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The forest canopy is home to a rich biota. One salient feature are the dynamics of the habitat‐building trees, which are growing and eventually vanishing. Tree species strongly differ in growth rates, final size and longevity. Nevertheless, these inherent dynamics have been a blind spot in studies on host specificity of vascular epiphytes (vascular plants dwelling on trees without parasitizing them)—not least because tree growth rates and longevity are usually unknown in highly diverse tropical forests. The present study aims at tackling this blind spot. We compared epiphyte abundances (>23,000 individuals) found on 285 individuals of four focal tree species in a lowland moist forest in Panama. Data on repeated dbh censuses from a permanent tree plot provided the unique opportunity to estimate the age of our sampled trees. We compared the relative importance of tree longevity for host biases with that of other host tree characteristics, namely microclimatic conditions and bark acidity, rugosity and stability. The studied tree species differ in host quality and epiphyte species partly differ in host preferences. The conclusions concerning relative host tree quality depend hugely on whether or not different tree growth rates are considered. Comparing these conclusions allows important insights into the role of tree longevity in shaping epiphyte communities. Relating tree trait differences to the observed distributions of epiphytes among the focal tree species shows how the simultaneous action of various tree characteristics causes host biases. Synthesis. This study highlights the substantial but, up to now, hidden role of different tree growth rates for host tree specificity of vascular epiphytes. Future investigations need to consider this possibly confounding factor adequately to avoid spurious conclusions. Differences in tree growth rates have been a blind spot in studies on host specificity of vascular epiphytes. We compared epiphyte abundances on four tree species in a lowland moist forest. Host quality ranking depends hugely on whether tree size or age is used as a covariate. Future investigations need to consider different tree growth rates to avoid spurious conclusions.

A type of monophasic group B Salmonella enterica with the antigenic formula 4,12:a:- (“Fulica-like”) has been described as associated with harbour porpoises ( Phocoena phocoena ), most frequently recovered from lung samples. In the present study, lung tissue samples from 47 porpoises found along the Swedish coast or as bycatch in fishing nets were analysed, two of which were positive for S. enterica . Pneumonia due to the infection was considered the likely cause of death for one of the two animals. The recovered isolates were whole genome sequenced and found to belong to sequence type (ST) 416 and to be closely related to ST416/ST417 porpoise isolates from UK waters as determined by core-genome MLST. Serovars Bispebjerg, Fulica and Abortusequi were identified as distantly related to the porpoise isolates, but no close relatives from other host species were found. All ST416/417 isolates had extensive loss of function mutations in key Salmonella pathogenicity islands, but carried accessory genetic elements associated with extraintestinal infection such as iron uptake systems. Gene ontology and pathway analysis revealed reduced secondary metabolic capabilities and loss of function in terms of signalling and response to environmental cues, consistent with adaptation for the extraintestinal niche. A classification system based on machine learning identified ST416/417 as more invasive than classical gastrointestinal serovars. Genome analysis results are thus consistent with ST416/417 as a host-adapted and extraintestinal clonal population of S. enterica , which while found in porpoises without associated pathology can also cause severe opportunistic infections.

In this viewpoint, by reviewing the recent findings on wild animals and their gut microbiomes, we found some potential new insights and challenges in the study of the evolution of wild animals and their gut microbiome. We suggested that wild animal gut microbiomes may come from microbiomes in the animals' living habitats along with animals' special behavior, and that the study of long‐term changes in gut microbiomes should consider both habitat and special behaviors. Also, host behavior would facilitate the gut microbiome transmission between individuals. We suggested that research should integrate the evolutionary history and physiological systems of wild animals to understand the evolution of animals and their gut microbiomes. Finally, we proposed the Noncultured‐Cultured‐Fermentation‐Model Animal pipeline to determine the function (diet digestion, physiology, and behavior) of these target strains in the wild animal gut. Future perspectives in the study of the evolution of wild animals and their gut microbiomes: Noncultured‐Cultured‐Fermentation‐Model Animal (NCFM). This research frame included the identification of the transmitted strains and the downstream analysis on the function of these transmitted strains.

Parasites are characteristically aggregated within hosts, but identifying the mechanisms underlying such aggregation can be difficult in wildlife populations. We examined the influence of host age and sex over an annual cycle on the eggs per gram of feces (EPG) of nematode parasites infecting wild Japanese macaques (Macaca fuscata yakui) on Yakushima Island. Five species of nematode were recorded from 434 fecal samples collected from an age-structured group of 50 individually recognizable macaques. All parasites exhibited aggregated EPG distributions. The age-infection profiles of all three directly transmitted species (Oesophagostomum aculeatum, Strongyloides fuelleborni, and Trichuris trichiura) exhibited convex curves, but concavity better characterized the age-infection curves of the two trophically transmitted species (Streptopharagus pigmentatus and Gongylonema pulchrum). There was a male bias in EPG and prevalence of infection with directly transmitted species, except in the prevalence of O. aculeatum, and no sex bias in the other parasites. Infection with O. aculeatum showed a female bias in prevalence among young adults, and additional interactions with sex and seasonality show higher EPG values in males during the mating season (fall) but in females during the birth season (spring). These patterns suggest that an immunosuppressive role by reproductive hormones may be regulating direct, but not indirect, life-cycle parasites. Exposure at an early age may trigger an immune response that affects all nematodes, but trophically transmitted species appear to accumulate thereafter. Although it is difficult to discern clear mechanistic explanations for parasite distributions in wildlife populations, it is critical to begin examining these patterns in host species that are increasingly endangered by anthropogenic threats.

