Stalemates in the Coevolutionary Arms Race: Syntheses, Synergisms, and Sundry Other Sins

1988 ◽  
pp. 113-132 ◽  
Author(s):  
MAY R. BERENBAUM ◽  
ARTHUR R. ZANGERL
Keyword(s):  
Arms Race ◽  
Coevolutionary Arms Race

scholarly journals Getting ahead of the Arms Race: Hothousing the Coevolution of VirusTotal with a Packer

Entropy ◽  
2021 ◽  
Vol 23 (4) ◽  
pp. 395
Author(s):  
Héctor D. Menéndez ◽  
David Clark ◽  
Earl T. Barr
Keyword(s):  
Machine Learning ◽  
Evolutionary Computation ◽  
Malware Detection ◽  
Cloud Service ◽  
False Positives ◽  
Arms Race ◽  
System Calls ◽  
A New Technique ◽  
Coevolutionary Arms Race

Malware detection is in a coevolutionary arms race where the attackers and defenders are constantly seeking advantage. This arms race is asymmetric: detection is harder and more expensive than evasion. White hats must be conservative to avoid false positives when searching for malicious behaviour. We seek to redress this imbalance. Most of the time, black hats need only make incremental changes to evade them. On occasion, white hats make a disruptive move and find a new technique that forces black hats to work harder. Examples include system calls, signatures and machine learning. We present a method, called Hothouse, that combines simulation and search to accelerate the white hat’s ability to counter the black hat’s incremental moves, thereby forcing black hats to perform disruptive moves more often. To realise Hothouse, we evolve EEE, an entropy-based polymorphic packer for Windows executables. Playing the role of a black hat, EEE uses evolutionary computation to disrupt the creation of malware signatures. We enter EEE into the detection arms race with VirusTotal, the most prominent cloud service for running anti-virus tools on software. During our 6 month study, we continually improved EEE in response to VirusTotal, eventually learning a packer that produces packed malware whose evasiveness goes from an initial 51.8% median to 19.6%. We report both how well VirusTotal learns to detect EEE-packed binaries and how well VirusTotal forgets in order to reduce false positives. VirusTotal’s tools learn and forget fast, actually in about 3 days. We also show where VirusTotal focuses its detection efforts, by analysing EEE’s variants.

scholarly journals A Single Adaptive Mutation in Sodium Taurocholate Cotransporting Polypeptide Induced by Hepadnaviruses Determines Virus Species Specificity

2018 ◽  
Vol 93 (5) ◽  
Author(s):  
Junko S. Takeuchi ◽  
Kento Fukano ◽  
Masashi Iwamoto ◽  
Senko Tsukuda ◽  
Ryosuke Suzuki ◽  
...  
Keyword(s):  
Amino Acid ◽  
Virus Infection ◽  
Positive Selection ◽  
Sodium Taurocholate ◽  
Arms Race ◽  
Adaptive Mutation ◽  
Molecular Evidence ◽  
Adaptive Mutations ◽  
Wide Range ◽  
Coevolutionary Arms Race

ABSTRACTHepatitis B virus (HBV) and its hepadnavirus relatives infect a wide range of vertebrates, from fish to human. Hepadnaviruses and their hosts have a long history of acquiring adaptive mutations. However, there are no reports providing direct molecular evidence for such a coevolutionary “arms race” between hepadnaviruses and their hosts. Here, we present evidence suggesting that the adaptive evolution of the sodium taurocholate cotransporting polypeptide (NTCP), an HBV receptor, has been influenced by virus infection. Evolutionary analysis of the NTCP-encoding genes from 20 mammals showed that most NTCP residues are highly conserved among species, exhibiting evolution under negative selection (dN/dSratio [ratio of nonsynonymous to synonymous evolutionary changes] of <1); this observation implies that the evolution of NTCP is restricted by maintaining its original protein function. However, 0.7% of NTCP amino acid residues exhibit rapid evolution under positive selection (dN/dSratio of >1). Notably, a substitution at amino acid (aa) 158, a positively selected residue, converting the human NTCP to a monkey-type sequence abrogated the capacity to support HBV infection; conversely, a substitution at this residue converting the monkey Ntcp to the human sequence was sufficient to confer HBV susceptibility. Together, these observations suggested a close association of the aa 158 positive selection with the pressure by virus infection. Moreover, the aa 158 sequence determined attachment of the HBV envelope protein to the host cell, demonstrating the mechanism whereby HBV infection would create positive selection at this NTCP residue. In summary, we provide the first evidence in agreement with the function of hepadnavirus as a driver for inducing adaptive mutation in host receptor.IMPORTANCEHBV and its hepadnavirus relatives infect a wide range of vertebrates, with a long infectious history (hundreds of millions of years). Such a long history generally allows adaptive mutations in hosts to escape from infection while simultaneously allowing adaptive mutations in viruses to overcome host barriers. However, there is no published molecular evidence for such a coevolutionary arms race between hepadnaviruses and hosts. In the present study, we performed coevolutionary phylogenetic analysis between hepadnaviruses and the sodium taurocholate cotransporting polypeptide (NTCP), an HBV receptor, combined with virological experimental assays for investigating the biological significance of NTCP sequence variation. Our data provide the first molecular evidence supporting that HBV-related hepadnaviruses drive adaptive evolution in the NTCP sequence, including a mechanistic explanation of how NTCP mutations determine host viral susceptibility. Our novel insights enhance our understanding of how hepadnaviruses evolved with their hosts, permitting the acquisition of strong species specificity.

