Microplastics (MPs) are ubiquitous in the aquatic environment and can be frequently ingested by zooplankton, leading to various effects. Brine shrimp (Artemia parthenogenetica) has an important role in the energy flow through trophic levels in different seawater systems. In this work, the influence of polyethylene (PE) and polystyrene (PS) MPs on the growth of brine shrimp and corresponding changes of gut microbiota were investigated. Our results showed that the MPs remarkably reduced the growth rate of brine shrimp, and the two types of MPs have different impacts. The average body length of brine shrimps was reduced by 17.92 and 14.95% in the PE group and PS group, respectively. MPs are mainly found in the intestine, and their exposure evidently affects the gut microbiota. By using 16S rRNA gene high-throughput sequencing, 32 phyla of bacteria were detected in the intestine, and the microbiome consisted mainly of Proteobacteria, Firmicutes, and Actinobacteria. MPs’ exposure significantly increased the gut microbial diversity. For the PE group, the proportion of Actinobacteria and Bacteroidetes increased by 45.26 and 2.73%, respectively. For the PS group, it was 54.95 and 1.27%, respectively. According to the analysis on genus level, the proportions of Ponticoccus, Seohaeicola, Polycyclovorans, and Methylophaga decreased by 46.38, 1.24, 1.07, and 2.66%, respectively, for the PE group and 57.87, 1.43, 0.88, and 2.24%, respectively, for the PS group. In contrast, the proportions of Stappia, Microbacterium, and Dietzia increased by 1.12, 23.27, and 11.59%, respectively, for the PE group, and 1.09, 3.79, and 42.96%, respectively, for the PS group. These experimental results demonstrated that the ingestion of MPs by brine shrimp can alter the composition of the gut microbiota and lead to a slow growth rate. This study provides preliminary data support for understanding the biotoxicity of MPs to invertebrate zooplankton and is conducive to the further risk assessment of MP exposure.

Severe fever with thrombocytopenia syndrome virus (SFTSV) is a tick-borne pathogen that causes severe hemorrhagic fever. Although SFTSV poses a serious threat to public health and was recently isolated, its pathogenesis remains unclear. In particular, the relationship between SFTSV infection and the host cell cycle has not been described. Here, we show for the first time that both asynchronized and synchronized SFTSV-susceptible cells arrest at the G ₂ /M checkpoint following SFTSV infection and that the accumulation of cells at this checkpoint facilitates viral replication. We also identify a key mechanism underlying SFTSV-induced G ₂ /M arrest, in which SFTSV NSs interacts with CDK1 to inhibit formation and nuclear import of the cyclin B1-CDK1 complex, thus preventing it from regulating cell cycle progression. Our study highlights the key role that NSs plays in SFTSV-induced G ₂ /M arrest.

Severe fever with thrombocytopenia syndrome virus (SFTSV) is a new tick-borne pathogen that can cause severe hemorrhagic fever. Fever with thrombocytopenia syndrome caused by SFTSV is a new infectious disease that has posed a great threat to public health. Therefore, a fast, sensitive, low-cost, and field-deployable detection method for diagnosing SFTSV is essential for virus surveillance and control. In this study, we developed a rapid, highly sensitive, instrument-flexible SFTSV detection method that utilizes recombinase polymerase amplification and the CRISPR/Cas12a system. We found that three copies of the L gene from the SFTSV genome per reaction were enough to ensure stable detection within 40 min. The assay clearly showed no cross-reactivity with other RNA viruses. Additionally, our method demonstrated 100% agreement with Q-PCR detection results for SFTSV in 46 clinical samples. We simplified the requirements for on-site detection instruments by combining the CRISPR/Cas12a tool and immunochromatographic strips to create a system that can reliably detect one copy/μl sample of the L gene, which showed extremely high sensitivity and specificity for detecting the virus. Taken together, these findings indicate that the new SFTSV detection method is a powerful and effective tool for on-site detection, which can contribute to diagnosing SFTSV quickly and sensitively.

EV-D68 is a serious threat to human health, and there are currently no effective treatments or vaccines. SGs play an important role in cellular innate immunity as a target with antiviral effects. This manuscript describes the formation of SGs induced by EV-D68 early infection but inhibited during the late stage of infection. Moreover, TIA1, HUR, and G3BP1 can chelate a specific site of the 3′ UTR of EV-D68 to inhibit viral replication, and this interaction is sequence and complex dependent. However, this inhibition can be antagonized by overexpression of the minireplicon. These findings increase our understanding of EV-D68 infection and may help identify new antiviral targets that can inhibit viral replication and limit the pathogenesis of EV-D68.

Influenza A virus (IAV) poses a significant threat to human health, which calls for the development of efficient detection methods. The present study constructed a fluorescence resonance energy transfer (FRET) system based on novel fluorescent probes and graphene oxide (GO) for detecting H5N1 IAV hemagglutinin (HA). Here, we synthesized small (sub-20 nm) sandwich-structured upconversion nanoparticles (UCNPs) (SWUCNPs for short) with a high energy transfer efficiency, which allows for controlling the emitter in a thin shell. The π–π stacking interaction between the aptamer and GO shortens the distance between the fluorescent probe and the receptor, thereby realizing fluorescence resonance energy transfer (FRET). When HA is present, the aptamer enables changes in their conformations and move away from GO surface. Fluorescence signals display a linear relationship between HA quantitation in the range of 0.1–15 ng mL^–1 and a limit of detection (LOD) of 60.9 pg mL^–1. The aptasensor was also applicable in human serum samples with a linear range from 0.2 to 12 ng mL^–1 and a limit of detection of 114.7 pg mL^–1. This strategy suggested the promising prospect of the aptasensor in clinical applications because of the excellent sensing performance and sensitivity. This strategy may be promising for vitro diagnostics and provides new insights into the functioning of the SWUCNPs system.

Human enterovirus 68 (EV-D68) has received considerable attention recently as a global reemergent pathogen because it causes severe respiratory tract infections and acute flaccid myelitis. The nonstructural protein 2A protease (2A^pro) of EV, which functions in cleavage of host proteins, comprises an essential part of the viral immune evasion process. However, the pathogenic mechanism of EV-D68 is not fully understood. Here, we show for the first time that EV-D68 inhibited antiviral type I interferon responses by cleaving tumor necrosis factor receptor-associated factor 3 (TRAF3). Furthermore, we identified the key cleavage site in TRAF3. Our study may suggest a new mechanism by which the 2A^proof EV facilitates subversion of host innate immune responses. These findings increase our understanding of EV-D68 infection and may help identify new antiviral targets against EV-D68.