Yajun Song

Academy of Military Medical Sciences

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Co-Authors

Ruifu Yang

Ningbo University

135

Zongmin Du

Academy of Military Medical Sciences

Yujun Cui

Academy of Military Medical Sciences

Dongsheng Zhou

Ningbo University

Zhaobiao Guo

Institute of Microbiology

Yanping Han

Academy of Military Medical Sciences

Yanfeng Yan

Institute of Microbiology

Yafang Tan

Academy of Military Medical Sciences

Junhui Zhai

Southeast University

Yujing Bi

Academy of Military Medical Sciences

Cooperative Institutions

Institute of Microbiology

196

Chinese Academy of Sciences

145

Academy of Military Medical Sciences

137

Chinese Academy of Medical Sciences & Peking Union Medical College

Sun Yat-sen University

University of Chinese Academy of Sciences

Peking University

Shanghai Jiao Tong University

Army Medical University

Chongqing Medical University

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[Relationship between core promoter mutation, clinical features and virus replication in HBV carriers].

Chinese Journal of Clinical Hepatology (2005)

Erhei Dai Heng-jun Liu Yajun Song Cuiying Chen Ruifu Yang

Objective To elucidate the relationship between HBV core promoter mutation and clinical features as well as its effects on serum e system and viral replication. Methods Semi-nested mutation specific PCR (msPCR) was employed for detecting core promoter mutation at nt 1 762-1 764 in 97 patients with HBV infection. Results The msPCR method was demonstrated to be specific and reliable for the mutation detection by sequencing the PCR products. The detection ratio of the mutation in patients with acute hepatitis, mild, moderate and severe chronic hepatitis and liver cirrhosis was 2/5, 7/43, 10/31, 1/3 and 7/15, respectively. The detection rate of the mutation in liver cirrhosis was significantly higher than that in light chronic hepatitis (P0.025). In 92 patients with chronic HBV infection, HBeAg positive rate in wild (25/92), mutant (42/92) and mixed (25/92) strain infection was 80.0%, 56.0% and 64.3%, HBV DNA level was (4.4±8.5)×10~8, (1.1±1.6)×10~9 and (1.4±1.8)×10~9 copies/ml, the rate of abnormal ALT was 44.0%, 52.0% and 42.6%;ALT level was (58.6±79.0), (57.1±75.2) and (62.6±90.3) IU/ L, respectively (P0.05). Conclusions The msPCR method for detecting core promoter mutation at nt 1 762-1 764 is specific and reliable. Core promoter mutation is associated with the severity of liver disease, but neither related to the status of e system in serum nor to the virus replication.

HBeAg

10.3760/cma.j.issn.1003-9279.2005.01.007

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Retrospective Serological Investigation of Severe Acute Respiratory Syndrome Coronavirus Antibodies in Recruits from Mainland China

Clinical and Vaccine Immunology (2005)

Yu SuMeng Maofeng Qiu Zeliang Chen Xiaobo Ye Yaling Gao

ABSTRACT Different assays were used to analyze 1,621 serum specimens collected from military recruits from the People's Republic of China in 2002 for severe acute respiratory syndrome (SARS) coronavirus antibodies. The results demonstrated that the subjects either had rarely been exposed to the virus before the 2003 SARS outbreak or had not been exposed but the nucleocapsid protein cross-reacted with other antibodies in humans.

Coronavirus

Sars virus

10.1128/cdli.12.4.552-554.2005

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Citations (11)

Sequencing and comparative genomics analysis of the IncHI2 plasmids pT5282-mphA and p112298-catA and the IncHI5 plasmid pYNKP001-dfrA

International Journal of Antimicrobial Agents (2017)

Quanhui Liang Zhe Yin Yachao Zhao Liqi Liang Jiao Feng

Citrobacter freundii

Insertion sequence

Enterobacter cloacae

10.1016/j.ijantimicag.2017.01.021

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Citations (45)

Attenuation of Yersinia pestis fyuA Mutants Caused by Iron Uptake Inhibition and Decreased Survivability in Macrophages

Frontiers in Cellular and Infection Microbiology (2022)

