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Background: A viral infection can modify the risk to subsequent viral infections via cross‐protective immunity, increased immunopathology, or disease‐driven behavioral change. There is limited understanding of virus–virus interactions due to lack of long‐term population‐level data. Methods: Our study leverages passive surveillance data of 10 human acute respiratory viruses from Beijing, Chongqing, Guangzhou, and Shanghai collected during 2009 to 2019: influenza A and B viruses; respiratory syncytial virus A and B; human parainfluenza virus (HPIV), adenovirus, metapneumovirus (HMPV), coronavirus, bocavirus (HBoV), and rhinovirus (HRV). We used a multivariate Bayesian hierarchical model to evaluate correlations in monthly prevalence of test‐positive samples between virus pairs, adjusting for potential confounders. Results: Of 101,643 lab‐tested patients, 33,650 tested positive for any acute respiratory virus, and 4,113 were co‐infected with multiple viruses. After adjusting for intrinsic seasonality, long‐term trends and multiple comparisons, Bayesian multivariate modeling found positive correlations for HPIV/HRV in all cities and for HBoV/HRV and HBoV/HMPV in three cities. Models restricted to children further revealed statistically significant associations for another ten pairs in three of the four cities. In contrast, no consistent correlation across cities was found among adults. Most virus–virus interactions exhibited substantial spatial heterogeneity. Conclusions: There was strong evidence for interactions among common respiratory viruses in highly populated urban settings. Consistent positive interactions across multiple cities were observed in viruses known to typically infect children. Future intervention programs such as development of combination vaccines may consider spatially consistent virus–virus interactions for more effective control. [ABSTRACT FROM AUTHOR]

Aim: To quantitatively and qualitatively compare the host proteomic profile in samples of symptomatic and asymptomatic apical periodontitis (AP) using nano‐liquid chromatography–electron spray tandem mass spectrometry. Methodology: Samples were obtained from 18 patients with radiographically evident AP, divided into symptomatic and asymptomatic groups (nine per group) according to clinical characteristics. After sample collection, protein extraction, purification and quantification of the samples were performed, which were analysed by reverse‐phase liquid chromatography coupled to mass spectrometry. Label‐free quantitative proteomic analysis was performed by Protein Lynx Global Service software. Differences in expression of proteins between the groups were calculated using the Monte Carlo algorithm, considering P < 0.05 for down‐regulated proteins and 1 − P > 0.95 for up‐regulated proteins. Proteins were identified with the embedded ion accounting algorithm in the software and a search of the Homo sapiens UniProt database. Results: A total of 853 individual human proteins were identified. In the quantitative analysis, common proteins to both groups accounted for 143 proteins. Differences in expression between groups resulted in 51 up‐regulated proteins (1 − P > 0.95) in the symptomatic group, including alpha‐1‐antitrypsin, protein S100‐A8, myeloperoxidase, peroxiredoxin and lactotransferrin. This group also had 43 down‐regulated proteins (P < 0.05), comprising immunoglobulin, neutrophil defensin, pyruvate kinase and alpha‐enolase. The qualitative analysis considered only the exclusive proteins of each group. For the symptomatic group, 318 complete proteins and 29 fragments were identified, such as dedicator of cytokinesis protein, intersectin, prostaglandin, phospholipase DDHD2 and superoxide dismutase. For the asymptomatic group, 326 complete proteins and 37 fragments were identified, including azurocidin, C‐reactive protein, collagen alpha, cathepsin, heat shock and laminin. Conclusions: Quantitative differences in the expression of common proteins in cases of symptomatic and asymptomatic AP were found, which were mostly related to host immune response in both groups. Exclusive proteins in the symptomatic group were mainly related to the host response to the presence of viruses in endodontic infections, oxidative stress and proteolytic enzymes. The results provide a basis for a better understanding of cellular and molecular pathways involved in AP, establishing specific proteomic profiles for symptomatic and asymptomatic conditions. [ABSTRACT FROM AUTHOR]

