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. 2018 Jun 12;9:1336. doi: 10.3389/fimmu.2018.01336

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Copyright © 2018 Temerozo, de Azevedo, Insuela, Vieira, Ferreira, Carvalho, Bello and Bou-Habib.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed model of the role of protein kinases A (PKA) and C (PKC) in the vasoactive intestinal peptide (VIP)/pituitary adenylate cyclase-activating polypeptide (PACAP)-mediated inhibition of HIV-1 replication in macrophages. The interaction of VIP and PACAP with their specific receptors in HIV-1-infected macrophages activates PKA (via induction of cAMP) and PKC, leading to inhibition of NF-kB activation and Cyclin D1 synthesis induced by HIV-1 infection, and to reduction of HIV-1 production. Also, PKA and PKC activation can trigger the phosphorylation of cAMP response element-binding protein (CREB) and the macrophage production of β-chemokines and IL-10, which diminish HIV-1 replication (27). In addition, PACAP introduces mutations on HIV-1 provirus that result in a reduction of HIV-1 replication fitness (the color green in the DNA represents the integrated HIV-1 provirus).