Inactivated Influenza A H1N1 (Brisbane/2/18)

Name: Inactivated Influenza A H1N1 (Brisbane/2/18)
SKU: VNV-106

Cat.No. : VNV-106

Storage: -80°C Shipping: Dry ice

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Product Infomation

Cat. No.	VNV-106
Description	Wild type influenza A H1N1 (Brisbane/2/18) particles which are inactivated by heat treatment. This product is intended for research use only.
Shipping	Dry ice
Storage	-80°C

Creative Biogene ensures high-quality lentivirus particles by optimizing and standardizing production protocols and performing stringent quality control (QC). The specific QC experiments performed vary between lentivirus particle lots.
Mycoplasma	Creative Biogene routinely tests for mycoplasma contamination using a mycoplasma detection kit. Cell lines are maintained for approximately 20 passages before being discarded and replaced with a new vial of early passage cells. Approximately 2 weeks after thawing, cell culture supernatants are tested for mycoplasma contamination. Creative Biogene ensures that lentiviral products are free of mycoplasma contamination.
Purity	Creative Biogene evaluates the level of impurities, such as residual host cell DNA or proteins, in prepared lentiviral vectors to ensure they meet quality standards.
Sterility	The lentiviral samples were inoculated into cell culture medium for about 5 days and the growth of bacteria and fungi was tested. Creative Biogene ensures that the lentiviral products are free of microbial contamination.
Transducibility	Upon requirement, Creative Biogene can perform in vitro or in vivo transduction assays to evaluate the ability of lentivirus to deliver genetic material into target cells, and assess gene expression and functional activities.
Proviral Identity Confirmation	All Creative Biogene lentiviral vectors are confirmed to have correctly integrated provirus using PCR. This test involves transducing cells with serial dilutions of the lentiviral vector, harvesting the cells a few days later, and isolating genomic DNA. This DNA is then used as a template to amplify a portion of the expected lentiviral insert.

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Influenza A(H1N1) virus (Brisbane/2/2018) is a seasonal influenza virus strain primarily transmitted through respiratory droplets produced when an infected person coughs, sneezes, or talks. It can also spread through direct contact with contaminated surfaces and subsequent mucosal self-inoculation. The virus is highly transmissible between humans, especially in crowded settings, which can lead to seasonal epidemics. After inhalation, the virus attacks epithelial cells lining the upper and lower respiratory tract and binds to sialic acid receptors (α-2,6-linked receptors in humans) through its hemagglutinin (HA) protein. Viral replication triggers rapid cell death and the release of proinflammatory cytokines, leading to symptoms such as fever, cough, sore throat, and myalgias. Severe cases may develop viral pneumonia or secondary bacterial infections, particularly in high-risk populations such as the elderly and immunocompromised individuals. The Brisbane/2/2018 strain is a descendant of the 2009 pandemic H1N1 lineage. It has retained adaptive mutations that enhance its adaptability in the human population while maintaining antigenic drift to evade pre-existing immunity.

The influenza A (H1N1) virus (Brisbane/2/2018) has a typical influenza A virus structure, consisting of a lipid envelope studded with the glycoproteins hemagglutinin (HA) and neuraminidase (NA), enclosing a segmented, single-stranded, negative-sense RNA genome. The HA protein facilitates host cell entry by mediating receptor binding and membrane fusion, while the NA protein cleaves sialic acid to release progeny viruses. Compared to earlier H1N1 strains, the Brisbane/2/2018 strain''s hemagglutinin (HA) exhibits antigenic changes (e.g., the Sa and Sb antigenic sites), which alter its immunogenicity. The viral genome consists of eight segments, encoding at least 11 proteins, including polymerase subunits (PA, PB1, PB2), nucleoprotein (NP), matrix proteins (M1, M2), and non-structural proteins (NS1, NS2). Segment reassortment and point mutations lead to genetic variation, thus enabling immune evasion

Infection with influenza A (H1N1) virus is a significant contributor to the global burden of acute respiratory diseases. Changes in glucose uptake and metabolism in different cell types have been reported following infection with different types of viruses, including influenza A virus. Alterations in glucose metabolism in immune cells can have significant health consequences. This study was designed to monitor glucose concentrations in U937 human monocytes stimulated and unstimulated with infectious or heat-inactivated H1N1 or Staphylococcus aureus, or stimulated with phorbol-12-myristate-13-acetate. Stimulated or unstimulated U937 human monocytes were infected with H1N1 at different time points, and glucose profiles in the growth medium were measured after infection. Results showed that challenge infection with H1N1 resulted in a significant decrease in blood glucose levels 36 h after infection, regardless of whether the initial stimulus to U937 cells came from a pathogen or a nonpathogen. In summary, H1N1 infection directly affects glucose uptake in U937 cells in vitro. This effect may be related to H1N1 infection or to the differentiated state of cells resulting from the applied stimulus.

U937 cells were induced with infectious or heat-inactivated H1N1 or S. aureus at a multiplicity of infection (MOI) of 0.1. Control cells were untreated. After 24 hours, stimulated and unstimulated cells were exposed to live H1N1 virus at a multiplicity of infection (MOI) of 0.1 for 12, 24, and 36 hours. Cell supernatants were harvested at each time point from uninfected unstimulated cells (NI), H1N1 infected unstimulated cells (VL), H1N1 infected previously infectious H1N1 stimulated cells (LV VI), H1N1 infected previously heat-inactivated H1N1 stimulated cells (KV VI), H1N1 infected previously infectious S. auerus stimulated cells (LB VI), H1N1 infected previously heat-inactivated S. auerus stimulated cells (KB VI), H1N1 infected previously HS stimulated cells (HS VI), H1N1 infected previously PMA stimulated cells (PMA VI), and H1N1 infected previously HS and PMA stimulated cells (HS PMA VI). Medium control (M Cont 0 h) was collected after culturing U937 cells for 0 h. Initially stimulated U937 cells with LV (A), KV (B), LB (C), or KB (D) all at MOI = 0.1 showed a significant decrease in glucose levels at 36 h PII compared with the M Cont 0 h and stimulated U937 control cells after 36 h (Figure 1).

Figure 1. Glucose profile in medium of U937 cells challenged with live or inactivated H1N1 or S. aureus then actively infected by H1N1. (Motawi T K, et al., 2020)

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