Yulu Chen Kai Song Xin Chen Ye Li Ruichen Lv

Yersinia pestis is the etiological agent of plague, a deadly infectious disease that has caused millions of deaths throughout history. Obtaining iron from the host is very important for bacterial pathogenicity. Y. pestis possesses many iron uptake systems. Yersiniabactin (Ybt) plays a major role in iron uptake in vivo and in vitro, and in virulence toward mice as well. FyuA, a β-barrel TonB-dependent outer membrane protein, serves as the receptor for Ybt. In this study, we examined the role of the fyuA gene in Y. pestis virulence using different challenging ways and explored the underlying mechanisms. The BALB/c mouse infection assay showed that the virulence of the mutant strains (ΔfyuA and ΔfyuAGCAdel) was lower when compared with that of the wild-type (WT) strain 201. Furthermore, the attenuation of virulence of the mutant strains via subcutaneous and intraperitoneal challenges was far greater than that via intravenous injection. Iron supplementation restored lethality during subcutaneous challenge with the two mutants. Thus, we speculated that the attenuated virulence of the mutant strains toward the mice may be caused by dysfunctional iron uptake. Moreover, ΔfyuA and ΔfyuAGCAdel strains exhibited lower survival rates in murine RAW264.7 macrophages, which might be another reason for the attenuation. We further explored the transcriptomic differences between the WT and mutant strains at different temperatures and found that the expressions of genes related to Ybt synthesis and its regulation were significantly downregulated in the mutant strains. This finding indicates that fyuA might exert a regulatory effect on Ybt. Additionally, the expressions of the components of the type III secretion system were unexpectedly upregulated in the mutants, which is inconsistent with the conventional view that the upregulation of the virulence genes enhances the virulence of the pathogens.

Yersinia pestis

Yersinia enterocolitica

Wild type

10.3389/fcimb.2022.874773

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Citations (4)

Identification and characterization of PhoP regulon members in Yersinia pestis biovar Microtus

BMC Genomics (2008)

Yingli Li He Gao Long Qin Bei Li Yanping Han

Abstract Background The transcription regulator PhoP has been shown to be important for Y. pestis survival in macrophages and under various in vitro stresses. However, the mechanism by which PhoP promotes bacterial intracellular survival is not fully understood. Our previous microarray analysis suggested that PhoP governed a wide set of cellular pathways in Y. pestis . A series of biochemical experiments were done herein to study members of the PhoP regulon of Y. pestis biovar Microtus . Results By using gel mobility shift assay and quantitative RT-PCR, a total of 30 putative transcription units were characterized as direct PhoP targets. The primer extension assay was further used to determine the transcription start sites of 18 PhoP-dependent promoters and to localize the -10 and -35 elements. The DNase I footprinting was used to identify the PhoP-binding sites within 17 PhoP-dependent promoters, enabling the identification of PhoP box and matrix that both represented the conserved signals for PhoP recognition in Y. pestis . Data presented here providing a good basis for modeling PhoP-promoter DNA interactions that is crucial to the PhoP-mediated transcriptional regulation. Conclusion The proven direct PhoP targets include nine genes encoding regulators and 21 genes or operons with functions of detoxification, protection against DNA damages, resistance to antimicrobial peptides, and adaptation to magnesium limitation. We can presume that PhoP is a global regulator that controls a complex regulatory cascade by a mechanism of not only directly controlling the expression of specific genes, but also indirectly regulating various cellular pathways by acting on a set of dedicated regulators. These results help us gain insights into the PhoP-dependent mechanisms by which Y. pestis survives the antibacterial strategies employed by host macrophages.

Yersinia pestis

Regulon

Biovar

Identification

Yersinia

10.1186/1471-2164-9-143

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Citations (32)

Microarray Analysis of Temperature‐Induced Transcriptome of Yersinia pestis

Microbiology and Immunology (2004)

Yanping Han Dongsheng Zhou Xin Pang Yajun Song Ling Zhang

Abstract Yersinia pestis , the etiologic agent of plague, must acclimatize itself to temperature shifts between the temperature (26 C) for flea blockage and the body temperature (37 C) of warm‐blooded hosts during its life cycle. Here a whole‐genome DNA microarray was used to investigate transcriptional regulation upon the upshift of growth temperature from 26 to 37 C in a chemically defined medium. Four hundred and one genes were regulated differentially under the two temperatures. About 39% of these genes were up‐regulated at 37 C, whereas 61% were down‐regulated. Temperature‐induced changes occurred at the level of transcription of genes encoding proven or predicted virulence factors, regulators, metabolism‐associated proteins, prophages, and hypothetical proteins. Strikingly, many gene clusters displayed a co‐transcription pattern in response to temperature upshift. Our data provided a genome‐wide profile of gene transcription induced by temperature shift and should shed light on the pathogenicity and host‐microbe interaction of this deadly pathogen.

