Identification of Hemagglutinin Mutations Caused by Neuraminidase Antibody Pressure

HA binds with the sialic acid receptor on the host cell and initiates the infection mode of influenza virus. NA cleaves the connection between receptor and HA of newborn virus at the end of viral production.

Chemotactic and temperature-dependent responses of the Strongyloidoidea superfamily of nematodes

Host-seeking behaviour and how a parasite identifies the correct host to infect remains a poorly understood area of parasitology. What is currently known is that host sensation and seeking behaviour is formed from a complex mixture of chemo-, thermo- and mechanosensory behaviours, of which chemosensation is the best studied. Previous studies of olfaction in parasitic nematodes suggested that this behaviour appears to be more closely related to target host and infection mode than phylogeny. However, there has not yet been a study comparing the chemotactic and temperature-dependent behaviours of very closely related parasitic and non-parasitic nematodes. To this end, we examined the temperature-dependent and chemotactic responses of the Strongyloidoidea superfamily of nematodes. We found differences in temperature response between the different species and within infective larvae. Chemotactic responses were highly divergent, with different attraction profiles between all species studied. When examining direct stimulation with fur, we found that it was insufficient to cause an attractive response. Overall, our results support the notion that olfactory sensation is more closely related to lifestyle and host range than phylogeny, and that multiple cues are required to initiate host-seeking behaviour.

Viral-eukaryotic gene exchange drives infection mode and cellular evolution

Gene exchange between viruses and their hosts acts as a key facilitator of horizontal gene transfer and is thought to be a major driver of evolutionary change 1–3. Our understanding of this process comes primarily from bacteria and phage co-evolution4, but the mode and functional significance of gene transfers between eukaryotes and their viruses remains more anecdotal. Here we show that viral-eukaryotic gene exchange can define infection strategies and has recurrently influenced eukaryotic evolution. Using a systematic, phylogenetically-informed approach, we characterized viral-eukaryotic gene exchange across diverse taxa, identifying thousands of transfers, and revealing their frequency, taxonomic distribution, and projected functions, across the eukaryotic tree of life. Eukaryote-derived viral genes revealed common viral host-manipulation strategies, including the key cellular pathways and compartments targeted during infection, identifying potential targets for broad-spectrum host-targeted antiviral therapeutics. Furthermore, viral-derived eukaryotic genes exposed a recurring role for viral glycosyltransferases in the diversification of eukaryotic morphology, as viral-derived genes have impacted the evolution of structures as diverse as algal cell walls, trypanosome mitochondria, and animal tissues. These findings illuminate the nature of viral-eukaryotic gene exchange and its impact on the biology of viruses and their eukaryotic hosts, providing novel perspectives for understanding viral infection mechanisms and revealing the influence of viruses on eukaryotic evolution.

Thermal stress triggers productive viral infection of a key coral reef symbiont

Climate change-driven ocean warming is increasing the frequency and severity of bleaching events, in which corals appear whitened after losing their dinoflagellate endosymbionts (family Symbiodiniaceae). Viral infections of Symbiodiniaceae may contribute to some bleaching signs, but little empirical evidence exists to support this hypothesis. We present the first temporal analysis of a viral lineage-the Symbiodiniaceae-infecting 'dinoRNAVs'-in coral colonies exposed to a 5-day heat treatment. Throughout the experiment, all colonies were dominated by Symbiodiniaceae in the genus Cladocopium, but 124 dinoRNAV major capsid protein 'aminotypes' (unique amino acid sequences) were detected across coral genets and treatments. Seventeen dinoRNAV aminotypes were found only in heat-treated fragments, and 22 aminotypes were detected at higher relative abundances in heat-treated fragments. DinoRNAVs also exhibited higher alpha diversity and dispersion under heat stress. Together, these findings provide the first empirical evidence that exposure to high temperatures triggers some dinoRNAVs to switch from a persistent to a productive infection mode within heat-stressed corals. Over extended time frames, we hypothesize that cumulative dinoRNAV lysis of Symbiodiniaceae cells during productive infections could decrease Symbiodiniaceae densities within corals, observable as bleaching signs. This study sets the stage for reef-scale investigations of dinoRNAV dynamics during bleaching events.

A Silent Infection Pandemic of COVID-19: Epidemiological Investigation and Hypothetical Models

To explore the epidemic mode of COVID-19, we made an epidemiological investigation, set up hypothetical models, and compared them with hepatitis A virus (HAV) age-specific epidemic characteristic. In the epidemiological investigation, we reported the first familial COVID-19 silent infection in the world. A 19-year-old healthy female COVID-19 virus carrier without any symptoms caused two mild and one severe pneumonia. In hypothetical models, the silent infection rate ranges from 60% to 80% based on 3 sources: China mainland, evacuation of 4 nationals, and the ship “Diamond Princess,” respectively. In comparison with HAV, COVID-19 shows the same infection mode in children (aged 0–9 years), but significant difference in young adults (aged 10–44 years) and the elderly (aged 45 years or older). Therefore, we prejudged that COVID-19 is a silent infection pandemic mainly in young adults but threatens the elderly.

The Microbiota-Gut-Brain Axis

The importance of the gut-brain axis in maintaining homeostasis has long been appreciated. However, the past 15 yr have seen the emergence of the microbiota (the trillions of microorganisms within and on our bodies) as one of the key regulators of gut-brain function and has led to the appreciation of the importance of a distinct microbiota-gut-brain axis. This axis is gaining ever more traction in fields investigating the biological and physiological basis of psychiatric, neurodevelopmental, age-related, and neurodegenerative disorders. The microbiota and the brain communicate with each other via various routes including the immune system, tryptophan metabolism, the vagus nerve and the enteric nervous system, involving microbial metabolites such as short-chain fatty acids, branched chain amino acids, and peptidoglycans. Many factors can influence microbiota composition in early life, including infection, mode of birth delivery, use of antibiotic medications, the nature of nutritional provision, environmental stressors, and host genetics. At the other extreme of life, microbial diversity diminishes with aging. Stress, in particular, can significantly impact the microbiota-gut-brain axis at all stages of life. Much recent work has implicated the gut microbiota in many conditions including autism, anxiety, obesity, schizophrenia, Parkinson’s disease, and Alzheimer’s disease. Animal models have been paramount in linking the regulation of fundamental neural processes, such as neurogenesis and myelination, to microbiome activation of microglia. Moreover, translational human studies are ongoing and will greatly enhance the field. Future studies will focus on understanding the mechanisms underlying the microbiota-gut-brain axis and attempt to elucidate microbial-based intervention and therapeutic strategies for neuropsychiatric disorders.

Cell-to-cell infection by HIV contributes over half of virus infection

Cell-to-cell viral infection, in which viruses spread through contact of infected cell with surrounding uninfected cells, has been considered as a critical mode of virus infection. However, since it is technically difficult to experimentally discriminate the two modes of viral infection, namely cell-free infection and cell-to-cell infection, the quantitative information that underlies cell-to-cell infection has yet to be elucidated, and its impact on virus spread remains unclear. To address this fundamental question in virology, we quantitatively analyzed the dynamics of cell-to-cell and cell-free human immunodeficiency virus type 1 (HIV-1) infections through experimental-mathematical investigation. Our analyses demonstrated that the cell-to-cell infection mode accounts for approximately 60% of viral infection, and this infection mode shortens the generation time of viruses by 0.9 times and increases the viral fitness by 3.9 times. Our results suggest that even a complete block of the cell-free infection would provide only a limited impact on HIV-1 spread.