scholarly journals Monkeying around with venom: an increased resistance to α-neurotoxins supports an evolutionary arms race between Afro-Asian primates and sympatric cobras

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Richard J. Harris ◽  
K. Anne-Isola Nekaris ◽  
Bryan G. Fry
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Selection Pressure ◽  
Arms Race ◽  
Last Common Ancestor ◽  
Geographic Ranges ◽  
Venomous Snakes ◽  
Snake Detection ◽  
Coevolutionary Arms Race

Abstract Background Snakes and primates have a multi-layered coevolutionary history as predators, prey, and competitors with each other. Previous work has explored the Snake Detection Theory (SDT), which focuses on the role of snakes as predators of primates and argues that snakes have exerted a selection pressure for the origin of primates’ visual systems, a trait that sets primates apart from other mammals. However, primates also attack and kill snakes and so snakes must simultaneously avoid primates. This factor has been recently highlighted in regard to the movement of hominins into new geographic ranges potentially exerting a selection pressure leading to the evolution of spitting in cobras on three independent occasions. Results Here, we provide further evidence of coevolution between primates and snakes, whereby through frequent encounters and reciprocal antagonism with large, diurnally active neurotoxic elapid snakes, Afro-Asian primates have evolved an increased resistance to α-neurotoxins, which are toxins that target the nicotinic acetylcholine receptors. In contrast, such resistance is not found in Lemuriformes in Madagascar, where venomous snakes are absent, or in Platyrrhini in the Americas, where encounters with neurotoxic elapids are unlikely since they are relatively small, fossorial, and nocturnal. Within the Afro-Asian primates, the increased resistance toward the neurotoxins was significantly amplified in the last common ancestor of chimpanzees, gorillas, and humans (clade Homininae). Comparative testing of venoms from Afro-Asian and American elapid snakes revealed an increase in α-neurotoxin resistance across Afro-Asian primates, which was likely selected against cobra venoms. Through structure-activity studies using native and mutant mimotopes of the α-1 nAChR receptor orthosteric site (loop C), we identified the specific amino acids responsible for conferring this increased level of resistance in hominine primates to the α-neurotoxins in cobra venom. Conclusion We have discovered a pattern of primate susceptibility toward α-neurotoxins that supports the theory of a reciprocal coevolutionary arms-race between venomous snakes and primates.

scholarly journals Divergent Evolution of PcF/SCR74 Effectors in Oomycetes Is Associated with Distinct Recognition Patterns in Solanaceous Plants

mBio ◽  
2020 ◽  
Vol 11 (3) ◽  
Author(s):  
Xiao Lin ◽  
Shumei Wang ◽  
Laura de Rond ◽  
Nicoletta Bertolin ◽  
Roland H. M. Wouters ◽  
...  
Keyword(s):  
Disease Resistance ◽  
Cell Surface ◽  
Immune Responses ◽  
Arms Race ◽  
Wild Potato ◽  
Content Type ◽  
Surface Receptors ◽  
Molecular Patterns ◽  
Solanaceous Plants ◽  
Coevolutionary Arms Race