Yersinia pestis

Prophage

Transcription

10.1111/j.1348-0421.2004.tb03605.x

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Citations (110)

The Genome of the Great Gerbil Reveals Species-Specific Duplication of an MHCII Gene

Genome Biology and Evolution (2020)

Pernille Nilsson Monica Hongrø Solbakken Boris V. Schmid Russell J. S. Orr Ruichen Lv

The great gerbil (Rhombomys opimus) is a social rodent living in permanent, complex burrow systems distributed throughout Central Asia, where it serves as the main host of several important vector-borne infectious pathogens including the well-known plague bacterium (Yersinia pestis). Here, we present a continuous annotated genome assembly of the great gerbil, covering over 96% of the estimated 2.47-Gb genome. Taking advantage of the recent genome assemblies of the sand rat (Psammomys obesus) and the Mongolian gerbil (Meriones unguiculatus), comparative immunogenomic analyses reveal shared gene losses within TLR gene families (i.e., TLR8, TLR10, and the entire TLR11-subfamily) for Gerbillinae, accompanied with signs of diversifying selection of TLR7 and TLR9. Most notably, we find a great gerbil-specific duplication of the MHCII DRB locus. In silico analyses suggest that the duplicated gene provides high peptide binding affinity for Yersiniae epitopes as well as Leishmania and Leptospira epitopes, putatively leading to increased capability to withstand infections by these pathogens. Our study demonstrates the power of whole-genome sequencing combined with comparative genomic analyses to gain deeper insight into the immunogenomic landscape of the great gerbil and its close relatives.

Yersinia pestis

Gerbil

10.1093/gbe/evaa008

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Citations (9)

Additional file 1: of Prevalence and associated knowledge of hepatitis B infection among healthcare workers in Freetown, Sierra Leone

Figshare (2018)

Yu-Ling Qin Bo Li Yue-Su Zhou Xin Zhang Lei Li

The original data of HBV surveillance for HCWs from Sierra Leone. (XLSX 25 kb)

Hepatitis B

10.6084/m9.figshare.6796298

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Historical variations in mutation rate in an epidemic pathogen, Yersinia pestis

Proceedings of the National Academy of Sciences (2012)

Yujun Cui Chang Yu Yanfeng Yan Dongfang Li Yanjun Li

The genetic diversity of Yersinia pestis , the etiologic agent of plague, is extremely limited because of its recent origin coupled with a slow clock rate. Here we identified 2,326 SNPs from 133 genomes of Y. pestis strains that were isolated in China and elsewhere. These SNPs define the genealogy of Y. pestis since its most recent common ancestor. All but 28 of these SNPs represented mutations that happened only once within the genealogy, and they were distributed essentially at random among individual genes. Only seven genes contained a significant excess of nonsynonymous SNP, suggesting that the fixation of SNPs mainly arises via neutral processes, such as genetic drift, rather than Darwinian selection. However, the rate of fixation varies dramatically over the genealogy: the number of SNPs accumulated by different lineages was highly variable and the genealogy contains multiple polytomies, one of which resulted in four branches near the time of the Black Death. We suggest that demographic changes can affect the speed of evolution in epidemic pathogens even in the absence of natural selection, and hypothesize that neutral SNPs are fixed rapidly during intermittent epidemics and outbreaks.

Yersinia pestis

Nonsynonymous substitution

Genetic drift

Rate of evolution

Nucleotide diversity

10.1073/pnas.1205750110

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Citations (380)

Draft Genome Sequence of “ Paramesorhizobium deserti ” A-3-E ^T , a Strain Highly Resistant to Diverse β-Lactam Antibiotics

Genome Announcements (2016)

Ruichen Lv Xianwei Yang Nan Fang Yuqin Song Xuesong Luo

Here, we report the draft genome sequence of "Paramesorhizobium deserti" A-3-E(T), a strain isolated from the Taklimakan Desert of Xinjiang, China, which is resistant to multiple β-lactam antibiotics and other antibiotics (kanamycin, erythromycin, streptomycin, etc.) as well.

Strain (injury)

Beta-lactam

Sequence (biology)

10.1128/genomea.00311-16

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Citations (2)