The limpet Lepetodrilus fucensis McLean is very abundant at hydrothermal vents on the Juan de Fuca and Explorer Ridges in the northeast Pacific Ocean. This limpet is parasitized by an undescribed chitonophilid copepod throughout the limpet's range. The parasite copepodite enters the mantle cavity and attaches to the afferent branchial vein. The initial invasive stage is a vermiform endosome within the vein that develops an extensive rootlet system causing an enlargement of the afferent branchial vein. Subsequently, an ectosomal female body grows outside the vein to sizes up to 2 mm in width. Once a dwarf male attaches, egg clusters form and nauplii are released. In over 3000 limpets examined from 30 populations, prevalence averaged about 5% with localized infections in female limpets over 25%. After the establishment of limpet populations at new vents, copepod prevalence increased over the succeeding months to 3 years. Host effects were marked and included castration of both sexes and deterioration in gill condition which affected both food acquisition and the gill symbiont. There was a significantly greater parasite prevalence in larger females which likely modifies the reproductive and competitive success of local host populations.

A considerable number of plants depend on structural support of other plants. To understand their diversity and ecology, it is essential to know how strongly potential host species differ in their suitability as hosts. This review focuses on vascular epiphytes, i.e. structurally dependent plants that do not parasitize their hosts. Despite a longstanding interest in the topic, our knowledge on the strength of their host specificity is still scanty. This is arguably due to conceptual confusion, but also because of the large complexity of the study system, which turns quantifying host specificity in the field into a challenge.Abstract Information on the degree of host specificity is fundamental for an understanding of the ecology of structurally dependent plants such as vascular epiphytes. Starting with the seminal paper of A.F.W. Schimper on epiphyte ecology in the late 19th century over 200 publications have dealt with the issue of host specificity in vascular epiphytes. We review and critically discuss this extensive literature. The available evidence indicates that host ranges of vascular epiphytes are largely unrestricted while a certain host bias is ubiquitous. However, tree size and age and spatial autocorrelation of tree and epiphyte species have not been adequately considered in most statistical analyses. More refined null expectations and adequate replication are needed to allow more rigorous conclusions. Host specificity could be caused by a large number of tree traits (e.g. bark characteristics and architectural traits), which influence epiphyte performance. After reviewing the empirical evidence for their relevance, we conclude that future research should use a more comprehensive approach by determining the relative importance of various potential mechanisms acting locally and by testing several proposed hypotheses regarding the relative strength of host specificity in different habitats and among different groups of structurally dependent flora.

The X chromosome and X-linked variants have largely been ignored in genome-wide and candidate association studies of infectious diseases due to the complexity of statistical analysis of the X chromosome. This exclusion is significant, since the X chromosome contains a high density of immune-related genes and regulatory elements that are extensively involved in both the innate and adaptive immune responses. Many diseases present with a clear sex bias, and apart from the influence of sex hormones and socioeconomic and behavioural factors, the X chromosome, X-linked genes and X chromosome inactivation mechanisms contribute to this difference. Females are functional mosaics for X-linked genes due to X chromosome inactivation and this, combined with other X chromosome inactivation mechanisms such as genes that escape silencing and skewed inactivation, could contribute to an immunological advantage for females in many infections. In this review, we discuss the involvement of the X chromosome and X inactivation in immunity and address its role in sexual dimorphism of infectious diseases using tuberculosis susceptibility as an example, in which male sex bias is clear, yet not fully explored.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which first occurred in Wuhan (China) in December of 2019, causes a severe acute respiratory illness with a high mortality rate, and has spread around the world. To gain an understanding of the evolution of the newly emerging SARS-CoV-2, we herein analyzed the codon usage pattern of SARS-CoV-2. For this purpose, we compared the codon usage of SARS-CoV-2 with that of other viruses belonging to the subfamily of Orthocoronavirinae. We found that SARS-CoV-2 has a high AU content that strongly influences its codon usage, which appears to be better adapted to the human host. We also studied the evolutionary pressures that influence the codon usage of five conserved coronavirus genes encoding the viral replicase, spike, envelope, membrane and nucleocapsid proteins. We found different patterns of both mutational bias and natural selection that affect the codon usage of these genes. Moreover, we show here that the two integral membrane proteins (matrix and envelope) tend to evolve slowly by accumulating nucleotide mutations on their corresponding genes. Conversely, genes encoding nucleocapsid (N), viral replicase and spike proteins (S), although they are regarded as are important targets for the development of vaccines and antiviral drugs, tend to evolve faster in comparison to the two genes mentioned above. Overall, our results suggest that the higher divergence observed for the latter three genes could represent a significant barrier in the development of antiviral therapeutics against SARS-CoV-2.

