Major Histocompatibility Complex class I and class II molecules presenting FLU-v peptides (MHC-FLU-v)

Major Histocompatibility Complex (MHC) class I and class II molecules presenting FLU-v peptides represent the functional immunological target of the universal influenza vaccine candidate, FLU-v. This target consists of MHC molecules on antigen-presenting cells (APCs) that have loaded four specific, highly conserved peptides derived from internal influenza virus proteins: nucleoprotein (NP), matrix proteins (M1 and M2), and polymerase acidic protein (PA) (Stoloff et al., 2016). Unlike traditional influenza vaccines that target the highly variable surface proteins hemagglutinin and neuraminidase, this target focuses on conserved epitopes to provide broad-spectrum protection against multiple influenza A and B strains, including those with pandemic potential (Pagnon et al., 2019). The interaction between these MHC-peptide complexes and T-cell receptors (TCRs) triggers a robust cellular immune response, characterized by the activation of CD8+ cytotoxic T cells and CD4+ helper T cells. Clinical trials have shown that targeting this complex leads to increased production of interferon-gamma and granzyme B, which are associated with reduced viral shedding and symptom severity (Imutex Ltd., 2024). This approach aims to provide long-lasting, "universal" immunity that does not require annual reformulation based on circulating strains.

Other names

HLA-FLU-v complexMHC-peptide complex (FLU-v)Human Leukocyte Antigen presenting FLU-v peptidesMHC-I/II FLU-v peptide complex

The FLU-v vaccine delivers four synthetic peptides derived from conserved internal influenza proteins (M1, M2, NP, and PA). These peptides are processed and presented by MHC class I and class II molecules on the surface of antigen-presenting cells. This presentation triggers the activation of CD8+ cytotoxic T cells and CD4+ helper T cells, which recognize and eliminate influenza-infected cells across various viral strains (Pagnon et al., 2019; Stoloff et al., 2016).