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In individuals with ME/CFS, ancestral HLA-II haplotypes, and latent EBV, these immunological alterations can be explained by the EBV-acquired immunodeficiency model, where the impairment of CD4 T-cell function and activation caused by these ancestral HLA-II haplotypes could generate T-cell depletion and thus an increase in EBV-infected ectopic lymphoid structures [8, 171]
The remaining four strains were excluded for the following reasons: (1) KCCM 12485 ( S
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