Bunyaviruses include Crimean-Congo Hemorrhagic Fever (CCHF) and Rift Valley Fever (RVF) viruses. Crimean-Congo Hemorrhagic Fever virus (CCHF) Glycoprotein pseudotyped lentiviruses based on NCBI reference sequence NC_005300.2. Rift Valley Fever virus (RFV) Glycoprotein pseudotyped lentiviruses based on NCBI reference sequence KX632067.1.
- CCHF and RVF pseudovirus transduction of target cells for viral entry and functional studies
- Anti-CCHF and Anti-RVF drug screening
- Anti-CCHF and Anti-RVF neutralizing antibody screening
We have developed several pre-assembled Crimean-Congo Hemorrhagic Fever (CCHF) and Rift Valley Fever (RVF) glycoprotein pseudotyped lentiviral particles that are available for your initial testing. These pseudoviruses are BSL-2 safe and ready to use for studying viral entry. Additionally, we help our customers to assemble custom CCHF and RVF glycoprotein pseudotyped lentiviruses at any scale. These particles carry reporters that can be used for antiviral drug screening or the quantification of neutralizing antibodies. Customers can provide us with the reporter construct of their choice, and we will assemble particles within a week. Please contact us by email: firstname.lastname@example.org
To enhance your pseudovirus entry, ask about receiving a free sample of our propriety Infectin that can significantly promote productive viral infection in a variety of host cells, enhancing viral infection rates by 3 to 20-fold.
Bunyaviruses are single-stranded negative-sense RNA viruses with 3-segmented genomes: small (S), medium (M), and large (L). The 3-segmented genomes encode viral nucleocapsid protein (NP) involved in transcription and replication, glycoprotein precursor generating two structural membrane proteins (Gc and Gn) and nonstructural proteins (GP38 and NSm), and RNA-dependent RNA polymerase (RdRp) proteins, respectively. Bunyaviruses enter the host cell via receptor-mediated endocytosis through the surface glycoprotein Gc, which is responsible for binding to the cellular receptors. Upon attachment, Gc responds to the reduced pH of endocytic compartments with a conformational change that results in a fusion loop, allowing it to insert into the endosomal membrane. Gc then folds back on itself, forcing the cell membrane (held by the fusion loop) and the viral membrane (held by a trans-membrane anchor) against each other, resulting in fusion and releasing the viral genome into the cytoplasm. Some of the receptors facilitating the viral entry that have been described include clathrin-dependent endocytosis, 3 integrins, nucleolin, and DC-SIGN (a C-type lectin restricted to interstitial dendric cells and certain tissue macrophages).
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