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How herbivorous insects adapt to host plants is a key question in ecological and evolutionary biology. The fall armyworm, (FAW) Spodoptera frugiperda (J.E. Smith), although polyphagous and a major pest on various crops, has been reported to have a rice and corn (maize) feeding strain in its native range in the Americas. The species is highly invasive and has recently established in China. We compared behavioral changes in larvae and adults of a corn population (Corn) when selected on rice (Rice) and the molecular basis of these adaptational changes in midgut and antennae based on a comparative transcriptome analysis. Larvae of S. frugiperda reared on rice plants continuously for 20 generations exhibited strong feeding preference for with higher larval performance and pupal weight on rice than on maize plants. Similarly, females from the rice selected population laid significantly more eggs on rice as compared to females from maize population. The most highly expressed DEGs were shown in the midgut of Rice vs. Corn. A total of 6430 DEGs were identified between the populations mostly in genes related to digestion and detoxification. These results suggest that potential adaptations for feeding on rice crops, may contribute to the current rapid spread of fall armyworm on rice crops in China and potentially elsewhere. Consistently, highly expressed DEGs were also shown in antennae; a total of 5125 differentially expressed genes (DEGs) s were identified related to the expansions of major chemosensory genes family in Rice compared to the Corn feeding population. These results not only provide valuable insight into the molecular mechanisms in host plants adaptation of S. frugiperda but may provide new gene targets for the management of this pest.

Background Human-to-human transmission of symbiotic, anaerobic bacteria is a fundamental evolutionary adaptation essential for membership of the human gut microbiota. However, despite its importance, the genomic and biological adaptations underpinning symbiont transmission remain poorly understood. The Firmicutes are a dominant phylum within the intestinal microbiota that are capable of producing resistant endospores that maintain viability within the environment and germinate within the intestine to facilitate transmission. However, the impact of host transmission on the evolutionary and adaptive processes within the intestinal microbiota remains unknown. Results We analyze 1358 genomes of Firmicutes bacteria derived from host and environment-associated habitats. Characterization of genomes as spore-forming based on the presence of sporulation-predictive genes reveals multiple losses of sporulation in many distinct lineages. Loss of sporulation in gut Firmicutes is associated with features of host-adaptation such as genome reduction and specialized metabolic capabilities. Consistent with these data, analysis of 9966 gut metagenomes from adults around the world demonstrates that bacteria now incapable of sporulation are more abundant within individuals but less prevalent in the human population compared to spore-forming bacteria. Conclusions Our results suggest host adaptation in gut Firmicutes is an evolutionary trade-off between transmission range and colonization abundance. We reveal host transmission as an underappreciated process that shapes the evolution, assembly, and functions of gut Firmicutes.

How viruses evolve largely depends on their hosts. To quantitatively characterize this dependence, we introduce Maximum Entropy Nucleotide Bias models (MENB) learned from single, di- and tri-nucleotide usage of viral sequences that infect a given host. We first use MENB to classify the viral family and the host of a virus from its genome, among four families of ssRNA viruses and three hosts. We show that both the viral family and the host leave a fingerprint in nucleotide motif usages that MENB models decode. Benchmarking our approach against state-of-the-art methods based on deep neural networks shows that MENB is rapid, interpretable and robust. Our approach is able to predict, with good accuracy, both the viral family and the host from a whole genomic sequence or a portion of it. MENB models also display promising out of sample generalization ability on viral sequences of new host taxa or new viral families. Our approach is also capable of identifying, within the limitations imposed by the three-host setting, intermediate hosts for well-known pathogenic strains of Influenza A subtypes and Human Coronavirus and recombinations and reassortments on specific genomic regions. Finally, MENB models can be used to track the adaptation to the new host, to shed light on the more relevant selective pressures that acted on motif usage during this process and to design new sequences with altered nucleotide usage at fixed amino-acid content.

As the number of human infections with avian and swine influenza viruses continues to rise, the pandemic risk posed by zoonotic influenza viruses cannot be underestimated. Implementation of global pandemic preparedness efforts has largely focused on H5 and H7 avian influenza viruses; however, the pandemic threat posed by other subtypes of avian influenza viruses, especially the H9 subtype, should not be overlooked. In this review, we summarize the literature pertaining to the emergence, prevalence and risk assessment of H9N2 viruses, and add new molecular analyses of key mammalian adaptation markers in the hemagglutinin and polymerase proteins. Available evidence has demonstrated that H9N2 viruses within the Eurasian lineage continue to evolve, leading to the emergence of viruses with an enhanced receptor binding preference for human-like receptors and heightened polymerase activity in mammalian cells. Furthermore, the increased prevalence of certain mammalian adaptation markers and the enhanced transmissibility of selected viruses in mammalian animal models add to the pandemic risk posed by this virus subtype. Continued surveillance of zoonotic H9N2 influenza viruses, inclusive of close genetic monitoring and phenotypic characterization in animal models, should be included in our pandemic preparedness efforts.

