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. 2016 Mar 3;8(3):67. doi: 10.3390/v8030067

Figure 5.

Figure 5

Remodeling of the plasma membrane by HIV-1 Nef and Vpu modulates immunometabolism and adaptive immunity. HIV-1 Nef and Vpu proteins work in concert to alter the expression of factors important for adaptive immune responses and optimal immunometabolic function, contributing to viral persistence during the later stages of HIV-1 acute infection. Downregulation of MHC-I on infected cells by Nef prevents their recognition and clearance by cytotoxic T lymphocyte (CTLs). Decreased surface expression of MHC-II on infected antigen-presenting cells (APCs) by Nef prevents optimal initiation of adaptive immune responses. Downregulation of both CD4 and BST2 by Nef and Vpu prevents the accumulation of CD4-induced (CD4i) gp120 epitopes at the cell surface, and therefore hampers anti-HIV antibody-dependent cell-mediated cytotoxicity (ADCC) responses. Reduction of sodium-coupled neutral amino acid transporter (SNAT)1 surface expression by Vpu reduces the intracellular alanine pool in infected CD4+ T cells, resulting in their decreased mitogenic capacity in response to TCR-activating stimuli. Downregulation of CD62L and CCR7 on infected cells may inhibit their trafficking to lymphoid structures, further decreasing the initiation of anti-HIV adaptive responses.