Pseudotyped Luciferase Lentivirus (COV-PSL1)

Product Overview
The Pseudotyped Luciferase Lentivirus was produced without envelope glycoproteins such as VSV-G or SARS-CoV-2 spike. It contains the eLuciferase gene driven by a CMV promoter as the reporter. The Pseudotyped Luciferase Lentivirus can serve as a negative control when studying virus entry initiated by specific interactions between virus particles and receptors.
Nature
Virus
Bio-activity
Since the virus is lacking the envelope glycoproteins and cannot be transfected to target cells, functional titer of this product cannot be determined. Based on p24 values, the approximate lentiviral particles (LP) of this product is ~ 10E+09 LP/ml.
Application Notes
Ideal as a negative control pseudovirus particles for the Pseudotyped Luciferase rSARS-CoV-2 Spike, CD Cat# COV-PS01 or other pseudovirus particles used to study the mechanism of viral transduction.
Size
1 mL
Buffer
The lentiviruses were produced from HEK293T cells in medium containing 90% DMEM + 10% FBS.
Storage
Store at -80°C. Multiple freeze/thaw cycles not recommended.
When using the virus, transfer the virus from the -80 ° C refrigerator and melt it in an ice bath.
Ship
Frozen on dry ice
Warnings
None of the HIV genes (gag, pol, rev) will be expressed in the transduced cells, as they are expressed from packaging plasmids lacking the packing signal. Although the pseudotyped lentiviruses are replication-incompetent, they require the use of a Biosafety Level 2 facility. It is the responsibility of the principal investigator to seek Institutional Biosafety Safety Committee approval for recombinant DNA, transgenic animal or infectious agent use within their laboratory spaces and maintain an Institutional Biosafety Safety Committee approval during the time period these materials are used.

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References


Air pollution in Ontario, Canada during the COVID-19 State of Emergency

SCIENCE OF THE TOTAL ENVIRONMENT

Authors: Adams, Matthew D.

In March of 2020, the province of Ontario declared a State of Emergency (SOE) to reduce the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes the coronavirus disease (COVID-19). This disruption to the economy provided an opportunity to measure change in air pollution when the population spends more time at home with fewer trips. Hourly air pollution observations were obtained for fine particulate matter, nitrogen dioxide, nitrogen oxides and ozone from the Ontario air monitoring network for 2020 and the previous five years. The analysis is focused on a five-week period during the SOE with a previous five-week period used as a control. Fine particulate matter did not show any significant reductions during the SOE. Ozone concentrations at 12 of the 32 monitors were lower than any of the previous five-years; however, four locations were above average. Average ozone concentrations were 1 ppb lower during the SOE, but this ranged at individual monitors from 15 ppb above to 42 ppb below long-term conditions. Nitrogen dioxide and nitrogen oxides demonstrated a reduction across Ontario, and both pollutants displayed their lowest concentrations for 22 of 29 monitors. Individual monitors ranged from 1 ppb (nitrogen dioxide) and 5 ppb (nitrogen oxides) above average to 4.5 (nitrogen dioxide) and 7.1 ppb (nitrogen oxides) below average. Overall, both nitrogen dioxide and nitrogen oxides demonstrated a reduction across Ontario in response to the COVID-19 SOE, ozone concentrations suggested a possible reduction, and fine particulate matter has not varied from historic concentrations. (C) 2020 Elsevier B.V. All rights reserved.

Unravelling host-pathogen interactions: ceRNA network in SARS-CoV-2 infection (COVID-19)

GENE

Authors: Arora, Shweta; Singh, Prithvi; Dohare, Ravins; Jha, Rishabh; Syed, Mansoor Ali

COVID-19 is a lurking calamitous disease caused by an unusual virus, SARS-CoV-2, causing massive deaths worldwide. Nonetheless, explicit therapeutic drugs or clinically approved vaccines are not available for COVID-19. Thus, a comprehensive research is crucially needed to decode the pathogenic tools, plausible drug targets, committed to the development of efficient therapy. Host-pathogen interactions via host cellular components is an emerging field of research in this respect. miRNAs have been established as vital players in host-virus interactions. Moreover, viruses have the capability to manoeuvre the host miRNA networks according to their own obligations. Besides protein coding mRNAs, noncoding RNAs might also be targeted in infected cells and viruses can exploit the host miRNA network via ceRNA effect. We have predicted a ceRNA network involving one miRNA (miR-124-3p), one mRNA (Ddx58), one lncRNA (Gm26917) and two circRNAs (Ppp1r10, C330019G07RiK) in SARS-CoV infected cells. We have identified 4 DEGs-Isg15, Ddx58, Oasl1, Usp18 by analyzing a mRNA GEO dataset. There is no notable induction of IFNs and IFN-induced ACE2, significant receptor responsible for S-protein binding mediated viral entry. Pathway enrichment and GO analysis conceded the enrichment of pathways associated with interferon signalling and antiviral-mechanism by IFN-stimulated genes. Further, we have identified 3 noncoding RNAs, playing as potential ceRNAs to the genes associated with immune mechanisms. This integrative analysis has identified noncoding RNAs and their plausible targets, which could effectively enhance the understanding of molecular mechanisms associated with viral infection. However, validation of these targets is further corroborated to determine their therapeutic efficacy.

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