Viral peptide–Human Leukocyte Antigen class I complex (Adenovirus, Cytomegalovirus, Epstein–Barr virus) (pHLA-I (AdV/CMV/EBV))

Viral peptide–Human Leukocyte Antigen (HLA) class I complexes are molecular assemblies found on the surface of cells infected with viruses such as Adenovirus, Cytomegalovirus (CMV), and Epstein–Barr virus (EBV) (NCBI, 2023). These complexes consist of a viral protein fragment (peptide) nested within the binding groove of an HLA class I molecule, which is then presented to the immune system (UniProt, 2024). Their primary biological function is to act as a signal for CD8+ cytotoxic T lymphocytes, which recognize the specific peptide-HLA combination via their T-cell receptors (TCRs) to initiate cell death (PubMed, 2021). In clinical settings, particularly in hematopoietic stem cell or solid organ transplant recipients, these complexes are the primary targets for adoptive T-cell therapies (Nature Reviews Immunology, 2022). Drugs like Tabelecleucel (Ebvallo) and Posoleucel (ALVR105) utilize virus-specific T-cells to target these complexes, providing a mechanism to control viral reactivation and associated diseases like post-transplant lymphoproliferative disorder (EMA, 2022; AlloVir, 2023). The specificity of this interaction is determined by both the viral peptide sequence and the host's HLA allele, necessitating HLA matching for therapeutic efficacy (PubMed, 2020). Therapeutic challenges include viral strategies to down-regulate HLA expression and the potential for off-target cross-reactivity with self-peptides (Frontiers in Immunology, 2021). Monitoring viral DNA load and using peptide-HLA multimers are common methods to assess the presence of these targets and the efficacy of the corresponding therapies (Journal of Clinical Investigation, 2019).

Other names

Viral peptide-MHC class I complexpMHC-I complexHLA-restricted viral antigensVirus-specific peptide-HLA complexes

Adoptive transfer of T-cells that recognize viral peptides presented by HLA class I molecules, leading to the activation of cytotoxic pathways (e.g., perforin/granzyme) and lysis of infected cells (Nature Reviews Immunology, 2022).