Apple Glomerella leaf spot (GLS) is an emerging fungal disease caused by Colletotrichum fructicola and other Colletotrichum species. These species are polyphyletic and it is currently unknown how these pathogens convergently evolved to infect apple. We generated chromosome-level genome assemblies of a GLS-adapted isolate and a non-adapted isolate in C. fructicola using long-read sequencing. Additionally, we resequenced 17 C. fructicola and C. aenigma isolates varying in GLS pathogenicity using short-read sequencing. Genome comparisons revealed a conserved bipartite genome architecture involving minichromosomes (accessory chromosomes) shared by C. fructicola and other closely related species within the C. gloeosporioides species complex. Moreover, two repeat-rich genomic regions (1.61 Mb in total) were specifically conserved among GLS-pathogenic isolates in C. fructicola and C. aenigma. Single-gene deletion of 10 accessory genes within the GLS-specific regions of C. fructicola identified three that were essential for GLS pathogenicity. These genes encoded a putative non-ribosomal peptide synthetase, a flavin-binding monooxygenase and a small protein with unknown function. These results highlight the crucial role accessory genes play in the evolution of Colletotrichum pathogenicity and imply the significance of an unidentified secondary metabolite in GLS pathogenesis.

Citrus target spot, caused by Pseudofabraea citricarpa, was formerly considered a cold-tolerant fungal disease. However, it has now spread from high-latitude regions to warmer low-latitude regions. Here, we conducted physiological observations on two different strains of the fungus collected from distinct regions, and evaluated their pathogenicity. Interestingly, the CQWZ collected from a low-latitude orchard, exhibited higher temperature tolerance and pathogenicity when compared to the SXCG collected from a high-latitude orchard. To further understand the evolution of temperature tolerance and virulence in these pathogens during the spread process, as well as the mechanisms underlying these differences, we performed genomic comparative analysis. The genome size of CQWZ was determined to be 44,004,669 bp, while the genome size of SXCG was determined to be 45,377,339 bp. Through genomic collinearity analysis, we identified two breakpoints and rearrangements during the evolutionary process of these two strains. Moreover, gene annotation results revealed that the CQWZ possessed 376 annotated genes in the \"Xenobiotics biodegradation and metabolism\" pathway, which is 79 genes more than the SXCG. The main factor contributing to this difference was the presence of salicylate hydroxylase. We also observed variations in the oxidative stress pathways and core pathogenic genes. The CQWZ exhibited the presence of a heat shock protein (HSP SSB), a catalase (CAT2), and 13 core pathogenic genes, including a LysM effector, in comparison to the SXCG. Furthermore, there were significant disparities in the gene clusters responsible for the production of seven metabolites, such as Fumonisin and Brefeldin. Finally, we identified the regulatory relationship, with the HOG pathway at its core, that potentially contributes to the differences in thermotolerance and virulence. As the global climate continues to warm, crop pathogens are increasingly expanding to new territories. Our findings will enhance understanding of the evolution mechanisms of pathogens under climate change.

Understanding changes in pathogen behavior (e.g. increased virulence, a shift in transmission channel) is critical for the public health management of emerging infectious diseases. Genome degradation via gene depletion or inactivation is recognized as a pathoadaptive feature of the pathogen evolving with the host. However, little is known about the exact role of genome degradation in affecting pathogenic behavior, and the underlying molecular detail has yet to be examined. Using large-scale global avian-restricted Salmonella genomes spanning more than a century, we projected the genetic diversity of Salmonella Pullorum (bvSP) by showing increasingly antimicrobial-resistant ST92 prevalent in Chinese flocks. The phylogenomic analysis identified three lineages in bvSP, with an enhancement of virulence in the two recently emerged lineages (L2/L3), as evidenced in chicken and embryo infection assays. Notably, the ancestor L1 lineage resembles the Salmonella serovars with higher metabolic flexibilities and more robust environmental tolerance, indicating stepwise evolutionary trajectories towards avian-restricted lineages. Pan-genome analysis pinpointed fimbrial degradation from a virulent lineage. The later engineered fim-deletion mutant, and all other five fimbrial systems, revealed behavior switching that restricted horizontal fecal-oral transmission but boosted virulence in chicks. By depleting fimbrial appendages, bvSP established persistent replication with less proinflammation in chick macrophages and adopted vertical transovarial transmission, accompanied by ever-increasing intensification in the poultry industry. Together, we uncovered a previously unseen paradigm for remodeling bacterial surface appendages that supplements virulence-enhanced evolution with increased vertical transmission.

