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  • 1
    Online Resource
    Online Resource
    Coronavirus Porcine Epidemic Diarrhea Virus Nucleocapsid Protein Interacts with p53 To Induce Cell Cycle Arrest in S-Phase and Promotes Viral Replication
    American Society for Microbiology ; 2021
    In:  Journal of Virology Vol. 95, No. 16 ( 2021-07-26)
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 95, No. 16 ( 2021-07-26)
    Abstract: Subversion of the host cell cycle to facilitate viral replication is a common feature of coronavirus infections. Coronavirus nucleocapsid (N) protein can modulate the host cell cycle, but the mechanistic details remain largely unknown. Here, we investigated the effects of manipulation of porcine epidemic diarrhea virus (PEDV) N protein on the cell cycle and the influence on viral replication. Results indicated that PEDV N induced Vero E6 cell cycle arrest at S-phase, which promoted viral replication ( P  〈   0.05). S-phase arrest was dependent on the N protein nuclear localization signal S 71 NWHFYYLGTGPHADLRYRT 90 and the interaction between N protein and p53. In the nucleus, the binding of N protein to p53 maintained consistently high-level expression of p53, which activated the p53-DREAM pathway. The key domain of the N protein interacting with p53 was revealed to be S 171 RGNSQNRGNNQGRGASQNRGGNN 194 (N S171–N194 ), in which G 183 RG 185 are core residues. N S171–N194 and G 183 RG 185 were essential for N-induced S-phase arrest. Moreover, small molecular drugs targeting the N S171–N194 domain of the PEDV N protein were screened through molecular docking. Hyperoside could antagonize N protein-induced S-phase arrest by interfering with interaction between N protein and p53 and inhibit viral replication ( P  〈   0.05). The above-described experiments were also validated in porcine intestinal cells, and data were in line with results in Vero E6 cells. Therefore, these results reveal the PEDV N protein interacts with p53 to activate the p53-DREAM pathway, and subsequently induces S-phase arrest to create a favorable environment for virus replication. These findings provide new insight into the PEDV-host interaction and the design of novel antiviral strategies against PEDV. IMPORTANCE Many viruses subvert the host cell cycle to create a cellular environment that promotes viral growth. PEDV, an emerging and reemerging coronavirus, has led to substantial economic loss in the global swine industry. Our study is the first to demonstrate that PEDV N-induced cell cycle arrest during the S-phase promotes viral replication. We identified a novel mechanism of PEDV N-induced S-phase arrest, where the binding of PEDV N protein to p53 maintains consistently high levels of p53 expression in the nucleus to mediate S-phase arrest by activating the p53-DREAM pathway. Furthermore, a small molecular compound, hyperoside, targeted the PEDV N protein, interfering with the interaction between the N protein and p53 and, importantly, inhibited PEDV replication by antagonizing cell cycle arrest. This study reveals a new mechanism of PEDV-host interaction and also provides a novel antiviral strategy for PEDV. These data provide a foundation for further research into coronavirus-host interactions.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.00187-21
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2021
    detail.hit.zdb_id: 1495529-5
    detail.hit.zdb_id: 80174-4
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  • 2
    Online Resource
    Online Resource
    Anaerobic Methyl tert -Butyl Ether-Degrading Microorganisms Identified in Wastewater Treatment Plant Samples by Stable Isotope Probing
    American Society for Microbiology ; 2012
    In:  Applied and Environmental Microbiology Vol. 78, No. 8 ( 2012-04-15), p. 2973-2980
    Details
    In: Applied and Environmental Microbiology, American Society for Microbiology, Vol. 78, No. 8 ( 2012-04-15), p. 2973-2980
    Abstract: Anaerobic methyl tert -butyl ether (MTBE) degradation potential was investigated in samples from a range of sources. From these 22 experimental variations, only one source (from wastewater treatment plant samples) exhibited MTBE degradation. These microcosms were methanogenic and were subjected to DNA-based stable isotope probing (SIP) targeted to both bacteria and archaea to identify the putative MTBE degraders. For this purpose, DNA was extracted at two time points, subjected to ultracentrifugation, fractioning, and terminal restriction fragment length polymorphism (TRFLP). In addition, bacterial and archaeal 16S rRNA gene clone libraries were constructed. The SIP experiments indicated bacteria in the phyla Firmicutes (family Ruminococcaceae ) and Alphaproteobacteria (genus Sphingopyxis ) were the dominant MTBE degraders. Previous studies have suggested a role for Firmicutes in anaerobic MTBE degradation; however, the putative MTBE-degrading microorganism in the current study is a novel MTBE-degrading phylotype within this phylum. Two archaeal phylotypes (genera Methanosarcina and Methanocorpusculum ) were also enriched in the heavy fractions, and these organisms may be responsible for minor amounts of MTBE degradation or for the uptake of metabolites released from the primary MTBE degraders. Currently, limited information exists on the microorganisms able to degrade MTBE under anaerobic conditions. This work represents the first application of DNA-based SIP to identify anaerobic MTBE-degrading microorganisms in laboratory microcosms and therefore provides a valuable set of data to definitively link identity with anaerobic MTBE degradation.
