myo‐Inositol phosphate synthase (MIPS) is the key enzyme of myo‐inositol synthesis, which is a central molecule required for cell metabolism and plant growth as a precursor to a large variety of compounds. A full‐length fragment of MfMIPS1 cDNA was cloned from Medicago falcata that is more cold‐tolerant than Medicago sativa. While MfMIPS1 transcript was induced in response to cold, dehydration and salt stress, MIPS transcript and myo‐inositol were maintained longer and at a higher level in M. falcata than in M. sativa during cold acclimation at 5 °C. MfMIPS1 transcript was induced by hydrogen peroxide (H₂O₂) and nitric oxide (NO), but was not responsive to abscisic acid (ABA). Pharmacological experiments revealed that H₂O₂ and NO are involved in the regulation of MfMIPS1 expression by cold and dehydration, but not by salt. Overexpression of MfMIPS1 in tobacco increased the MIPS activity and levels of myo‐inositol, galactinol and raffinose, resulting in enhanced resistance to chilling, drought and salt stresses in transgenic tobacco plants. It is suggested that MfMIPS1 is induced by diverse environmental factors and confers resistance to various abiotic stresses.

Newcastle disease virus (NDV) infection causes severe inflammation and is a highly contagious disease in poultry. Virulent NDV strains (GM) induce large quantities of interleukin-1β (IL-1β), which is the central mediator of the inflammatory reaction. Excessive expression of IL-1β exacerbates inflammatory damage. Therefore, exploring the mechanisms underlying NDV-induced IL-1β expression can aid in further understanding the pathogenesis of Newcastle disease. Here, we showed that anti-IL-1β neutralizing antibody treatment decreased body temperature and mortality following infection with virulent NDV. We further explored the primary molecules involved in NDV-induced IL-1β expression from the perspective of both the host and virus. This study showed that overexpression of NLRP3 resulted in increased IL-1β expression, whereas inhibition of NLRP3 or caspase-1 caused a significant reduction in IL-1β expression, indicating that the NLRP3/caspase-1 axis is involved in NDV-induced IL-1β expression. Moreover, ultraviolet-inactivated GM (chicken/Guangdong/GM/2014) NDV failed to induce the expression of IL-1β. We then collected virus from GM-infected cell culture supernatant using ultracentrifugation, extracted the viral RNA, and stimulated the cells further with GM RNA. The results revealed that RNA alone was capable of inducing IL-1β expression. Moreover, NLRP3/caspase-1 was involved in GM RNA-induced IL-1β expression. Thus, our study elucidated the critical role of IL-1β in the pathogenesis of Newcastle disease while also demonstrating that inhibition of IL-1β via anti-IL-1β neutralizing antibodies decreased the damage associated with NDV infection; furthermore, GM RNA induced IL-1β expression via NLRP3/caspase-1.

Pigeon paramyxovirus type 1 (PPMV-1) infection causes high morbidity in pigeons, resulting in a significant burden to the poultry industry. In this study, we isolated three PPMV-1 strains from diseased pigeons collected in Guangdong Province, South China, from June 2017 to April 2019. Genetic analysis revealed that these three PPMV-1 strains and most of the PPMV-1 strains isolated from China after 2011 were clustered into sub-genotype VI.2.1.1.2.2. Our Bayesian analysis revealed that the VI.2.1.1.2.2 viruses might have originated in Europe. Phylogeographic analyses revealed that East and South China might have played a key role in seeding the VI.2.1.1.2.2 PPMV-1 epidemic in China. To characterize the effect of age at infection on the outcome of PPMV-1 infection in pigeons, we investigated the pathogenesis and transmission of the pigeon/Guangdong/GZ08/2017 (GZ08) virus in 3-, 6-, and 12-week-old pigeons. Two of six 12-week-old pigeons inoculated with GZ08 survived, and all of the 3- and 6-week-pigeons inoculated with GZ08 died. Moreover, the GZ08 virus could be transmitted to 3-, 6-, and 12-week-old naïve contact pigeons. The lethality of the GZ08 virus through contact with 3-, 6-, and 12-week-old pigeons was 100%, 66.7%, and 0%, respectively, suggesting that the transmissibility of the GZ08 virus was stronger in young pigeons. These findings demonstrated that East and South China was the epicenter for dissemination of VI.2.1.1.2.2 PPMV-1, and age at infection has an impact on the outcome of PPMV-1 infection in pigeons.

Wild birds play an important role in the emergence, evolution, and spread of zoonotic avian influenza viruses (AIVs). However, there are few studies on the cross-species transmission of the H3N8 AIV originating from wild birds. In this study, we investigated the transmissibility and pathogenicity of two H3N8 low pathogenic avian influenza viruses (LPAIVs) isolated from wild birds, GZA1 and XJ47, to mammals. The HA genes of both strains belonged to Eurasian isolates, while the other genes were derived from a variety of other subtypes of AIVs. Both strains can infect specific-pathogen-free (SPF) chickens, BALB/c mice, and guinea pigs. The XJ47 strain spread horizontally in SPF chickens and guinea pigs. The GZA1 strain did not spread horizontally but caused higher weight loss and mild lung inflammation in mice. P12-GZA1- and P12-XJ47-adapted strains obtained after 12 passages in the lung of mice showed enhanced pathogenicity in mice, which led to obvious clinical symptoms, lung inflammation, and 100% death. Both adapted strains have the reported mutation T97I in the PA, and the reported mutation D701N in PB2 has been found in the P12-GZA1-adapted strain. This study provides an important scientific basis for the continuous monitoring of wild AIVs and the mechanism underlying AIV cross-species transmission.