Synonymous codon usage (codon bias) greatly influences not only translation but also mRNA stability. In vertebrates, highly expressed genes preferentially use codons with an optimal tRNA adaptation index (tAI) that mostly end in C or G. Surprisingly, the codon usage of viruses infecting humans often deviates from optimality, showing an enrichment in A/U-ending codons, which are generally associated with slow decoding and reduced mRNA stability. This observation is particularly evident in RNA viruses causing respiratory illnesses in humans. This review analyzes the mutational and selective forces that shape nucleotide composition and codon usage drift in human RNA viruses, as well as their impact on translation, viral fitness, and evolution. It also describes how some viruses overcome suboptimal codon usage to outcompete host mRNA for translation. Finally, the roles of viral tropism and host adaptation in codon usage bias of prototypical viruses are discussed.

AbstractObjectiveTo compare the efficacy of covid-19 vaccines between immunocompromised and immunocompetent people.DesignSystematic review and meta-analysis.Data sourcesPubMed, Embase, Central Register of Controlled Trials, COVID-19 Open Research Dataset Challenge (CORD-19), and WHO covid-19 databases for studies published between 1 December 2020 and 5 November 2021. ClinicalTrials.gov and the WHO International Clinical Trials Registry Platform were searched in November 2021 to identify registered but as yet unpublished or ongoing studies.Study selectionProspective observational studies comparing the efficacy of covid-19 vaccination in immunocompromised and immunocompetent participants.MethodsA frequentist random effects meta-analysis was used to separately pool relative and absolute risks of seroconversion after the first and second doses of a covid-19 vaccine. Systematic review without meta-analysis of SARS-CoV-2 antibody titre levels was performed after first, second, and third vaccine doses and the seroconversion rate after a third dose. Risk of bias and certainty of evidence were assessed.Results82 studies were included in the meta-analysis. Of these studies, 77 (94%) used mRNA vaccines, 16 (20%) viral vector vaccines, and 4 (5%) inactivated whole virus vaccines. 63 studies were assessed to be at low risk of bias and 19 at moderate risk of bias. After one vaccine dose, seroconversion was about half as likely in patients with haematological cancers (risk ratio 0.40, 95% confidence interval 0.32 to 0.50, I2=80%; absolute risk 0.29, 95% confidence interval 0.20 to 0.40, I2=89%), immune mediated inflammatory disorders (0.53, 0.39 to 0.71, I2=89%; 0.29, 0.11 to 0.58, I2=97%), and solid cancers (0.55, 0.46 to 0.65, I2=78%; 0.44, 0.36 to 0.53, I2=84%) compared with immunocompetent controls, whereas organ transplant recipients were 16 times less likely to seroconvert (0.06, 0.04 to 0.09, I2=0%; 0.06, 0.04 to 0.08, I2=0%). After a second dose, seroconversion remained least likely in transplant recipients (0.39, 0.32 to 0.46, I2=92%; 0.35, 0.26 to 0.46), with only a third achieving seroconversion. Seroconversion was increasingly likely in patients with haematological cancers (0.63, 0.57 to 0.69, I2=88%; 0.62, 0.54 to 0.70, I2=90%), immune mediated inflammatory disorders (0.75, 0.69 to 0.82, I2=92%; 0.77, 0.66 to 0.85, I2=93%), and solid cancers (0.90, 0.88 to 0.93, I2=51%; 0.89, 0.86 to 0.91, I2=49%). Seroconversion was similar between people with HIV and immunocompetent controls (1.00, 0.98 to 1.01, I2=0%; 0.97, 0.83 to 1.00, I2=89%). Systematic review of 11 studies showed that a third dose of a covid-19 mRNA vaccine was associated with seroconversion among vaccine non-responders with solid cancers, haematological cancers, and immune mediated inflammatory disorders, although response was variable in transplant recipients and inadequately studied in people with HIV and those receiving non-mRNA vaccines.ConclusionSeroconversion rates after covid-19 vaccination were significantly lower in immunocompromised patients, especially organ transplant recipients. A second dose was associated with consistently improved seroconversion across all patient groups, albeit at a lower magnitude for organ transplant recipients. Targeted interventions for immunocompromised patients, including a third (booster) dose, should be performed.Systematic review registrationPROSPERO CRD42021272088.