ABSTRACT Plants deploy cell surface receptors known as pattern-recognition receptors (PRRs) that recognize non-self molecules from pathogens and microbes to defend against invaders. PRRs typically recognize microbe-associated molecular patterns (MAMPs) that are usually widely conserved, some even across kingdoms. Here, we report an oomycete-specific family of small secreted cysteine-rich (SCR) proteins that displays divergent patterns of sequence variation in the Irish potato famine pathogen Phytophthora infestans. A subclass that includes the conserved effector PcF from Phytophthora cactorum activates immunity in a wide range of plant species. In contrast, the more diverse SCR74 subclass is specific to P. infestans and tends to trigger immune responses only in a limited number of wild potato genotypes. The SCR74 response was recently mapped to a G-type lectin receptor kinase (G-LecRK) locus in the wild potato Solanum microdontum subsp. gigantophyllum. The G-LecRK locus displays a high diversity in Solanum host species compared to other solanaceous plants. We propose that the diversification of the SCR74 proteins in P. infestans is driven by a fast coevolutionary arms race with cell surface immune receptors in wild potato, which contrasts the presumed slower dynamics between conserved apoplastic effectors and PRRs. Understanding the molecular determinants of plant immune responses to these divergent molecular patterns in oomycetes is expected to contribute to deploying multiple layers of disease resistance in crop plants. IMPORTANCE Immune receptors at the plant cell surface can recognize invading microbes. The perceived microbial molecules are typically widely conserved and therefore the matching surface receptors can detect a broad spectrum of pathogens. Here we describe a family of Phytophthora small extracellular proteins that consists of conserved subfamilies that are widely recognized by solanaceous plants. Remarkably, one subclass of SCR74 proteins is highly diverse, restricted to the late blight pathogen Phytophthora infestans and is specifically detected in wild potato plants. The diversification of this subfamily exhibits signatures of a coevolutionary arms race with surface receptors in potato. Insights into the molecular interaction between these potato-specific receptors and the recognized Phytophthora proteins are expected to contribute to disease resistance breeding in potato.

scholarly journals A Single Adaptive Mutation in Sodium Taurocholate Cotransporting Polypeptide Induced by Hepadnaviruses Determines Virus Species-specificity

2018 ◽  
Author(s):  
Junko S Takeuchi ◽  
Kento Fukano ◽  
Masashi Iwamoto ◽  
Senko Tsukuda ◽  
Ryosuke Suzuki ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Positive Selection ◽  
Sodium Taurocholate ◽  
Arms Race ◽  
Adaptive Mutation ◽  
Molecular Evidence ◽  
Adaptive Mutations ◽  
Wide Range ◽  
B Virus ◽  
Coevolutionary Arms Race

AbstractHepatitis B virus (HBV) and its hepadnavirus relatives infect a wide range of vertebrates from fish to human. Hepadnaviruses and their hosts have a long history of acquiring adaptive mutations. However, there are no reports providing direct molecular evidence for such a coevolutionary “arms race” between hepadnaviruses and their hosts. Here, we present evidence suggesting the adaptive evolution of the sodium taurocholate cotransporting polypeptide (NTCP), an HBV receptor, has been influenced by virus infection. Evolutionary analysis of the NTCP-encoding genes from 20 mammals showed that most NTCP residues are highly conserved among species, exhibiting evolution under negative selection (dN/dS < 1); this observation implies that the evolution of NTCP is restricted by maintaining its original protein function. However, 0.7 % of NTCP amino acid (aa) residues exhibit rapid evolution under positive selection (dN/dS > 1). Notably, a substitution at aa 158, a positively selected residue, converting the human NTCP to a monkey-type sequence abrogated the capacity to support HBV infection; conversely, a substitution at this residue converting the monkey Ntcp to the human sequence was sufficient to confer HBV susceptibility. Together, these observations suggested that positive selection at aa 158 was induced by virus infection. Moreover, the aa 158 sequence determined attachment of the HBV envelope protein to host cell, demonstrating the mechanism whereby HBV infection would create positive selection at this residue in NTCP. In summary, we provide the first evidence in agreement with the function of hepadnavirus as a driver for inducing an adaptive mutation in host receptor.ImportanceHepatitis B virus (HBV) and its hepadnavirus relatives infect a wide range of vertebrates, with a long infectious history (hundreds of millions of years). Such a long history generally allows adaptive mutations in hosts to escape from infection, while simultaneously allowing adaptive mutations in viruses to overcome host barriers. However, there is no published molecular evidence for such a coevolutionary “arms race” between hepadnaviruses and hosts. In the present study, we performed coevolutionary phylogenetic analysis between hepadnaviruses and the sodium taurocholate cotransporting polypeptide (NTCP), an HBV receptor, combined with virological experimental assays for investigating the biological significance of NTCP sequence variation. Our data provide the first molecular evidences supporting that HBV-related hepadnaviruses drive adaptive evolution in the NTCP sequence, including a mechanistic explanation of how NTCP mutations determine host viral susceptibility. Our novel insights enhance our understanding of how hepadnaviruses evolved with their hosts, permitting the acquisition of strong species-specificity.

scholarly journals Bacteriophage ICP1: A Persistent Predator of Vibrio cholerae

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Caroline M. Boyd ◽  
Angus Angermeyer ◽  
Stephanie G. Hays ◽  
Zachary K. Barth ◽  
Kishen M. Patel ◽  
...  
Keyword(s):  
Vibrio Cholerae ◽  
Diarrheal Disease ◽  
Arms Race ◽  
Clinical Samples ◽  
Annual Review ◽  
Publication Date ◽  
Variable Regions ◽  
Disease Research ◽  
System A ◽  
Coevolutionary Arms Race