The Tasmanian salmon industry had remained relatively free of major viral diseases until the emergence of pilchard orthomyxovirus (POMV). Originally isolated from wild pilchards, POMV is of concern to the industry as it can cause high mortality in farmed salmon (Salmo salar). Field observations suggest the virus can spread from pen to pen and between farms, but evidence of passive transmission in sea water was unclear. Our aim was to establish whether direct contact between infected and naïve fish was required for transmission, and to examine viral infection dynamics. Atlantic salmon post‐smolts were challenged with POMV by either direct exposure via cohabitation or indirect exposure via virus‐contaminated sea water. POMV was transmissible in sea water and direct contact between fish was not required for infection. Head kidney and heart presented the highest viral loads in early stages of infection. POMV survivors presented low viral loads in most tissues, but these remained relatively high in gills. A consistent feature was the infiltration of viral‐infected melanomacrophages in different tissues, suggesting an important role of these in the immune response to POMV. Understanding POMV transmission and host–pathogen interactions is key for the development of improved surveillance tools, transmission models and ultimately for disease prevention. [ABSTRACT FROM AUTHOR]

Polysulfated nanomaterials that mimic the extracellular cell matrix are of great interest for their potential to modulate cellular responses and to bind and neutralize pathogens. However, control over the density of active functional groups on such biomimetics is essential for efficient interactions, and this remains a challenge. In this regard, producing polysulfated graphene derivatives with control over their functionality is an intriguing accomplishment in order to obtain highly effective 2D platforms for pathogen interactions. Here, a facile and efficient method for the controlled attachment of a heparin sulfate mimic on the surface of graphene is reported. Dichlorotriazine groups are conjugated to the surface of graphene by a one-pot [2+1] nitrene cycloaddition reaction at ambient conditions, providing derivatives with defined functionality. Consecutive step by step conjugation of hyperbranched polyglycerol to the dichlorotriazine groups and eventual conversion to the polyglycerol sulfate result in the graphene based heparin biomimetics. Scanning force microscopy, cryo-transmission electron microscopy, and in vitro bioassays reveal strong interactions between the functionalized graphene (thoroughly covered by a sulfated polymer) and vesicular stomatitis virus. Infection experiments with highly sulfated versions of graphene drastically promote the infection process, leading to higher viral titers compared to nonsulfated analogues. [ABSTRACT FROM AUTHOR]

The rates and ratios of environmental nutrient supplies can determine plant community composition. However, the effect of nutrient supplies on within-host microbial interactions is poorly understood. Resource competition is a promising theory for understanding microbial interactions, because microparasites require nitrogen (N) and phosphorus (P) for synthesis of macromolecules such as nucleic acids and proteins., To better understand the effects of nutrient supplies to hosts on pathogen interactions, we singly inoculated and coinoculated Avena sativa with two virus species, barley yellow dwarf virus-PAV ( BYDV- PAV) and cereal yellow dwarf virus-RPV ( CYDV- RPV). Host plants were grown across a factorial combination of N and P supply rates that created a gradient of N : P supply ratios, one being replicated at low and high nutrient supply., Nutrient supply affected prevalence and the interaction strength among viruses. P addition lowered CYDV- RPV prevalence. The two viruses had a distinct competitive hierarchy: the coinoculation of BYDV- PAV lowered CYDV- RPV infection rate, but the reverse was not true. This antagonistic interaction occurred at low nutrient supply rates and disappeared at high N supply rate., Given the global scale of human alterations of N and P cycles, these results suggest that elevated nutrient supply will increase risks of virus coinfection with likely effects on virus epidemiology, virulence and evolution. [ABSTRACT FROM AUTHOR]

In a disease complex, different pathogen species cause similar symptoms on a common host plant species. These pathogens commonly develop simultaneously in a field and can then infect the same host individuals. Co-occurring pathogens may affect each other, through antagonism and/or synergism. An important question is the ecological and pathological consequences of co-occurrence of pathogenic species within a disease complex. By using two pathogens ( Mycosphaerella pinodes and Phoma medicaginis var . pinodella) of the Ascochyta blight complex, this study aimed at describing how co-occurrence affects the development of pathogens and disease severity, and at defining the prerequisites for interactions between pathogens. Results showed that the presence of the two pathogens on the same host plant organ limited the disease development and their reproduction. Damages caused by the two pathogens, however, increased when plants that had been previously inoculated were inoculated with the other species. The development of one pathogen species can be affected by a subsequent pathogen inoculation. Co-occurrence of pathogens within a disease complex can then limit or favour plant damages and pathogens reproduction. It would be one of the main forces that shape pathogen community structures and therefore the dynamics of diseases in field. [ABSTRACT FROM AUTHOR]