    Type of Medium: Online Resource
    ISSN: 0099-2240 , 1098-5336
    URL: Article
    DOI: 10.1128/AEM.07253-11
    RVK:
    WA 15000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2012
    detail.hit.zdb_id: 223011-2
    detail.hit.zdb_id: 1478346-0
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Diversity and Metabolic Potentials of As(III)-Oxidizing Bacteria in Activated Sludge
    American Society for Microbiology ; 2021
    In:  Applied and Environmental Microbiology Vol. 87, No. 23 ( 2021-11-10)
    Details
    In: Applied and Environmental Microbiology, American Society for Microbiology, Vol. 87, No. 23 ( 2021-11-10)
    Abstract: Biological arsenite [As(III)] oxidation is an important process in the removal of toxic arsenic (As) from contaminated water. However, the diversity and metabolic potentials of As(III)-oxidizing bacteria (AOB) responsible for As(III) oxidation in wastewater treatment facilities are not well documented. In this study, two groups of bioreactors inoculated with activated sludge were operated under anoxic or oxic conditions to treat As-containing synthetic wastewater. Batch tests of inoculated sludges from the bioreactors further indicated that microorganisms could use nitrate or oxygen as electron acceptors to stimulate biological As(III) oxidation, suggesting the potentials of this process in wastewater treatment facilities. In addition, DNA-based stable isotope probing (DNA-SIP) was performed to identify the putative AOB in the activated sludge. Bacteria associated with Thiobacillus were identified as nitrate-dependent AOB, while bacteria associated with Hydrogenophaga were identified as aerobic AOB in activated sludge. Metagenomic binning reconstructed a number of high-quality metagenome-assembled genomes (MAGs) associated with the putative AOB. Functional genes encoding As resistance, As(III) oxidation, denitrification, and carbon fixation were identified in these MAGs, suggesting their potentials for chemoautotrophic As(III) oxidation. In addition, the presence of genes encoding secondary metabolite biosynthesis and extracellular polymeric substance metabolism in these MAGs may facilitate the proliferation of these AOB in activated sludge and enhance their capacity for As(III) oxidation. IMPORTANCE AOB play an important role in the removal of toxic arsenic from wastewater. Most of the AOB have been isolated from natural environments. However, knowledge regarding the structure and functional roles of As(III)-oxidizing communities in wastewater treatment facilities is not well documented. The combination of DNA-SIP and metagenomic binning provides an opportunity to elucidate the diversity of in situ AOB community inhabiting the activated sludges. In this study, the putative AOB responsible for As(III) oxidation in wastewater treatment facilities were identified, and their metabolic potentials, including As(III) oxidation, denitrification, carbon fixation, secondary metabolite biosynthesis, and extracellular polymeric substance metabolism, were investigated. This observation provides an understanding of anoxic and/or oxic AOB during the As(III) oxidation process in wastewater treatment facilities, which may contribute to the removal of As from contaminated water.
