**1. Introduction**

Human immunodeficiency viruses 1 and 2 (HIV-1 and HIV-2) infection leads to immunological failure and Acquired Immunodeficiency Syndrome (AIDS). During transmission and dissem‐ ination within a new host, HIV must overcome several cellular mechanisms aiming to inhibit or restrict its infection and its spread to other host cells. Not surprisingly, as a well-adapted human pathogen, HIV has evolved in order to counteract and subvert these cellular inhibitory factors. Defining how viral and cellular proteins interact remains a critical area of research with direct implications in the knowledge of transmission, pathogenic mechanisms, vaccine design and molecular targets for therapeutic intervention.

In this chapter, the mechanisms involved in the inhibitory activity of some cellular proteins and the way HIV evades those host cell restrictions will be focused on. Particular attention will be given to the tripartite motif 5 (TRIM5) protein family, involved in viral uncoating; the retroviral protection factors, apolipoprotein B mRNA-editing enzyme catalytic polypeptidelike (APOBEC) and Tetherin, involved in the reverse transcription and viral release respec‐ tively; and to the sterile alpha motif [SAM] and histidine/aspartic acid [HD] domain-containing protein 1 (SAMHD1), which mediates the restriction of HIV-1 replication in dendritic cells. This review will also delve into the mechanisms of two recently described factors: MxB, which restricts HIV nuclear import and integration, and cholesterol-25-hydroxylase that converts cholesterol to a soluble antiviral factor (25-hydroxycholesterol) that blocks HIV fusion with target cells.

© 2015 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
