Cat.No. : VNV-122
Storage: -80°C Shipping: Dry ice
| Cat. No. | VNV-122 |
| Description | Wild type mpox virus (strain: USA/MA001/2022) 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. |
Monkeypox is a viral zoonosis caused by monkeypox virus (MPXV). During MPXV infection, macrophages are recruited to the site of infection and are thought to be involved in the spread of the virus. Vertical transmission of MPXV from infected pregnant women to the developing fetus in utero has been reported, resulting in high viral loads in placental tissues and miscarriage. Here, researchers aimed to understand the impact of MPXV infection on the maternal-fetal interface by studying the function of macrophages. Using a term placental explant model, macrophages were recruited to the site of infection. Isolated naive macrophages were susceptible to MPXV infection and secreted high levels of proinflammatory cytokines with a strong M1 polarization signature. Antiviral gene expression analysis revealed that interferon (IFN) and IFN-related genes were upregulated, suggesting that MPXV induced the expression of certain antiviral response components by macrophages that were unable to clear the virus. These studies suggest that macrophages are tolerant to MPXV and are able to subvert inflammatory and antiviral mechanisms without clearing the virus. These findings contribute to a better understanding of the pathogenic mechanisms of vertical transmission of MPXV.
Researchers investigated whether infection of macrophages was associated with an antiviral response to MPXV by assessing the expression of several antiviral effectors and type I interferon genes. The response of macrophages to MPXV infection was distinct from that of cells incubated in vitro with heat-inactivated MPXV or incubated under resting conditions (Figure 1A). Principal component analysis and hierarchical clustering revealed that the response of macrophages to MPXV infection was also distinct from that of MPXV-infected MDM, suggesting specific regulation of antiviral response components in placental cell populations (Figure 1B). Expression of IFNA transcripts was increased in macrophages following MPXV stimulation, whereas IFNB and IFNB1 were not modulated (Figure 1C). Interestingly, heat-inactivated MPXV significantly modulated the expression of IFNB and IFNB1 in macrophages, but the amount of regulation was very small compared to that of IFNA. In macrophages, expression of IFIT1 (p = 0.0147), IFIT2 (p = 0.0118), IFIT3 (p = 0.0135), and IFIH1 (p = 0.0001) transcripts was induced in response to MPXV (Figure 1D). No differences were observed in MDMs. In contrast, virus-induced antiviral responses and type I interferon genes were modulated in infected monocytes. These results suggest that macrophages specifically respond to MPXV infection by modulating certain components of the antiviral response compared to MDMs.
Figure 1. Macrophages present an antiviral reply against MPXV infection. (Andrieu J, et al., 2025)
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This Inactivated Wild-Type Mpox Virus (USA/MA001/2022) provided exceptional performance in PCR controls and serological testing. The viral genome integrity remained intact post-inactivation, allowing accurate quantification in our outbreak surveillance studies. Shipping documentation met all regulatory requirements flawlessly.
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