Influenza A virus (IAV) infection is a global respiratory disease, which annually leads to 3-5 million cases of severe illness, resulting in 290,000-650,000 deaths. Additionally, during the past century, four global IAV pandemics have claimed millions of human lives. The epithelial lining of the trachea plays a vital role during IAV infection, both as point of viral entry and replication as well as in the antiviral immune response. Tracheal tissue is generally inaccessible from human patients, which makes animal models crucial for the study of the tracheal host immune response. In this study, pigs were inoculated with swine- or human-adapted H1N1 IAV to gain insight into how host adaptation of IAV shapes the innate immune response during infection. In-depth multi-omics analysis (global proteomics and RNA sequencing) of the host response in upper and lower tracheal tissue was conducted, and results were validated by microfluidic qPCR. Additionally, a subset of samples was selected for histopathological examination. A classical innate antiviral immune response was induced in both upper and lower trachea after infection with either swine- or human-adapted IAV with upregulation of genes and higher abundance of proteins associated with viral infection and recognition, accompanied by a significant induction of interferon stimulated genes with corresponding higher proteins concentrations. Infection with the swine-adapted virus induced a much stronger immune response compared to infection with a human-adapted IAV strain in the lower trachea, which could be a consequence of a higher viral load and a higher degree of inflammation. Central components of the JAK-STAT pathway, apoptosis, pyrimidine metabolism, and the cytoskeleton were significantly altered depending on infection with swine- or human-adapted virus and might be relevant mechanisms in relation to antiviral immunity against putative zoonotic IAV. Based on our findings, we hypothesize that during host adaptation, IAV evolve to modulate important host cell elements to favor viral infectivity and replication.

RNA modifications are involved in numerous biological processes and are present in all RNA classes. These modifications can be constitutive or modulated in response to adaptive processes. RNA modifications play multiple functions since they can impact RNA base-pairings, recognition by proteins, decoding, as well as RNA structure and stability. However, their roles in stress, environmental adaptation and during infections caused by pathogenic bacteria have just started to be appreciated. With the development of modern technologies in mass spectrometry and deep sequencing, recent examples of modifications regulating host-pathogen interactions have been demonstrated. They show how RNA modifications can regulate immune responses, antibiotic resistance, expression of virulence genes, and bacterial persistence. Here, we illustrate some of these findings, and highlight the strategies used to characterize RNA modifications, and their potential for new therapeutic applications.

Within-host adaptation is a typical feature of chronic, persistent Staphylococcus aureus infections. Research projects addressing adaptive changes due to bacterial in-host evolution increase our understanding of the pathogen’s strategies to survive and persist for a long time in various hosts such as human and bovine. In this study, we investigated the adaptive processes of S. aureus during chronic, persistent bovine mastitis using a previously isolated isogenic strain pair from a dairy cow with chronic, subclinical mastitis, in which the last variant (host-adapted, Sigma factor SigB-deficient) quickly replaced the initial, dominant variant. The strain pair was cultivated under specific in vitro infection-relevant growth-limiting conditions (iron-depleted RPMI under oxygen limitation). We used a combinatory approach of surfaceomics, molecular spectroscopic fingerprinting and in vitro phenotypic assays. Cellular cytotoxicity assays using red blood cells and bovine mammary epithelial cells (MAC-T) revealed changes towards a more cytotoxic phenotype in the host-adapted isolate with an increased alpha-hemolysin (α-toxin) secretion, suggesting an improved capacity to penetrate and disseminate the udder tissue. Our results foster the hypothesis that within-host evolved SigB-deficiency favours extracellular persistence in S. aureus infections. Here, we provide new insights into one possible adaptive strategy employed by S. aureus during chronic, bovine mastitis, and we emphasise the need to analyse genotype–phenotype associations under different infection-relevant growth conditions.