    Type of Medium: Online Resource
    ISSN: 0099-2240 , 1098-5336
    URL: Article
    DOI: 10.1128/AEM.01769-21
    RVK:
    WA 15000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2021
    detail.hit.zdb_id: 223011-2
    detail.hit.zdb_id: 1478346-0
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    A survey of fecal virome and bacterial community of the diarrhea-affected cattle in northeast China reveals novel disease-associated ecological risk factors
    American Society for Microbiology ; 2024
    In:  mSystems Vol. 9, No. 1 ( 2024-01-23)
    Details
    In: mSystems, American Society for Microbiology, Vol. 9, No. 1 ( 2024-01-23)
    Abstract: The lack of data on the virome and bacterial community restricts our capability to recognize ecological risk factors for bovine diarrhea disease, thereby hindering our overall comprehension of the disease’s cause. In this study, we found that, for the diarrheal samples, the identified virome and bacterial community varied in terms of composition, abundance, diversity, configuration, and geographic distribution in relation to different disease-associated ecological factors. A series of significant correlations were observed between the prevalence of individual viruses and the disease-associated ecological factors. Our study aims to uncover novel ecological risk factors of bovine diarrheal disease by examining the pathogenic microorganism-host-environment disease ecology, thereby providing a new perspective on the control of bovine diarrheal diseases.
    Type of Medium: Online Resource
    ISSN: 2379-5077
    URL: Article
    DOI: 10.1128/msystems.00842-23
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2024
    detail.hit.zdb_id: 2844333-0
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  • 5
    Online Resource
    Online Resource
    Zoonotic Risk, Pathogenesis, and Transmission of Avian-Origin H3N2 Canine Influenza Virus
    American Society for Microbiology ; 2017
    In:  Journal of Virology Vol. 91, No. 21 ( 2017-11)
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 91, No. 21 ( 2017-11)
    Abstract: Two subtypes of influenza A virus (IAV), avian-origin canine influenza virus (CIV) H3N2 (CIV-H3N2) and equine-origin CIV H3N8 (CIV-H3N8), are enzootic in the canine population. Dogs have been demonstrated to seroconvert in response to diverse IAVs, and naturally occurring reassortants of CIV-H3N2 and the 2009 H1N1 pandemic virus (pdmH1N1) have been isolated. We conducted a thorough phenotypic evaluation of CIV-H3N2 in order to assess its threat to human health. Using ferret-generated antiserum, we determined that CIV-H3N2 is antigenically distinct from contemporary human H3N2 IAVs, suggesting that there may be minimal herd immunity in humans. We assessed the public health risk of CIV-H3N2 × pandemic H1N1 (pdmH1N1) reassortants by characterizing their in vitro genetic compatibility and in vivo pathogenicity and transmissibility. Using a luciferase minigenome assay, we quantified the polymerase activity of all possible 16 ribonucleoprotein (RNP) complexes (PB2, PB1, PA, NP) between CIV-H3N2 and pdmH1N1, identifying some combinations that were more active than either parental virus complex. Using reverse genetics and fixing the CIV-H3N2 hemagglutinin (HA), we found that 51 of the 127 possible reassortant viruses were viable and able to be rescued. Nineteen of these reassortant viruses had high-growth phenotypes in vitro , and 13 of these replicated in mouse lungs. A single reassortant with the NP and HA gene segments from CIV-H3N2 was selected for characterization in ferrets. The reassortant was efficiently transmitted by contact but not by the airborne route and was pathogenic in ferrets. Our results suggest that CIV-H3N2 reassortants may pose a moderate risk to public health and that the canine host should be monitored for emerging IAVs. IMPORTANCE IAV pandemics are caused by the introduction of novel viruses that are capable of efficient and sustained transmission into a human population with limited herd immunity. Dogs are a a potential mixing vessel for avian and mammalian IAVs and represent a human health concern due to their susceptibility to infection, large global population, and close physical contact with humans. Our results suggest that humans are likely to have limited preexisting immunity to CIV-H3N2 and that CIV-H3N2 × pdmH1N1 reassortants have moderate genetic compatibility and are transmissible by direct contact in ferrets. Our study contributes to the increasing evidence that surveillance of the canine population for IAVs is an important component of pandemic preparedness.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.00637-17
