Marshgunter0950

Polybrominated diphenyl ethers (PBDEs) are widely detected in coastal wetlands but their remediation is still difficult. In this study, different carbon sources, namely formate, acetate, pyruvate, lactate, succinate, methanol and ethanol, were added to mangrove sediments contaminated with BDE-47, a common PBDE congener, to enhance its degradation. After 2-month incubation, all carbon addition significantly enhanced degradation percentages. The residual BDE-47 percentage significantly correlated with the abundance of total bacteria and Dehalococcoides spp. The addition of methanol, acetate and succinate also achieved significantly higher degradation rates and shorter half-lives than sediments without carbon amendment at the end of 5-month incubation, although degradation percentages were comparable between sediments with and without extra carbon. The degradation pathway based on the profiles of degradation products was also similar among treatments. The results indicated the stimulatory effect of extra carbon sources on BDE-47 degradation in contaminated sediments was carbon- and time-specific. In this study, we analyzed heavy metals in 404 surface sediment samples from the Bohai Sea to measure contamination status and distribution. We found Zn levels to be the highest, whereas Hg concentrations were the lowest of measured heavy metals. We found that the samples containing the most heavy metals were those collected from Fuzhou Bay, Jinzhou Bay, central Bohai Sea mud area, and the Yellow River Delta. Further analyses suggest that these heavy metals in surface sediments in the Jinzhou Bay and Fuzhou Bay pose a serious ecological risk, with substantial Cd and Hg accumulation in the Jinzhou Bay and Yellow River Delta regions being indicative of intense human activities. An essential step in the morphogenesis of tailed bacteriophages is the joining of heads and tails to form infectious virions. Our understanding of the maturation of complete virus particles remains incomplete. Through an unknown mechanism, phage T4 gene product 4 (gp4) plays an essential role in the head-tail joining step of T4-like phages. Alignment of T4 gp4 homologs identified a type II restriction endonuclease motif. Purified gp4 from both T4 and a marine T4-like bacteriophage, YC, have non-specific nuclease activity in vitro. Mutation of a single conserved amino acid residue in the endonuclease fold of T4 and YC gp4 abrogates nuclease activity. When expressed in trans, the wild type T4 gp4, but neither the mutated T4 protein nor the YC homolog, rescues a T4 gene 4 amber mutant phage. Thus the nuclease activity appears essential for morphogenesis, potentially by cleaving packaged DNA to enable the joining of heads to tails. Hantaviruses are rodent-borne hemorrhagic fever viruses leading to serious diseases. Viral attachment and entry represent the first steps in virus transmission and are promising targets for antiviral therapeutic intervention. Here we investigated receptor use in human airway epithelium of the Old and New World hantaviruses Hantaan virus (HTNV) and Andes virus (ANDV). Using a biocontained recombinant vesicular stomatitis virus pseudotype platform, we provide first evidence for a role of the cellular phosphatidylserine (PS) receptors of the T-cell immunoglobulin and mucin (TIM) protein family in HTNV and ANDV infection. In line with previous studies, HTNV, but not ANDV, was able to use glycosaminoglycan heparan sulfate and αvβ3 integrin as co-receptors. In sum, our studies demonstrate for the first time that hantaviruses make use of apoptotic mimicry for infection of human airway epithelium, which may explain why these viruses can easily break the species barrier. Viruses possessing class I fusion proteins require proteolytic activation by host cell proteases to mediate fusion with the host cell membrane. The mammalian SPINT2 gene encodes a protease inhibitor that targets trypsin-like serine proteases. Here we show the protease inhibitor, SPINT2, restricts cleavage-activation efficiently for a range of influenza viruses and for human metapneumovirus (HMPV). SPINT2 treatment resulted in the cleavage and fusion inhibition of full-length influenza A/CA/04/09 (H1N1) HA, A/Aichi/68 (H3N2) HA, A/Shanghai/2/2013 (H7N9) HA and HMPV F when activated by trypsin, recombinant matriptase or KLK5. click here We also demonstrate that SPINT2 was able to reduce viral growth of influenza A/CA/04/09 H1N1 and A/X31 H3N2 in cell culture by inhibiting matriptase or TMPRSS2. Moreover, inhibition efficacy did not differ whether SPINT2 was added at the time of infection or 24 h post-infection. Our data suggest that the SPINT2 inhibitor has a strong potential to serve as a novel broad-spectrum antiviral. Zika Virus (ZIKV) is a Flavivirus transmitted primarily via the bite of infected Aedes aegypti mosquitoes. Globally, 87 countries and territories have recorded autochthonous mosquito-borne transmission of ZIKV as at July 2019 and distributed across four of the six WHO Regions. Outbreaks of ZIKV infection peaked in 2016 and declined substantially throughout 2017 and 2018 in the Americas region. There is the likely risk for ZIKV to spread to more countries. There is also the potential for the re-emergence of ZIKV in all places with prior reports of the virus transmission. The current status of ZIKV transmission and spread is, however, a global health threat, and from the aforementioned, has the potential to re-emerge as an epidemic. This review summarizes the past and present spread of ZIKV outbreak-2007-2019, the genome, transmission cycle, clinical manifestations, vaccine and antiviral drug advancement. When purified from persistent infections, the genomes of most human polyomaviruses contain single enhancers. However, when isolated from productively infected cells from immunocompromised individuals, the genomes of several polyomaviruses contain duplicated enhancers that promote a number of polyoma-based diseases. The mechanism(s) that gives rise to the duplicated enhancers in the polyomaviruses is, however, not known. Herein we propose a model for the duplication of the enhancers that is based on recent advances in our understanding of; 1) the initiation of polyomavirus DNA replication, 2) the formation of long flaps via displacement synthesis and 3) the subsequent generation of duplicated enhancers via double stranded break repair. Finally, we discuss the possibility that the polyomavirus based replication dependent enhancer duplication model may be relevant to the enhancer-associated rearrangements detected in human genomes that are associated with various diseases, including cancers.