Our results raise the question whether the impact of HBV coinfection on T-cell clonality is to alter the nature or magnitude of specific T-cell populations, for example, by stimulating T-cell proliferation, expression of CD25 (interleukin 2 receptor alpha chain [13]), or the frequency of CD4+FoxP3+ regulatory T cells [14]. The gene discussed is FOXP3; the disease is coinfection.