by Background: The duration of viable viral shedding is important to be defined in regards of viral transmission in SARS-CoV-2 infection with the backdrop of the current worldwide effort for revising isolation polices and establishing the duration of infectiousness.
Methods: In this review we searched databases including Medline and google scholar for research articles published between January 2020 and January 2022. We included case reports, case series, cross sectional, cohort, and randomized control trials that reported the duration of shedding of viable SARS-CoV-2 virus. After evaluating the criteria for inclusion, 32 articles (2721 patients) were included.
Result: This review showed that the median for the last day of successful viral isolation was 11 (8.5-14.5 95% CI) , 20 (9.0-57.5 95 %CI), 20 (9.0-103 95 %CI) for the general population, critical patients and immunocompromised individuals, respectively, with significant association between prolonged viral shedding, disease severity (P-Value 0.024) and immunosuppressive status (P-Value 0.023).The corresponding higher cutoff of CTv to culturable virus ranged between 26.25 and 34.00 (95% confidence interval) with median of 30.5, and higher values were observed when critical (25.0-37.37 95 %CI) and immunocompromised patients (20.0-37.82 95 %CI) have been excluded, this deviation did not represent a statistical significance (P-Value 0.997 and 0.888) respectively.
Conclusion: Our review highlights that repeating SARS-CoV-2 viral RNA test solely in recovering patients has no importance in determining infectivity and emphasizes the individualization of de-isolation decisions based on the host factors and a combined symptom and testing-based approaches with the later benefiting most of correlation with recently introduced rapid antigen test. Our finding in the review also opposes the most recent CDC Guidance on shortening isolation duration in term of the last days of viable transmissible virus, therefore caution should be considered when revising such protocols.
Curcumin analog HO-3867 triggers apoptotic pathways through activating JNK1/2 signalling in human oral squamous cell carcinoma cells
Human oral squamous cell carcinoma (OSCC) is the common head and neck malignancy in the world. While surgery, radiotherapy and chemotherapy are emerging as the standard treatment for OSCC patients, the outcome is limited to the recurrence and side effects. Therefore, patients with OSCC require alternative strategies for treatment. In this study, we aimed to explore the therapeutic effect and the mode of action of the novel curcumin analog, HO-3867, against human OSCC cells. We analysed the cytotoxicity of HO-3867 using MTT assay. In vitro mechanic studies were performed to determine whether MAPK pathway is involved in HO-3867 induced cell apoptosis.
As the results, we found HO-3867 suppressed OSCC cells growth effectively. The flow cytometry data indicate that HO-3867 induce the sub-G1 phase. Moreover, we found that HO-3867 induced cell apoptosis by triggering formation of activated caspase 3, caspase 8, caspase 9 and PARP. After dissecting MAPK pathway, we found HO-3867 induced cell apoptosis via the c-Jun N-terminal kinase (JNK)1/2 pathway. Our results suggest that HO-3867 is an effective anticancer agent as its induction of cell apoptosis through JNK1/2 pathway in human oral cancer cells.
Gut-on-chip for ecological and causal human gut microbiome research
There is a growing interest to understand if and how the gut microbiome is causally linked to the pathogenesis and/or progression of diseases. While in vitro cell line models are commonly used for studying specific aspects of the host-microbe interaction, gnotobiotic murine models are considered the preferred platform for studying causality in microbiome research. Nevertheless, findings from animal studies provide limited opportunity for delineating various areas of interest to the human gut microbiome research.
Gut-on-chips are biomimetics recapitulating intestinal physiology which enable investigation of bidirectional effects of the host and microbiome. We posit that they could advance causal and ecological gut microbiome research in three major areas: (i) diet-microbiome and drug-microbiome interaction; (ii) microbiome-targeted therapeutics pharmacoecology; and (iii) mechanistic studies of gut microbiome and microbiome-targeted intervention in extraintestinal pathologies.
Rare isolation of human-tropic recombinant porcine endogenous retroviruses PERV-A/C from Göttingen minipigs
Background: Porcine endogenous retroviruses (PERVs) can infect human cells and pose a risk for xenotransplantation when pig cells, tissues or organs are transplanted to human recipients. Xenotransplantation holds great promise to overcome the shortage of human donor organs after solving the problems of rejection, functionality and virus safety. We recently described the transmission of a human-tropic recombinant PERV-A/C, designated PERV-F, from peripheral blood mononuclear cells (PBMCs) of a Göttingen Minipig (GöMP) to human 293 cells (Krüger et al., in Viruses 12(1):38, 2019). The goal of this study was to characterize PERV-F in more detail and to analyze the probability of virus isolation from other animals.
