The peptide GLCTLVAML is a linear peptidic epitope (epitope ID 20788) studied as part of the protein „mRNA export factor ICP27 homolog“ (UniProt:Q04360) from Epstein Barr virus (Human herpesvirus 4). The open reading frame „BMLF1“ is coding for this early protein of Epstein Barr virus' lytic cycle.

The Epstein Barr virus can cause infectious mononucleosis and in affected patients, CD8+ cytotoxic T lymphocytes react to antigens of the lytic cycle such as BMLF1. In ex vivo assays, the response to BMLF1-280-288 (HLA-A*02:01) in the primary cytotoxic T lymphocyte population was as strong as to the B7-restricted EBNA3A 379-387 epitope, an immunodominant peptide of latent EBV infection. [1]

In recent work, EBV BMLF-1 280–288 (GLCTLVAML) was used, for example, to generate recombinant HLA monomers. [2] To do this, scientists let Escherichia coli form recombinant HLA‐A*02:01, ‐A*24:02, and ‐B*07:02 heavy chains. They then generated peptide‐HLA class I complexes through in vitro refolding reactions with E. coli‐derived β2M in the presence of the EBV peptide GLCTLVAML and the RSV peptide NPKASLLSL. The scientists biotinylated the peptide-HLA class I complexes, purified them by gel filtration high performance liquid chromatography, and stored them at −70 °C.

Using BMLF-1 280–288 (GLCTLVAML), scientists also investigated the extent to which the novel peptide alarm therapy (PAT) can be applied to the aggressive, treatment-resistant glioblastoma multiforme. [3] Peptide alarm therapy is based on activating virus-specific memory T cells that are common in tumors. These tissue-resident memory T cells (TRM) patrol the tissue and are capable of rapid and effective immune activation upon re-exposure to antigens.

To determine whether virus-specific CD8 + T cells are present in human glioblastomas, the scientists used the following immunodominant peptides from common viral infections: GLCTLVAML and CLGGLLTMV from the Epstein-Barr virus, NLVPMVATV from the cytomegalovirus, and GILGFVFTL from the influenza A virus. They were able to detect virus-specific CD8+ T cells in human glioblastomas that express markers for tissue residency. Furthermore, they could reactivate virus-specific memory CD8+ T cells in a murine glioblastoma model by intratumoral delivery of adjuvant-free virus-derived peptides.

The literature references can be found under the "References" tab above.