Therefore, we propose that latency and recurrent EBV reactivation could generate an acquired immunodeficiency syndrome in three steps: first, an acquired EBV immunodeficiency develops in individuals with weak EBV HLA-II haplotypes, which prevents the control of latency I cells
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However, very large VLDL particles cannot be secreted if their diameter exceeds that of the sinusoidal endothelial pores, and this limitation may ultimately result in lipid retention and NAFLD [120]
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