Bacteriophages or phages—viruses of bacteria—are abundant and considered to be highly diverse. Interestingly, a particular group of lytic Vibrio cholerae–specific phages (vibriophages) of the International Centre for Diarrheal Disease Research, Bangladesh cholera phage 1 (ICP1) lineage show high levels of genome conservation over large spans of time and geography, despite a constant coevolutionary arms race with their host. From a collection of 67 sequenced ICP1 isolates, mostly from clinical samples, we find these phages have mosaic genomes consisting of large, conserved modules disrupted by variable sequences that likely evolve mostly through mobile endonuclease-mediated recombination during coinfection. Several variable regions have been associated with adaptations against antiphage elements in V. cholerae; notably, this includes ICP1’s CRISPR-Cas system. The ongoing association of ICP1 and V. cholerae in cholera-endemic regions makes this system a rich source for discovery of novel defense and counterdefense strategies in bacteria-phage conflicts in nature. Expected final online publication date for the Annual Review of Virology, Volume 8 is September 2021. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

scholarly journals Sustained coevolution of phage Lambda and Escherichia coli involves inner as well as outer membrane defenses and counter-defenses

2021 ◽  
Author(s):  
Alita R. Burmeister ◽  
Rachel M. Sullivan ◽  
Jenna Gallie ◽  
Richard E. Lenski
Keyword(s):  
Escherichia Coli ◽  
Outer Membrane ◽  
Arms Race ◽  
Host Defenses ◽  
Arms Races ◽  
Surface Receptors ◽  
E Coli ◽  
Encoding Genes ◽  
Coevolutionary Arms Race ◽  
Gene For Gene

AbstractBacteria often evolve resistance to phage through the loss or modification of cell-surface receptors. In Escherichia coli and phage λ, such resistance can catalyze a coevolutionary arms race focused on host and phage structures that interact at the outer membrane. Here, we analyze another facet of this arms race involving interactions at the inner membrane, whereby E. coli evolves mutations in mannose permease-encoding genes manY and manZ that impair λ’s ability to eject its DNA into the cytoplasm. We show that these man mutants arose concurrently with the arms race at the outer membrane. We tested the hypothesis that λ evolved an additional counter-defense that allowed them to infect bacteria with deleted man genes. The deletions severely impaired the ancestral λ, but some evolved phage grew well on the deletion mutants, indicating they regained infectivity by evolving the ability to infect hosts independently of the mannose permease. This coevolutionary arms race fulfills the model of an inverse-gene-for-gene infection network. Taken together, the interactions at both the outer and inner membranes reveal that coevolutionary arms races can be richer and more complex than is often appreciated.IMPACT STATEMENTLaboratory studies of coevolution help us understand how host defenses and pathogen counter-defenses change over time, which is often essential for predicting the future dynamics of host-pathogen interactions. One particular model, termed “inverse-gene-for-gene” coevolution, predicts that coevolution proceeds through alternating steps, whereby hosts lose the features exploited by pathogens, and pathogens evolve to exploit alternative features. Using a classic model system in molecular biology, we describe the nature and timing of a previously overlooked step in the coevolution of E. coli and bacteriophage lambda. Our work demonstrates that this mode of coevolution can profoundly re-shape the interactions between bacteria and phage.

Defense and Counterdefense During Plant-Pathogenic Oomycete Infection

2019 ◽  
Vol 73 (1) ◽  
pp. 667-696 ◽  
Author(s):  
Yan Wang ◽  
Brett M. Tyler ◽  
Yuanchao Wang
Keyword(s):  
Cell Death ◽  
Immune System ◽  
Plant Immunity ◽  
Arms Race ◽  
Signal Integration ◽  
Natural Ecosystems ◽  
Numerous Species ◽  
Physical Barriers ◽  
Signaling Components ◽  
Coevolutionary Arms Race

Plant-pathogenic oomycetes include numerous species that are ongoing threats to agriculture and natural ecosystems. Understanding the molecular dialogs between oomycetes and plants is instrumental for sustaining effective disease control. Plants respond to oomycete infection by multiple defense actions including strengthening of physical barriers, production of antimicrobial molecules, and programmed cell death. These responses are tightly controlled and integrated via a three-layered immune system consisting of a multiplex recognition layer, a resilient signal-integration layer, and a diverse defense-action layer. Adapted oomycete pathogens utilize apoplastic and intracellular effector arsenals to counter plant immunity mechanisms within each layer, including by evasion or suppression of recognition, interference with numerous signaling components, and neutralization or suppression of defense actions. A coevolutionary arms race continually drives the emergence of new mechanisms of plant defense and oomycete counterdefense.

Sign in / Sign up

Export Citation Format

Share Document