Polyphagous aphids often consist of host‐specialized lineages, which have greater fitness on their native hosts than on others. The underlying causes are important for understanding of the evolution of diet breadth and host shift of aphids. The cotton‐melon aphid Aphis gossypii Glover is extremely polyphagous with many strict host‐specialized lineages. Whether and how the lineage specialized on the primary host hibiscus shifts to the secondary host cucumber remains elusive. We found that the hibiscus‐specialized lineage suffered high mortality and gave birth to very few nymphs developing into yellow dwarfs on fresh cucumber leaves, and did not inflict any damage symptoms on cucumber plants. The poor performance did not improve with prolonged exposure to cucumber; however, it did significantly improve when the cucumber leaves were pre‐infected with a biotrophic phytopathogen Pseudoperonospora cubensis. More importantly, the hibiscus‐specialized lineage with two‐generation feeding experience on pre‐infected cucumber leaves performed as well as the cucumber‐specialized lineage did on fresh cucumber leaves, and inflicted typical damage symptoms on intact cucumber plants. Electrical penetration graph (EPG) indicated that the hibiscus‐specialized lineage did not ingest phloem sap from fresh cucumber leaves but succeeded in ingesting phloem sap from pre‐infected cucumber leaves, which explained the performance improvement of the hibiscus‐specialized lineage on pre‐infected cucumber leaves. This study revealed a new pathway for the hibiscus‐specialized lineage to quickly acclimate to cucumber under the assistance of the phytopathogen. We considered that the short feeding experience on pre‐infected cucumber may activate expression of effector genes that are related to specific host utilization. We suggest to identify host‐specific effectors by comparing proteomes or/and transcriptomes of the hibiscus‐specialized lineage before and after acclimating to cucumber. The hibiscus‐specialized Aphis gossypii cannot use cucumber as host plant but performed well on cucumber that has been pre‐infected with the phytopathogen Pseudoperonospora cubensis; a short feeding experience on the pre‐infected cucumber enables the hibiscus‐specialized A. gossypii to fully adapt to fresh cucumber.

Avian pathogenic (APEC) is a critical bacterial pathogen that causes severe infections in poultry. Diverse serotypes increase the complexity of treatment and controlling APEC infections. Recent epidemiological investigations indicate O145 is emerging as a predominant serogroup of APEC in China. However, limited information is known about this newly emerged serogroup. A virulent strain, NC22, was selected to elucidate the mechanisms underlying APEC O145-related pathogenicity and host adaptation. Whole-genome sequencing and pathogenicity assays was conducted on this strain. We further performed a transcriptional analysis of the bacteria during the early colonization stage in the duck liver and compared them with those in liquid cultures . Subcutaneous inoculation of NC22 induced typical symptoms in ducks. The bacterial loads in the blood and various tissues peaked at 2 and 3 days post infection, respectively. The affected tissues included the heart, liver, spleen, lung, kidney, bursa of Fabricius, duodenum, jejunum, and cecum. We then analyzed the transcriptome profiles of NC22 during growth in duck liver versus lysogeny broth and identified 87 genes with differential expression levels.These included key metabolic enzymes and recognized host adaptation factors. Analysis of the metabolic pathways revealed an inhibition of the metabolic shift from glycolysis towards pentose phosphate pathway and an interference of the citrate cycle. Moreover, significantly differentially expressed small regulatory RNAs were examined, such as SroC, CsrC, and GadY. These findings enhance our understanding of the pathogenicity of APEC O145 and the molecular mechanisms underlying APEC-related pathogen-host interactions.

Starting at birth, newborn infants are exposed to numerous microorganisms. Adaptation of the innate immune system to them is a delicate process, with potentially advantageous and harmful implications for health development. Cytomegaloviruses (CMVs) are highly adapted to their specific mammalian hosts, with which they share millions of years of co-evolution. Throughout the history of mankind, human CMV has infected most infants in the first months of life without overt implications for health. Thus, CMV infections are intertwined with normal immune development. Nonetheless, CMV has retained substantial pathogenicity following infection or in situations of immunosuppression, leading to pathology in virtually any organ and particularly the central nervous system (CNS). CMVs enter the host through mucosal interfaces of the gastrointestinal and respiratory tract, where macrophages (MACs) are the most abundant immune cell type. Tissue MACs and their potential progenitors, monocytes, are established target cells of CMVs. Recently, several discoveries have revolutionized our understanding on the pre- and postnatal development and site-specific adaptation of tissue MACs. In this review, we explore experimental evidences and concepts on how CMV infections may impact on MAC development and activation as part of host-virus co-adaptation.