**Acknowledgements**

CD317), acts in late steps of viral replication cycle, by preventing viruses from leaving the cell during budding and release of viral particles. The recently described factors MxB and choles‐ terol 25-hydroxylase seem to inhibit the nuclear import/integration of viral DNA and the viral fusion events, respectively. Remarkably, despite this array of restriction factors, HIV had created viral proteins to subdue these restrictions emphasizing how well adapted this virus is

88 Trends in Basic and Therapeutic Options in HIV Infection - Towards a Functional Cure

**Figure 3. Schematic representation of a simplified replication cycle of HIV and the different steps that are blocked by cellular restriction factors**. The cholesterol-25-hydroxylase blocks viral fusion with target cell membrane; TRIM5α, SAMHD1 and APOBEC3G impair viral DNA synthesis either by accelerating capsid disintegration, reducing dNTPs

to human host.

This work was supported by grants from Fundação para a Ciência e Tecnologia and Ministério da Saúde de Portugal (VIH/SAU/0006/2011) and from Gilead Sciences Portugal (Programa Gilead Génese).
