- Marburg and Ebola pseudovirus transduction of target cells for viral entry and functional studies
- Rapid Anti-Marburg and Anti-Ebola drug screening
- Rapid Anti-Marburg and Anti-Ebola neutralizing antibody screening
A novel rapid hybrid alpha-pseudovirus for Marburg (MARV) and Ebolaviruses (EBOV) that are available for your initial testing. These pseudoviruses are BSL-2 safe and ready to use for studying viral entry. HA-MARV and HA-EBOV particles are pseudoviruses assembled from the structural proteins of the filovirus glycoprotein (GP), VP40 matrix protein, and the Nucleoprotein (NP) and package an alphaviral vector for reporter gene expression. The alpha-pseudoviruses are single-cycle viruses with self-replicating RNA for rapid quantification of neutralizing antibodies and entry-inhibiting drugs. Additionally, we help our customers to assemble HA-MARV and HA-EBOV pseudoviruses at any scale.
Additionally, we help our customers to assemble custom Marburg virus (MARV) and Ebolavirus (EBOV) pseudoviruses. These particles carry reporters that can be used for antiviral drug screening or the quantification of neutralizing antibodies or entry inhibitors. Please contact us by email: firstname.lastname@example.org
To enhance your pseudovirus entry, ask about receiving a free sample of our propriety InfectinTM which can significantly promote productive viral infection in a variety of host cells, enhancing viral infection rates by 3 to 20-fold.
Ebolavirus is the causative agent of ebolavirus disease (EDV) characterized by severe hemorrhagic fever. EVD is a disease of human and non-human primates that is characterized by a high fatality rate (30–90%). Ebolavirus is an enveloped, negative-stranded RNA virus characterized by a viron of ≈80 nm in diameter and a length ranging from hundreds of nanometers to micrometers. The genome encodes for seven structural proteins: the nucleoprotein (N), the virion protein (VP) 24, VP35, VP30, VP40, the glycoprotein (GP), and the RNA-dependent RNA polymerase (L). The virus enters the cell by fusion following the attachment of the viral Glycoprotein (GP) to the cell surface receptor Tim-1 and NPC1. This mechanism of entry allows for a broad host cell range.