Journal of Microbiology

Yaqing Liu

1 Article

The effect of the HRB linker of Newcastle disease virus fusion protein on the fusogenic activity: Yaqing Liu , Ying Liu , Yanan Huang , Hongling Wen , Li Zhao , Yanyan Song , Zhiyu Wang; J. Microbiol. 2021;59(5):513-521. Published online March 29, 2021; DOI: https://doi.org/10.1007/s12275-021-0539-4

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Newcastle disease, designated a class A disease of poultry by the Office international des epizooties (OIE), is an acute infection caused by Newcastle disease virus (NDV). The merging of the envelope of NDV with the membrane of a target host cell is the key step in the infection pathway, which is driven by the concerted action of two glycoproteins: haemagglutinin- neuraminidase (HN) and fusion (F) protein. When the HN protein binds to the host cell surface receptor, the F protein is activated to mediate fusion. The three-dimensional structure of the F protein has been reported to have low electron density between the DIII domain and the HRB domain, and this electron-poor region is defined as the HRB linker. To clarify the contributing role of the HRB linker in the NDV F protein-mediated fusion process, 6 single amino acid mutants were obtained by site-directed mutagenesis of the HRB linker. The expression of the mutants and their abilities to mediate fusion were analysed, and the key amino acids in the HRB linker were identified as L436, E439, I450, and S453, as they can modulate the fusion ability or expression of the active form to a certain extent. The data shed light on the crucial role of the F protein HRB linker in the acquisition of a normal fusogenic phenotype.

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Evaluation of Newcastle disease virus LaSota strain attenuated by codon pair deoptimization of the HN and F genes for in ovo vaccination
Fatma Eldemery, Changbo Ou, Taejoong Kim, Stephen Spatz, John Dunn, Robert Silva, Qingzhong Yu
Veterinary Microbiology.2023; 277: 109625. CrossRef
Prevalence and Molecular Characterization of Bovine Parainfluenza Virus Type 3 in Cattle Herds in China
Yunxin Ren, Cheng Tang, Hua Yue
Animals.2023; 13(5): 793. CrossRef
Direct interaction of the molecular chaperone GRP78/BiP with the Newcastle disease virus hemagglutinin-neuraminidase protein plays a vital role in viral attachment to and infection of culture cells
Chenxin Han, Ziwei Xie, Yadi Lv, Dingxiang Liu, Ruiai Chen
Frontiers in Immunology.2023;[Epub] CrossRef
Adaptor complex-mediated trafficking of Newcastle disease virus fusion protein is regulated by the YLMY motif of its cytoplasmic tail
Yawen Bu, Qingyuan Teng, Delan Feng, Rong Liang, Haoran Wang, Xuehui Zhang, Xiao Li, Wenfeng Jia, Jia Xue, Ye Zhao, Guozhong Zhang
Virulence.2022; 13(1): 1849. CrossRef
YLMY Tyrosine Residue within the Cytoplasmic Tail of Newcastle Disease Virus Fusion Protein Regulates Its Surface Expression to Modulate Viral Budding and Pathogenicity
Yawen Bu, Qingyuan Teng, Delan Feng, Lu Sun, Jia Xue, Guozhong Zhang, Peter Pelka
Microbiology Spectrum.2021;[Epub] CrossRef

Yaqing Liu

1 Article

The key pathways and genes related to oncolytic Newcastle disease virus-induced phenotypic changes in ovarian cancer cells: Wei Song, Yuan Yuan, Fangfang Cao, Huazheng Pan, Yaqing Liu; J. Microbiol. 2025;63(4):e2411018. Published online April 29, 2025; DOI: https://doi.org/10.71150/jm.2411018

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Abstract PDF Supplementary Material: The poor prognosis and high recurrence rate of ovarian cancer highlight the urgent need to develop new therapeutic strategies. Oncolytic Newcastle disease virus (NDV) can kill cancer cells directly and regulate innate and adaptive immunity. In this study, ovarian cancer cells infected with or without velogenic NDV-BJ were subjected to a CCK-8 assay for detecting cell proliferation, flow cytometry for detecting the cell cycle and apoptosis, and wound healing and transwell assays for detecting cell migration and invasion. Transcriptomic sequencing was conducted to identify the differentially expressed genes (DEGs). GO and KEGG enrichment analyses were performed to explore the mechanism underlying the oncolytic effect of NDV on ovarian cancer cells. The results showed that infection with NDV inhibited ovarian cancer cell proliferation, migration, and invasion; disrupted the cell cycle; and promoted apoptosis. Compared with those in negative control cells, the numbers of upregulated and downregulated genes in ovarian cancer cells infected with NDV were 1,499 and 2,260, respectively. Thirteen KEGG pathways related to cell growth and death, cell mobility, and signal transduction were significantly enriched. Among these pathways, 48 DEGs, especially SESN2, HLA B/C/E, GADD45B, and RELA, that may be involved in the oncolytic process were screened, and qPCR analysis verified the reliability of the transcription data. This study discovered some key pathways and genes related to oncolytic NDV-induced phenotypic changes in ovarian cancer cells, which will guide our future research directions and help further explore the specific mechanisms by which infection with NDV suppresses ovarian cancer development.

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