistance determinants for C. difficile infection-triggering antimicrobials, including fluoroquinolones and clindamycin, were comparatively rare in RT078. Tetracyclines are used intensively in agriculture; this selective pressure, plus rapid, international spread via the food chain, may explain the increased RT078 prevalence in humans. Our work indicates that the use of antimicrobials outside the health care environment has selected for resistant organisms, and in the case of RT078, has contributed to the emergence of a human pathogen. IMPORTANCE Clostridium difficile PCR ribotype 078 (RT078) has multiple reservoirs; many are agricultural. Since 2005, this genotype has been increasingly associated with human infections in both clinical settings and the community. Investigations of RT078 whole-genome sequences revealed that tetracycline resistance had been acquired on multiple independent occasions. Phylogenetic analysis revealed a rapid, recent increase in numbers of closely related tetracycline-resistant RT078 (clonal expansions), suggesting that tetracycline selection has strongly influenced its recent evolutionary history. We demonstrate recent international spread of emergent, tetracycline-resistant RT078. A similar tetracycline-positive clonal expansion was also identified in unrelated nontoxigenic C. difficile, suggesting that this process may be widespread and may be independent of disease-causing ability. Resistance to typical C. difficile infection-associated antimicrobials (e.g., fluoroquinolones, clindamycin) occurred only sporadically within RT078. Selective pressure from tetracycline appears to be a key factor in the emergence of this human pathogen and the rapid international dissemination that followed, plausibly via the food chain.

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