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Rift Valley Fever Virus and Yellow Fever Virus in Urine: A Potential Source of Infection
Meng Li, Beibei Wang, Liqiang Li, Gary Wong, Yingxia Liu, Jinmin Ma, Jiandong Li, Hongzhou Lu, Mifang Liang, Ang Li, Xiuqing Zhang, Yuhai Bi, Hui Zeng
当前状态: , doi: 10.1007/s12250-019-00096-2
[摘要] [PDF] Springerlink
In recent years, the incidence of human infections caused by emerging or re-emerging pathogens has rapidly increased. Diseases that were once regional now have the ability to spread globally in a short amount of time and pose a wider threat to public health (Weaver et al. 2018). Yellow fever virus (YFV, family Flaviviridae, genus Flavivirus) is a mosquito-borne flavivirus that causes yellow fever in humans and has been endemic in Africa and Latin America for many years (Domingo et al. 2018). The most recent large-scale outbreak of YFV occurred in Brazil in which the mortality rate as of February 28, 2018 is 32.78% (WHO 2018). Rift Valley fever virus (RVFV, family Bunyaviridae, genus Phlebovirus) is another mosquitoborne virus and primarily circulates in Africa and the Middle East, and in recent years in Europe (Mansfield et al. 2015). During the initial stage of infection, most patients infected with YFV or RVFV present nonspecific symptoms such as fever, headache, and vomiting, which often lead to a misdiagnosis (Mansfield et al. 2015; Domingo et al. 2018). The cases of YFV and RVFV in China were first reported in March and July 2016, respectively, in travelers returning from Angola (Chen et al. 2016; Liu et al. 2017).
Bacteriophages Isolated in China for the Control of Pectobacterium carotovorum Causing Potato Soft Rot in Kenya
Peter Muturi, Junping Yu, Alice Nyambura Maina, Samuel Kariuki, Francis B. Mwaura, Hongping Wei
当前状态: , doi: 10.1007/s12250-019-00091-7
[摘要] [PDF] Springerlink
Soft rot is an economically significant disease in potato and one of the major threats to sustainable potato production. This study aimed at isolating lytic bacteriophages and evaluating methods for and the efficacy of applying phages to control potato soft rot caused by Pectobacterium carotovorum. Eleven bacteriophages isolated from soil and water samples collected in Wuhan, China, were used to infect P. carotovorum host strains isolated from potato tubers showing soft rot symptoms in Nakuru county, Kenya. The efficacy of the phages in controlling soft rot disease was evaluated by applying individual phage strains or a phage cocktail on potato slices and tubers at different time points before or after inoculation with a P. carotovorum strain. The phages could lyse 20 strains of P. carotovorum, but not Pseudomonas fluorescenscontrol strains. Among the 11 phages, Pectobacterium phage Wc5r, interestingly showed cross-activity against Pectobacterium atrosepticum and two phage-resistant P. carotovorum strains. Potato slice assays showed that the phage concentration and timing of application are crucial factors for effective soft rot control. Phage cocktail applied at a concentration of 1 × 109 plaque-forming units per milliliter before or within an hour after bacterial inoculation on potato slices, resulted in ≥90% reduction of soft rot symptoms. This study provides a basis for the development and application of phages to reduce the impact of potato soft rot disease.
Cleavage of the Babuvirus Movement Protein B4 into Functional Peptides Capable of Host Factor Conjugation is Required for Virulence
Jun Zhuang, Wenwu Lin, Christopher J. Coates, Pengxiang Shang, Taiyun Wei, Zujian Wu, Lianhui Xie
当前状态: , doi: 10.1007/s12250-019-00094-4
[摘要] [PDF] Springerlink
Banana bunchy top virus (BBTV) poses a serious danger to banana crops worldwide. BBTV-encoded protein B4 is a determinant of pathogenicity. However, the relevant molecular mechanisms underlying its effects remain unknown. In this study, we found that a functional peptide could be liberated from protein B4, likely via proteolytic processing. Site-directed mutagenesis indicated that the functional processing of protein B4 is required for its pathogenic effects, including dwarfism and sterility, in plants. The released protein fragment targets host proteins, such as the large subunit of RuBisCO (RbcL) and elongation factor 2 (EF2), involved in protein synthesis. Therefore, the peptide released from B4 (also a precursor) may act as a non-canonical modifier to influence host–pathogen interactions involving BBTV and plants.