Methods: The recombination site in the envelope (env) gene, the long terminal repeats (LTR), the proteins and the morphology of the recombinant PERV-F were characterized by polymerase chain reaction (PCR), sequencing, Western blot analysis, immunofluorescence, and transmissible electron microscopy. Mitogen-stimulated PBMCs from 47 additional pigs, including 17 new GöMP, were co-cultured with highly susceptible human 293 T cells, and the PERV-A/C prevalence and PERV transmission was analyzed by PCR.
Results: PERV-F, isolated from a GöMP, is an infectious human-tropic PERV-A/C virus with a novel type of recombination in the env gene. The length of the LTR of PERV-F increased after passaging on human cells. In a few minipigs, but not in German landrace pigs, PERV-A/C were found. There was no transmission of human-tropic PERV-A/C from additional 47 pigs, including 17 GöMP, to human cells.
Conclusion: These data show that human-tropic recombinant PERV-A/C proviruses can only be found in a very small number of minipigs, but not in other pigs, and that their isolation as infectious virus able to replicate on human cells is an extremely rare event, even when using highly susceptible 293 cells.
Human CellExp? Human CD40/ TNFRSF5, Human recombinant |
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| 9230-10 | Biovision | each | 333.6 EUR |
Human CellExp? Human CD40/ TNFRSF5, Human recombinant |
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| 9230-50 | Biovision | each | 868.8 EUR |
Humanin (human) |
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| 5-01353 | CHI Scientific | 4 x 1mg | Ask for price |
Humanin (human) |
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| H-5574.0500 | Bachem | 0.5mg | 312 EUR |
Humanin (human) |
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| H-5574.1000 | Bachem | 1.0mg | 507.6 EUR |
Human CellExp? SHH, human recombinant |
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| 7223-10 | Biovision | each | 255.6 EUR |
Human CellExp? EGF, human recombinant |
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| 7228-10 | Biovision | each | 352.8 EUR |
Human CellExp? UPA, human recombinant |
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| 7248-10 | Biovision | each | 398.4 EUR |
Human CellExp? UPA, human recombinant |
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| 7248-50 | Biovision | each | 1324.8 EUR |
Human CellExp? LIF, human recombinant |
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| 7267-10 | Biovision | each | 464.4 EUR |
Human CellExp?CD4, human recombinant |
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| 7834-100 | Biovision | each | 861.6 EUR |
Human CellExp?CD4, human recombinant |
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| 7834-20 | Biovision | each | 320.4 EUR |
Human CellExp? EPO, Human Recombinant |
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| 6447-10 | Biovision | each | 646.8 EUR |
Human CellExp? EPO, Human Recombinant |
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| 6447-50 | Biovision | each | 2017.2 EUR |
Human CellExp? HGF, Human Recombinant |
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| 6456-10 | Biovision | each | 464.4 EUR |
Human CellExp? HGF, Human Recombinant |
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| 6456-50 | Biovision | each | 1677.6 EUR |
Human CellExp? HGH, Human Recombinant |
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| 6457-10 | Biovision | each | 405.6 EUR |
Human CellExp? HGH, Human Recombinant |
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| 6457-50 | Biovision | each | 1455.6 EUR |
Human CellExp? SCF, Human Recombinant |
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| 6478-10 | Biovision | each | 411.6 EUR |
Human CellExp? SCF, Human Recombinant |
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| 6478-50 | Biovision | each | 1599.6 EUR |
Human CellExp? TPO, Human Recombinant |
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| 6483-10 | Biovision | each | 438 EUR |
Human CellExp? TPO, Human Recombinant |
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| 6483-50 | Biovision | each | 2376 EUR |
Human CellExp? NOV, human recombinant |
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| P1022-10 | Biovision | each | 235.2 EUR |
Human CellExp? NOV, human recombinant |
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| P1022-25 | Biovision | each | 352.8 EUR |
Nuclear genome of Bulinus truncatus, an intermediate host of the carcinogenic human blood fluke Schistosoma haematobium
Some snails act as intermediate hosts (vectors) for parasitic flatworms (flukes) that cause neglected tropical diseases, such as schistosomiases. Schistosoma haematobium is a blood fluke that causes urogenital schistosomiasis and induces bladder cancer and increased risk of HIV infection. Understanding the molecular biology of the snail and its relationship with the parasite could guide development of an intervention approach that interrupts transmission. Here, we define the genome for a key intermediate host of S. haematobium-called Bulinus truncatus-and explore protein groups inferred to play an integral role in the snail’s biology and its relationship with the schistosome parasite. Bu. truncatus shared many orthologous protein groups with Biomphalaria glabrata-the key snail vector for S. mansoni which causes hepatointestinal schistosomiasis in people.
Conspicuous were expansions in signalling and membrane trafficking proteins, peptidases and their inhibitors as well as gene families linked to immune response regulation, such as a large repertoire of lectin-like molecules. This work provides a sound basis for further studies of snail-parasite interactions in the search for targets to block schistosomiasis transmission.
