Elevated global temperatures and increased concentrations of carbon dioxide (CO2) in the atmosphere associated with climate change will exert profound effects on rice cropping systems, particularly on their greenhouse gas emitting potential. Incorporating biochar into paddy soil has been shown previously to reduce methane (CH4) emission from paddy rice under ambient temperature and CO2. We examined the ability of rice straw-derived biochar to reduce CH4 emission from paddy soil under elevated temperature and CO2 concentrations expected in the future. Adding biochar to paddy soil reduced CH4 emission under ambient conditions and significantly reduced emissions by 39.5% (ranging from 185.4 mg kg−1 dry weight soil, dws season−1 to 112.2 mg kg−1 dws season−1) under simultaneously elevated temperature and CO2. Reduced CH4 release was mainly attributable to the decreased activity of methanogens along with the increased CH4 oxidation activity and pmoA gene abundance of methanotrophs. Our findings highlight the valuable services of biochar amendment for CH4 control from paddy soil in a future that will be shaped by climate change.

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The broad‐leaved and Korean pine mixed forest in Changbai Mountain, China is an important component of boreal forest; the area is sensitive to global climate change. To understand spatial distribution patterns of soil bacterial community along elevation, we analyzed the soil bacterial community diversity and composition along an elevational gradient of 699–1177 m in a primitive Korean pine forest in Changbai Mountain using the high‐throughput sequencing. In total, 149,519 optimized sequences were obtained. Bacterial Shannon index increased along elevation from 699 m to 937 m and started to decrease at the elevation of 1,044 m, showing a humpback curve along elevation. Evenness (ACE index) and richness (Chao index) of the soil bacterial community both decreased with elevation (the highest values of 770 and 762 at 699 m and the lowest values of 548 and 539 at 1,177 m, respectively), all the indices are significantly different between elevations. Bacterial composition at phylum and genus levels had some differences between elevations, but the dominant bacterial populations were generally consistent. Beta‐diversity analysis showed a distance‐decay pattern of bacterial community similarity at different samples. Soil physical and chemical properties explained 70.78% of the variation in bacterial community structure (soil pH explained 19.95%), and elevational distance only explained 8.42%. In conclusion, the contemporary environmental disturbances are the critical factors in maintaining the bacterial spatial distribution compared with historical contingencies.

As a prevalent agent in cats, feline herpesvirus 1 (FHV-1) infection contributes to feline respiratory disease and acute and chronic conjunctivitis. FHV-1 can successfully evade the host innate immune response and persist for the lifetime of the cat. Several mechanisms of immune evasion by human herpesviruses have been elucidated, but the mechanism of immune evasion by FHV-1 remains unknown. In this study, we screened for FHV-1 open reading frames (ORFs) responsible for inhibiting the type I interferon (IFN) pathway with an IFN-β promoter reporter and analysis of IFN-β mRNA levels in HEK 293T cells and the Crandell-Reese feline kidney (CRFK) cell line, and we identified the Ser/Thr kinase US3 as the most powerful inhibitor. Furthermore, we found that the anti-IFN activity of US3 depended on its N terminus (amino acids 1 to 75) and was independent of its kinase activity. Mechanistically, the ectopic expression of US3 selectively inhibited IFN regulatory factor 3 (IRF3) promoter activation. Furthermore, US3 bound to the IRF association domain (IAD) of IRF3 and prevented IRF3 dimerization. Finally, US3-deleted recombinant FHV-1 and US3-repaired recombinant FHV-1 (rFHV-dUS3 and rFHV-rUS3, respectively) were constructed. Compared with wild-type FHV-1 and rFHV-rUS3, infection with rFHV-dUS3 induced large amounts of IFN-β and More importantly, US3 deletion significantly attenuated virulence, reduced virus shedding, and blocked the invasion of trigeminal ganglia. These results indicate that FHV-1 US3 efficiently inhibits IFN induction by using a novel immune evasion mechanism and that FHV-1 US3 is a potential regulator of neurovirulence. Despite widespread vaccination, the prevalence of FHV-1 remains high, suggesting that it can successfully evade the host innate immune response and infect cats. In this study, we screened viral proteins for inhibiting the IFN pathway and identified the Ser/Thr kinase US3 as the most powerful inhibitor. In contrast to other members of the alphaherpesviruses, FHV-1 US3 blocked the host type I IFN pathway in a kinase-independent manner and via binding to the IRF3 IAD and preventing IRF3 dimerization. More importantly, the depletion of US3 attenuated the anti-IFN activity of FHV-1 and prevented efficient viral replication and Also, US3 deletion significantly attenuated virulence and blocked the invasion of trigeminal ganglia. We believe that these findings not only will help us to better understand the mechanism of how FHV-1 manipulates the host IFN response but also highlight the potential role of US3 in the establishment of latent infection .

Feline calicivirus (FCV) often causes respiratory tract and oral disease in cats and is a highly contagious virus. Widespread vaccination does not prevent the spread of FCV. Furthermore, the low fidelity of the RNA-dependent RNA polymerase of FCV leads to the emergence of new variants, some of which show increased virulence. Currently, few effective anti-FCV drugs are available. Here, we found that germacrone, one of the main constituents of volatile oil from rhizoma curcuma, was able to effectively reduce the growth of FCV strain F9 in vitro. This compound exhibited a strong anti-FCV effect mainly in the early phase of the viral life cycle. The antiviral effect depended on the concentration of the drug. In addition, germacrone treatment had a significant inhibitory effect against two other reference strains, 2280 and Bolin, and resulted in a significant reduction in the replication of strains WZ-1 and HRB-SS, which were recently isolated in China. This is the first report of antiviral effects of germacrone against a calicivirus, and extensive in vivo research is needed to evaluate this drug as an antiviral therapeutic agent for FCV.

Tembusu virus (TMUV) is a flavivirus responsible for panzootic outbreaks of severe egg-drop and fatal encephalitis of domestic waterfowl in China. Although TMUV can be attenuated by in vitro passaging, experimental evidence supporting the role of specific genetic changes in virulence attenuation is currently lacking. Here, we performed site-directed mutagenesis on five envelope (E) protein amino acid residues in accordance with the attenuated TMUV generated in our recent study. Our results showed that the Thr-to-Lys mutation of residue 367 in E protein (E367) plays a predominant role in viral cell adaptation and virulence attenuation in ducks compared with mutations in other residues. We further demonstrated that the positively charged basic amino acid substitution at E367 enhanced the viral binding affinity for glycosaminoglycans (GAGs) and reduced viremia levels and the efficiency of replication in major target organs in subcutaneously inoculated ducks. Interestingly, the T367K mutation increased viral neutralization sensitivity to the early immune sera. Together, our findings provide the first evidence that a basic amino acid substitution at E367 strongly impacts the in vitro and in vivo infection of TMUV. IMPORTANCE Outbreaks of Tembusu virus (TMUV) infection have caused huge economic losses in the production of domestic waterfowl since the virus was first recognized in China in 2010. To control TMUV infection, a live-attenuated vaccine candidate of TMUV was developed in our previous study, but the mechanisms of virulence attenuation are not fully understood. Here, we found that the Thr-to-Lys substitution at E367 is a crucial determinant of TMUV virulence attenuation in ducks. We demonstrated that the T367K mutation attenuates TMUV through reducing viral replication in the blood, brain, heart (ducklings), and ovaries. These data provide new insights into understanding the pathogenesis of TMUV and the rational development of novel TMUV vaccines.