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Preface
Preface
Zhi-Ming Zheng, Ke Lan, Eric O. Freed, Zheng-Li Shi
2019, 34(2): 117-118.   doi: 10.1007/s12250-019-00118-z
[HTML全文] [PDF 357KB] Springerlink
Review
Multiple Roles of HIV-1 Capsid during the Virus Replication Cycle
Mariia Novikova, Yulan Zhang, Eric O. Freed, Ke Peng
2019, 34(2): 119-134.   doi: 10.1007/s12250-019-00095-3
[HTML全文] [PDF 1752KB] Springerlink
Human immunodeficiency virus-1 capsid (HIV-1 CA) is involved in different stages of the viral replication cycle. During virion assembly, CA drives the formation of the hexameric lattice in immature viral particles, while in mature virions CA monomers assemble in cone-shaped cores surrounding the viral RNA genome and associated proteins. In addition to its functions in late stages of the viral replication cycle, CA plays key roles in a number of processes during early phases of HIV-1 infection including trafficking, uncoating, recognition by host cellular proteins and nuclear import of the viral preintegration complex. As a result of efficient cooperation of CA with other viral and cellular proteins, integration of the viral genetic material into the host genome, which is an essential step for productive viral infection, successfully occurs. In this review, we will summarize available data on CA functions in HIV-1 replication, describing in detail its roles in late and early phases of the viral replication cycle.
卡波氏肉瘤相关疱疹病毒生活周期:转录和转录后调控及致瘤机制
严莉君, VladimirMajerciak, 郑志明, 蓝柯
2019, 34(2): 135-161.   doi: 10.1007/s12250-019-00114-3
[HTML全文] [PDF 1571KB] Springerlink
卡波氏肉瘤相关疱疹病毒是一种重要的人类肿瘤病毒,在其生活周期中表现出潜伏感染和裂解复制两相生命周期。除了引发典型的卡波氏肉瘤之外,该病毒还会引发多中心性卡斯特曼疾病以及原发性渗出性淋巴瘤。卡波氏肉瘤同时也是艾滋病患者中常见的肿瘤之一。在病毒与宿主长期进化和共存的过程中,病毒利用宿主的系统来发展生命周期并不断进化出各种策略以拮抗宿主内的免疫系统从而最终导致肿瘤的发生。因此,更好地了解病毒两相生命周期及其调控的相关机制对我们揭示该病毒致瘤过程是十分有必要的。
Flu DRiPs in MHC Class Ⅰ Immunosurveillance
Jiajie Wei, Jonathan W. Yewdell
2019, 34(2): 162-167.   doi: 10.1007/s12250-018-0061-y
[HTML全文] [PDF 390KB] Springerlink
Since the publication of the DRiP (defective ribosomal product) hypothesis in 1996, numerous studies have addressed the contribution of DRiPs to generating viral antigenic peptides for CD8+ T cell immunosurveillance. Here, we review studies characterizing the generation of antigenic peptides from influenza A virus encoded DRiPs, discuss the many remaining mysteries regarding the nature of their co-translational generation, and speculate on where the future might lead.
