[1] In 2010 the World Health Organization Naming Committee for Factors of the HLA System revised the nomenclature for HLAs.

[3] Serotyping can identify as far as HLA-A*02, which is typically enough to prevent transplant rejection (the original motivation for HLA identification).

In essence, there are indicators, albeit from a small study comparing HLA expression in fertile and infertile couples, that HLA-A*02 may induce increased maternal immune response to the fetus.

HLA-A*02 appears to stimulate peripheral blood mononuclear cells in a manner that inhibits HIV replication.

HIV produces a protein called Nef that binds to the cytoplasmic tail of HLA-A and B and diverts it to the lysosomes for destruction.

[8] In addition, there are several HLA-A*02 haplotypes that appear to contribute heavily to higher or lower viral loads in HIV patients.

HLA-A*02 has been linked with decreased risk of developing Epstein-Barr virus (EBV)-positive Hodgkin lymphoma(HL).

[10] This high affinity increases the probability of CD8+ t-cell recognition of EBV peptides held by HLA-A*02 complexes.

This, in turn, enhances the immune system's ability to control and clear the EBV, which decreases the change of developing Hodgkin Lymphoma as a result of the infection.