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2017
    detail.hit.zdb_id: 1495529-5
    detail.hit.zdb_id: 80174-4
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  • 6
    Online Resource
    Online Resource
    African Swine Fever Virus L83L Negatively Regulates the cGAS-STING-Mediated IFN-I Pathway by Recruiting Tollip To Promote STING Autophagic Degradation
    American Society for Microbiology ; 2023
    In:  Journal of Virology Vol. 97, No. 2 ( 2023-02-28)
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 97, No. 2 ( 2023-02-28)
    Abstract: African swine fever (ASF) is a devastating infectious disease of pigs caused by the African swine fever virus (ASFV), which poses a great danger to the global pig industry. Many viral proteins can suppress with interferon signaling to evade the host's innate immune responses. Therefore, the development of an effective vaccine against ASFV has been dampened. Recent studies have suggested that the L83L gene may be integrated into the host genome, weakening the host immune system, but the underlying mechanism is unknown. Our study found that L83L negatively regulates the cGAS-STING-mediated type I interferon (IFN-I) signaling pathway. Overexpression of L83L inhibited IFN-β promoter and ISRE activity, and knockdown of L83L induced higher transcriptional levels of interferon-stimulated genes (ISGs) and phosphorylation levels of IRF3 in primary porcine alveolar macrophages. Mechanistically, L83L interacted with cGAS and STING to promote autophagy-lysosomal degradation of STING by recruiting Tollip, thereby blocking the phosphorylation of the downstream signaling molecules TBK1, IRF3, and IκBα and reducing IFN-I production. Altogether, our study reveals a negative regulatory mechanism involving the L83L-cGAS-STING-IFN-I axis and provides insights into an evasion strategy involving autophagy and innate signaling pathways employed by ASFV. IMPORTANCE African swine fever virus (ASFV) is a large double-stranded DNA virus that primarily infects porcine macrophages. The ASFV genome encodes a large number of immunosuppressive proteins. Current options for the prevention and control of this pathogen remain pretty limited. Our study showed that overexpression of L83L inhibited the cGAS-STING-mediated type I interferon (IFN-I) signaling pathway. In contrast, the knockdown of L83L during ASFV infection enhanced IFN-I production in porcine alveolar macrophages. Additional analysis revealed that L83L protein downregulated IFN-I signaling by recruiting Tollip to promote STING autophagic degradation. Although L83L deletion has been reported to have little effect on viral replication, its immune evade mechanism has not been elucidated. The present study extends our understanding of the functions of ASFV-encoded pL83L and its immune evasion strategy, which may provide a new basis for developing a live attenuated vaccine for ASF.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.01923-22
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2023
    detail.hit.zdb_id: 1495529-5
    detail.hit.zdb_id: 80174-4
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  • 7
    Online Resource
    Online Resource
    Hydrocarbon-Degrading Microbial Communities Are Site Specific, and Their Activity Is Limited by Synergies in Temperature and Nutrient Availability in Surface Ocean Waters
    American Society for Microbiology ; 2019
    In:  Applied and Environmental Microbiology Vol. 85, No. 15 ( 2019-08)
    Details
    In: Applied and Environmental Microbiology, American Society for Microbiology, Vol. 85, No. 15 ( 2019-08)
    Abstract: The objective of this study was to quantify the potential for hydrocarbon biodegradation in surface waters of three sites, representing geographic regions of major oil exploration (Beaufort Sea in the Arctic, northern Gulf of Mexico [GOM], and southern GOM), in a systematic experimental design that incorporated gradients in temperature and the availability of major nutrients. Surface seawater was amended in microcosms with Macondo surrogate oil to simulate an oil slick, and microcosms were incubated, with or without nutrient amendment, at temperatures ranging from 4 to 38 º C. Using respiration rate as a proxy, distinct temperature responses were observed in surface