Development of Neutralizing Antibodies against Zika Virus Based on Its Envelope Protein Structure
Chunpeng Yang, Rui Gong, Natalia de Val
2019, 34(2): 168-174.   doi: 10.1007/s12250-019-00093-5
[HTML全文] [PDF 1223KB] Springerlink
As we know more about Zika virus (ZIKV), as well as its linkage to birth defects (microcephaly) and autoimmune neurological syndromes, we realize the importance of developing an efficient vaccine against it. Zika virus disease has affected many countries and is becoming a major public health concern. To deal with the infection of ZIKV, plenty of experiments have been done on selection of neutralizing antibodies that can target the envelope (E) protein on the surface of the virion. However, the existence of antibody-dependent enhancement (ADE) effect might limit the use of them as therapeutic candidates. In this review, we classify the neutralizing antibodies against ZIKV based on the epitopes and summarize the resolved structural information on antibody/antigen complex from X-ray crystallography and cryo-electron microscopy (cryo-EM), which might be useful for further development of potent neutralizing antibodies and vaccines toward clinical use.
Viral Regulation of RNA Granules in Infected Cells
Qiang Zhang, Nishi R. Sharma, Zhi-Ming Zheng, Mingzhou Chen
2019, 34(2): 175-191.   doi: 10.1007/s12250-019-00122-3
[HTML全文] [PDF 1155KB] Springerlink
RNA granules are cytoplasmic, microscopically visible, non-membrane ribo-nucleoprotein structures and are important posttranscriptional regulators in gene expression by controlling RNA translation and stability. TIA/G3BP/PABP-specific stress granules (SG) and GW182/DCP-specific RNA processing bodies (PB) are two major distinguishable RNA granules in somatic cells and contain various ribosomal subunits, translation factors, scaffold proteins, RNA-binding proteins, RNA decay enzymes and helicases to exclude mRNAs from the cellular active translational pool. Although SG formation is inducible due to cellular stress, PB exist physiologically in every cell. Both RNA granules are important components of the host antiviral defense. Virus infection imposes stress on host cells and thus induces SG formation. However, both RNA and DNA viruses must confront the hostile environment of host innate immunity and apply various strategies to block the formation of SG and PB for their effective infection and multiplication. This review summarizes the current research development in the field and the mechanisms of how individual viruses suppress the formation of host SG and PB for virus production.
Manipulating the Interferon Signaling Pathway: Implications for HIV Infection
Krystelle Nganou-Makamdop, Daniel C. Douek
2019, 34(2): 192-196.   doi: 10.1007/s12250-019-00085-5
[HTML全文] [PDF 387KB] Springerlink
During human immunodeficiency virus (HIV) infection, type Ⅰ interferon (IFN-Ⅰ) signaling induces an antiviral state that includes the production of restriction factors that inhibit virus replication, thereby limiting the infection. As seen in other viral infections, type Ⅰ IFN can also increase systemic immune activation which, in HIV disease, is one of the strongest predictors of disease progression to acquired immune deficiency syndrome (AIDS) and non-AIDS morbidity and mortality. Moreover, IFN-Ⅰ is associated with CD4 T cell depletion and attenuation of antigen-specific T cell responses. Therefore, therapeutic manipulation of IFN-Ⅰ signaling to improve HIV disease outcome is a source of much interest and debate in the field. Recent studies have highlighted the importance of timing (acute vs. chronic infection) and have suggested that specific targeting of type Ⅰ IFNs and their subtypes may help harness the beneficial roles of the IFN-Ⅰ system while avoiding its deleterious activities.
