Anti-LCMV nucleoprotein – Purified <i>in vivo</i> PLATINUM™ Functional Grade (L331-GRP)

Lymphocytic choriomeningitis virus (LCMV) is a neglected human pathogenic arenavirus with worldwide distribution 1,2. Arenaviruses cause human infection through mucosal exposure to aerosols or by direct contact with abraded skin of infected rodents 1. LCMV infection may carry health risks for humans who are immunocompromised or pregnant 2. LCMV infection in mice can be acute or persistent depending on age, immunocompetence, genetic background, route of infection, strain, and dosage 1. Due to the versatility of outcome, LCMV mouse models are extensively used to examine basic questions of immunology and virology, including: virus-induced immunopathological disease, MHC restriction, T cell and B cell regulation, T cell-mediated killing, and immune T cell therapy in clearing viral infection 1,2. LCMV mouse models were used to identify PD-1 as a critical regulator of T cell exhaustion 2 and have also been used to study the synergy between PD-1 blockade and IL-2 cytokine in cancer immunotherapy 3. LCMV is an enveloped virus with a bi-segmented negative-stranded, ambisense RNA genome 1,2. LCMV has a non-cytolytic life cycle restricted to the cell cytoplasm. Cell entry is cholesterol-dependent but clathrin-, dynamin-, caveolin-, ARF6-, flotillin-, and actin-independent and occurs via receptor-mediated endocytosis utilizing alpha-dystroglycan as the main extracellular matrix protein receptor 1. Most of the disease caused by LCMV is mediated by the host T cell response 2. Arenavirus nucleoprotein (NP) is the most abundant viral protein component in virions as well as in infected cells 4. NP encapsidates the viral genomic RNA and is part of the viral ribonucleoprotein complex that directs viral RNA replication and gene transcription in the cytoplasm of infected cells. NP also counteracts host type I interferon response during infection via a functional 3’–5’ exonuclease domain in its C-terminal region 5,6. The same domain also interacts with LCMV Z, as well as Lassa Virus Z, but different residues are involved 4. This NP-Z interaction is a novel target for antiviral drug development. VL-4 antibody was generated by immunizing a (Louvain X DA) F1 rat with LCMV strain WE and fusing the resulting spleen cells with the YM3 myeloma cell line 7.