seawater microcosms based on geographic origin; biodegradation was nearly always more rapid in the Arctic site samples than in the GOM samples. Nutrient amendment enhanced respiration rates by a factor of approximately 6, stimulated microbial growth, and generally elevated the taxonomic diversity of microbial communities within the optimal temperature range for activity at each site, while diversity remained the same or was lower at temperatures deviating from optimal conditions. Taken together, our results advance the understanding of how bacterioplankton communities from different geographic regions respond to oil perturbation. A pulsed disturbance of oil is proposed to favor copiotrophic r-strategists that are adapted to pointed seasonal inputs of phytoplankton carbon, displaying carbon and nutrient limitations, rather than oil exposure history. Further understanding of the ecological mechanisms underpinning the complex environmental controls of hydrocarbon degradation is required for improvement of predictive models of the fate and transport of spilled oil in marine environments. IMPORTANCE The risk of an oil spill accident in pristine regions of the world’s oceans is increasing due to the development and transport of crude oil resources, especially in the Arctic region, as a result of the opening of ice-free transportation routes, and there is currently no consensus regarding the complex interplay among the environmental controls of petroleum hydrocarbon biodegradation for predictive modeling. We examined the hydrocarbon biodegradation potential of bacterioplankton from three representative geographic regions of oil exploration. Our results showed that rates of aerobic respiration coupled to hydrocarbon degradation in surface ocean waters are controlled to a large extent by effects of temperature and nutrient limitation; hydrocarbon exposure history did not appear to have a major impact. Further, the relationship between temperature and biodegradation rates is linked to microbial community structure, which is specific to the geographic origin.
    Type of Medium: Online Resource
    ISSN: 0099-2240 , 1098-5336
    URL: Article
    DOI: 10.1128/AEM.00443-19
    RVK:
    WA 15000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2019
    detail.hit.zdb_id: 223011-2
    detail.hit.zdb_id: 1478346-0
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Mast Cell-Induced Lung Injury in Mice Infected with H5N1 Influenza Virus
    American Society for Microbiology ; 2012
    In:  Journal of Virology Vol. 86, No. 6 ( 2012-03-15), p. 3347-3356
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 86, No. 6 ( 2012-03-15), p. 3347-3356
    Abstract: Although an important role for mast cells in several viral infections has been demonstrated, its role in the invasion of highly pathogenic H5N1 influenza virus is unknown. In the present study, we demonstrate that mast cells were activated significantly by H5N1 virus (A/chicken/Henan/1/2004) infection both in vivo and in vitro . Mast cells could possibly intensify the lung injury that results from H5N1 infection by releasing proinflammatory mediators, including histamine, tryptase, and gamma interferon (IFN-γ). Lung lesions and apoptosis induced by H5N1 infection were reduced dramatically by treatment with ketotifen, which is a mast cell degranulation inhibitor. A combination of ketotifen and the neuraminidase inhibitor oseltamivir protected 100% of the mice from death postinfection. In conclusion, our data suggest that mast cells play a crucial role in the early stages of H5N1 influenza virus infection and provide a new approach to combat highly pathogenic influenza virus infection.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.06053-11
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2012
    detail.hit.zdb_id: 1495529-5
    detail.hit.zdb_id: 80174-4
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  • 9
    Online Resource
    Online Resource
    Erratum for Sun et al., “Zoonotic Risk, Pathogenesis, and Transmission of Avian-Origin H3N2 Canine Influenza Virus”
    American Society for Microbiology ; 2018
    In:  Journal of Virology Vol. 92, No. 8 ( 2018-04-15)
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 92, No. 8 ( 2018-04-15)
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.02227-17
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2018
    detail.hit.zdb_id: 1495529-5
    detail.hit.zdb_id: 80174-4
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