Research Article
MicroRNA-135a Modulates Hepatitis C Virus Genome Replication through Downregulation of Host Antiviral Factors
Catherine Sodrosk, Brianna Lowey, Laura Hertz, T. Jake Liang, Qisheng Li
2019, 34(2): 197-210.   doi: 10.1007/s12250-018-0055-9
[HTML全文] [PDF 3041KB] Springerlink ESM
Cellular microRNAs (miRNAs) have been shown to modulate HCV infection via directly acting on the viral genome or indirectly through targeting the virus-associated host factors. Recently we generated a comprehensive map of HCV– miRNA interactions through genome-wide miRNA functional screens and transcriptomics analyses. Many previously unappreciated cellular miRNAs were identified to be involved in HCV infection, including miR-135a, a human cancerrelated miRNA. In the present study, we investigated the role of miR-135a in regulating HCV life cycle and showed that it preferentially enhances viral genome replication. Bioinformatics-based integrative analyses and subsequent functional assays revealed three antiviral host factors, including receptor interacting serine/threonine kinase 2 (RIPK2), myeloid differentiation primary response 88 (MYD88), and C-X-C motif chemokine ligand 12 (CXCL12), as bona fide targets of miR-135a. These genes have been shown to inhibit HCV infection at the RNA replication stage. Our data demonstrated that repression of key host restriction factors mediated the proviral effect of miR-135a on HCV propagation. In addition, miR-135a hepatic abundance is upregulated by HCV infection in both cultured hepatocytes and human liver, likely mediating a more favorable environment for viral replication and possibly contributing to HCV-induced liver malignancy. These results provide novel insights into HCV–host interactions and unveil molecular pathways linking miRNA biology to HCV pathogenesis.
HPV18 Utilizes Two Alternative Branch Sites for E6*I Splicing to Produce E7 Protein
Ayslan Castro Brant, Vladimir Majerciak, Miguel Angelo Martins Moreira, Zhi-Ming Zheng
2019, 34(2): 211-221.   doi: 10.1007/s12250-019-00098-0
[HTML全文] [PDF 951KB] Springerlink ESM
Human papillomavirus 18 (HPV18) E6 and E7 oncogenes are transcribed as a single bicistronic E6E7 pre-mRNA. The E6 ORF region in the bicistronic E6E7 pre-mRNA contains an intron. Splicing of this intron disrupts the E6 ORF integrity and produces a spliced E6*I RNA for efficient E7 translation. Here we report that the E6 intron has two overlapped branch point sequences (BPS) upstream of its 3' splice site, with an identical heptamer AACUAAC, for E6*I splicing. One heptamer has a branch site adenosine (underlined) at nt 384 and the other at nt 388. E6*I splicing efficiency correlates to the expression level of E6 and E7 proteins and depends on the selection of which branch site. In general, E6*I splicing prefers the 3'ss-proximal branch site at nt 388 over the distal branch site at nt 384. Inactivation of the nt 388 branch site was found to activate a cryptic acceptor site at nt 636 for aberrant RNA splicing. Together, these data suggest that HPV18 modulates its production ratio of E6 and E7 proteins by alternative selection of the two mapped branch sites for the E6*I splicing, which could be beneficial in its productive or oncogenic infection according to the host cell environment.
肿瘤细胞表达的朊病毒蛋白抵抗内质网应激导致的细胞凋亡
高振兴, 彭敏, 谌亮, 杨小文, 李欢, 师润, 吴桂茹, 蔡丽丽, 宋启斌, 李朝阳
2019, 34(2): 222-234.   doi: 10.1007/s12250-019-00107-2
[HTML全文] [PDF 6855KB] Springerlink ESM
未折叠蛋白反应(UPR)是内质网应激(ER stress)引起的一种适应性反应。在肺癌、胰腺癌等多种癌症中,癌细胞可利用ER stress促进自身的生存发展。朊病毒蛋白(PrP)是一种细胞表面糖蛋白,在多种癌症中表达上调且是胰腺癌,胃癌和乳腺癌患者预后差的生物学标记物。PrP在ER stress 的条件下表达上调,作为易于错误折叠的蛋白质,PrP的上调是否增强ER stress,其功能是什么目前所知极少。我们的研究发现尽管BFA、Thps、TM激活UPR,但只有ATF4是持续性增强,而不是ER stress的其他分支通路。而且在肺癌中经典的PERK-eIF2α-ATF4通路不能解释ATF4的激活,相关机制正在研究中。此外,只有BFA显著增强胞质中的简单糖基化的PrP。最后我们发现PrP的表达可以抵抗BFA诱导的癌细胞死亡。因此,BFA诱导持续的ER stress通路可以为肺癌、胰腺癌的靶向治疗提供新思路。