Fusarium oxysporum f. sp. cucumerinum (Foc) is a prominent pathogen that adversely affects cucumber (Cucumis sativus) production. In the pathogen\'s parasitic lifestyle, the pathogenesis and virulence evolution may be regulated by lysine acetylation, as demonstrated in many living organisms. However, its specific function in Foc remains poorly understood. In this study, the acetylome profiles of a mild virulence strain (foc-3b) and its derived virulence-enhanced strain (Ra-4) were analyzed before and post-inoculation on cucumber plants. In total, 10,664 acetylation sites were identified corresponding to 3874 proteins, and 45 conserved acetylation motifs were detected. Through comparison of the acetylomes, numerous differentially lysine-acetylated proteins were enriched in energy metabolism and protein processing processes, indicating the critical role of lysine acetylation during the transition from the saprotrophic lifestyle to the parasitic lifestyle. Comparative acetylome analyses on the two virulence-differentiated strains revealed that several differentially lysine-acetylated proteins were involved in pathways of defense response and energy metabolism. Ra-4 showed enhanced energy metabolism compared to foc-3b. This indicates that robust metabolic activity is required to achieve high virulence and facilitating adaptive evolution. Additionally, faster host responses are supported by an ample energy supply enhancing virulence. Thus, lysine acetylation plays a crucial role in the pathogenesis and virulence evolution of Foc.

Cucumber plants commonly suffer from Fusarium wilt disease, which is caused by Fusarium oxysporum f. sp. cucumerinum (Foc). Although resistant cultivars assist with Fusarium wilt disease control, enhancement of the virulence of Foc has been identified after monoculture of wilt-resistant cultivars. To investigate the biological characteristics that contribute to the virulence evolution of Foc, a wildtype strain foc-3b (WT) and its virulence-enhanced variant Ra-4 (InVir) were compared in terms of their growth, reproduction, stress tolerance, and colonization in cucumber plants. The InVir strain showed similar culture characteristics on PDA media to the WT strain but produced significantly more conidia (>two fold), with a distinctly higher germination rate (>four fold) than the WT strain. The colony diameter of the InVir strain increased faster than the WT strain on PDA plates; however, the mycelia dry weight of the InVir was significantly lower (<70%) than that of the WT harvested from PDB. The InVir strain exhibited a significant increase in tolerance to osmolality (1 M NaCl, 1 M KCl, etc.). The GFP-labeled InVir strain propagated in the cucumber vascular faster than the WT strain. These results suggest that increased conidia production and germination in vitro may correlate with virulence enhancement in Fusarium oxysporum f. sp. cucumerinum. This study will provide an insight into its virulence evolution and help us understand the mechanisms underlying the evolutionary biology of F. oxysporum.

Current research on the virulence evolution of Toxoplasma gondii is mainly conducted via experiments, and studies using mathematical models are still limited. Here, we constructed a complex cycle model of T. gondii in a multi-host system considering multiple transmission routes and cat-mouse interaction. Based on this model, we studied how the virulence of T. gondii evolves with the factors related to transmission routes and the regulation of infection on host behavior under an adaptive dynamics framework. The study shows that all factors that enhance the role of mice favored decreased virulence of T. gondii, except the decay rate of oocysts that led to different evolutionary trajectories under different vertical transmission. The same was true of the environmental infection rate of cats, whose effect was different under different vertical transmission. The effect of the regulation factor on the virulence evolution of T. gondii was the same as that of the inherent predation rate depending on its net effect on direct and vertical transmissions. The global sensitivity analysis on the evolutionary outcome suggests that changing the vertical infection rate and decay rate was most effective in regulating the virulence of T. gondii. Furthermore, the presence of coinfection would favor virulent T. gondii and make evolutionary bifurcation easy to occur. The results reveal that the virulence evolution of T. gondii had a compromise between adapting to different transmission routes and maintaining the cat-mouse interaction thereby leading to different evolutionary scenarios. This highlights the significance of evolutionary ecological feedback to evolution. In addition, the qualitative verification of T. gondii virulence evolution in different areas by the present framework will provide a new perspective for the study of evolution.

