Spatial patterns of urban expansion and cropland loss during 2017-2022 in Guangdong, China.

Urban expansion often occurs at the expense of cropland loss, posing challenges to sustainable urban growth and food security. However, detailed investigations into urban expansion and cropland loss remain limited, particularly in regions with varying levels of urbanization. Here, we take Guangdong Province, China, as a case study to exemplify how urban expansion affects cropland using remotely sensed land use products. We adopted geospatial analysis, correlation indicators, and landscape metrics to uncover their spatial relationships at 10-m spatial resolutions. Results showed that urban areas increased by 6335 km2 while cropland decreased by 3780 km2 from 2017 to 2022. Notably, 41 % of newly expanded urban areas were from croplands, and 45 % of lost croplands were converted to urban areas. Western Guangdong experienced the largest extent of urban expansion and cropland loss, emerging as a hotspot region in recent years. Additionally, our analysis observed the increasing compactness of urban areas and the growing fragmentation of cropland landscapes over time. These findings shed light on the intricate dynamics between urban expansion and cropland loss in rapidly urbanizing regions, which provide valuable insights for sustainable urban development, agricultural practice, and land management in the future.

SC75741 antagonizes vesicular stomatitis virus, duck Tembusu virus, and duck plague virus infection in duck cells through promoting innate immune responses.

Duck Tembusu virus (DTMUV) and duck plague virus (DPV) are typical DNA and RNA viruses of waterfowl, causing drastic economic losses to the duck farm industry in terms of high mortality and decreased egg production. These 2 viruses reappear from time to time because the available vaccines fail to provide complete immunity and no clinical antiviral drugs are available for them. In the present study, we evaluated the antiviral activity of SC75741 for DTMUV, DPV, and the model virus, vesicular stomatitis virus infection in duck cells. SC75741, a nuclear factor-kappa B (NF-κB)-specific inhibitor in mammal cells, revealed the highest antiviral activity among the inhibitors specific to c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, p38 mitogen-activated protein kinase (p38), and NF-κB signaling. The antiviral activity of SC75741 was dose-dependent and showed effects in different duck cell types. Time-addition and duration assay demonstrated that SC75741 inhibited virus infection in the middle of and after virus infection at least for 72 h in duck embro fibroblast cells. The DPV viral adsorption and genomic copy number were reduced, indicating that SC75741 blocks the phase of the virus life cycle at viral entry and genomic replication. In addition, SC75741 enhanced the expression of interferon only when stimulator of interferon genes (STING) was overexpressed or pre-activated by the virus infection, suggesting that SC75741 acts as a STING agonist. In conclusion, SC75741 is a candidate antiviral agent for DTMUV and DPV.

Duck enteritis virus pUL47, as a late structural protein localized in the nucleus, mainly depends on residues 40 to 50 and 768 to 777 and inhibits IFN-ß signalling by interacting with STAT1.

Duck enteritis virus (DEV) is a member of the Alphaherpesvirinae subfamily. The characteristics of some DEV genes have been reported. However, information regarding the DEV UL47 gene is limited. In this study, we identified the DEV UL47 gene encoding a late structural protein located in the nucleus of infected cells. We further found that two domains of DEV pUL47, amino acids (aa) 40 to 50 and 768 to 777, could function as nuclear localization sequence (NLS) to guide the nuclear localization of pUL47 and nuclear translocation of heterologous proteins, including enhanced green fluorescent protein (EGFP) and beta-galactosidase (ß-Gal). Moreover, pUL47 significantly inhibited polyriboinosinic:polyribocytidylic acid [poly(I:C)]-induced interferon beta (IFN-ß) production and downregulated interferon-stimulated gene (ISG) expression, such as Mx and oligoadenylate synthetase-like (OASL), by interacting with signal transducer and activator of transcription-1 (STAT1).

Alphaherpesvirus Major Tegument Protein VP22: Its Precise Function in the Viral Life Cycle.

Alphaherpesviruses are zoonotic pathogens that can cause a variety of diseases in humans and animals and severely damage health. Alphaherpesvirus infection is a slow and orderly process that can lie dormant for the lifetime of the host but may be reactivated when the immune system is compromised. All alphaherpesviruses feature a protein layer called the tegument that lies between the capsid and the envelope. Virus protein (VP) 22 is one of the most highly expressed tegument proteins; there are more than 2,000 copies of this protein in each viral particle. VP22 can interact with viral proteins, cellular proteins, and chromatin, and these interactions play important roles. This review summarizes the latest literature and discusses the roles of VP22 in viral gene transcription, protein synthesis, virion assembly, and viral cell-to-cell spread with the purpose of enhancing understanding of the life cycle of herpesviruses and other pathogens in host cells. The molecular interaction information herein provides important reference data.