Hosts can activate a defensive response to clear the parasite once being infected. To explore how host survival and fecundity are affected by host-parasite coevolution for chronic parasitic diseases, in this paper, we proposed an age-structured epidemic model with infection age, in which the parasite transmission rate and parasite-induced mortality rate are structured by the infection age. By use of critical function analysis method, we obtained the existence of the host immune evolutionary singular strategy which is a continuous singular strategy (CSS). Assume that parasite-induced mortality begins at infection age [Formula: see text] and is constant v thereafter. We got that the value of the CSS, [Formula: see text], monotonically decreases with respect to infection age [Formula: see text] (see Case (I)), while it is non-monotone if the constant v positively depends on the immune trait c (see Case (II)). This non-monotonicity is verified by numerical simulations and implies that the direction of immune evolution depends on the initial value of immune trait. Besides that, we adopted two special forms of the parasite transmission rate to study the parasite\'s virulence evolution, by maximizing the basic reproduction ratio [Formula: see text]. The values of the convergence stable parasite\'s virulence evolutionary singular strategies [Formula: see text] and [Formula: see text] increase monotonically with respect to time lag L (i.e., the time lag between the onset of transmission and mortality). At the singular strategy [Formula: see text] and [Formula: see text], we further obtained the expressions of the case mortalities [Formula: see text] and how they are affected by the time lag L. Finally, we only presented some preliminary results about host and parasite coevolution dynamics, including a general condition under which the coevolutionary singular strategy [Formula: see text] is evolutionarily stable.

This is the first attempt to investigate the effects of the factors related to non-pharmaceutical interventions (NPIs) and the physical condition of the public on virulence evolution of SARS-CoV-2 and the trend of the epidemics of COVID-19 under an adaptive dynamics framework. Qualitative agreement of the prediction on the epidemics of COVID-19 with the actual situations convinced the rationality of the present model. The study showed that enhancing both NPIs (including public vigilance, quarantine measures, and hospitalization) and the physical condition of the public (including susceptibility and recovery speed) contributed to decreasing the prevalence of COVID-19 but only increasing public vigilance and decreasing the susceptibility of the public could also reduce the virulence of SARS-CoV-2. Therefore, controlling the contact rate and infection rate was the key to control not only the epidemic scale of COVID-19 but also the extent of its harm. On the other hand, the best way to control the epidemics was to increase the public vigilance and physical condition because both of them could reduce the prevalence and case fatality rate (CFR) of COVID-19. In addition, the enhancement of quarantine measures and hospitalization could bring the (slight) increase in the CFR of COVID-19.

COVID-19 is a disease caused by infection with the virus 2019-nCoV, a single-stranded RNA virus. During the infection and transmission processes, the virus evolves and mutates rapidly, though the disease has been quickly controlled in Wuhan by \'Fangcang\' hospitals. To model the virulence evolution, in this paper, we formulate a new age structured epidemic model. Under the tradeoff hypothesis, two special scenarios are used to study the virulence evolution by theoretical analysis and numerical simulations. Results show that, before \'Fangcang\' hospitals, two scenarios are both consistent with the data. After \'Fangcang\' hospitals, Scenario I rather than Scenario II is consistent with the data. It is concluded that the transmission pattern of COVID-19 in Wuhan obey Scenario I rather than Scenario II. Theoretical analysis show that, in Scenario I, shortening the value of L (diagnosis period) can result in an enormous selective pressure on the evolution of 2019-nCoV.

Sequence type 11 (ST11) carbapenem-resistant Klebsiella pneumoniae (CRKP) has become the dominant clone in China. In this review, we trace the prevalence of ST11 CRKP in the China Antimicrobial Surveillance Network (CHINET), the key antimicrobial resistance mechanisms and virulence evolution. The recent emergence of ST11 carbapenem-resistant hypervirulent K. pneumoniae (CR-hvKP) strains in China due to the acquisition of a pLVPK-like virulence plasmid, which may cause severe infections in relatively healthy individuals that are difficult to treat with current antibiotics, has attracted worldwide attention. There is a very close linkage among IncF plasmids, NTEKPC and ST11 K. pneumoniae in China. Hybrid conjugative virulence plasmids are demonstrated to readily convert a ST11 CRKP strain to a CR-hvKP strain via conjugation. Understanding the molecular evolutionary mechanisms of resistance and virulence-bearing plasmids as well as the prevalence of ST11 CRKP in China allows improved tracking and control of such organisms.