**Author details**

patients may

individuals (**Figure 3**).

**3. Conclusions**

356 Endothelial Dysfunction - Old Concepts and New Challenges

Interestingly, HIV<sup>+</sup>

**Figure 3.** Endothelial dysfunction in HIV<sup>+</sup>

multiple trigger factors.

As described in the present chapter, endothelial dysfunction occurring in HIV<sup>+</sup>

morphology of ECs by altering their homeostasis and function.

disposed to endothelial dysfunction is a common feature in HIV<sup>+</sup>

be considered as a multifactorial pathology in which the HIV-1 virus itself and, most of all, its structural and regulatory proteins are able to induce strong changes in the physiology and

the presence of suppressive cART [69, 70], although low-level transcription of HIV-1 genes continues even after years of cART [71, 72]. Many studies demonstrated the persistence of HIV-1-encoded proteins in different tissues and organs also during pharmacological control of infection. Since these proteins are able to induce a direct endothelial damage and to develop an inflammatory microenvironment, it is possible to hypothesize that viral proteins are among the most important factors involved in endothelial dysfunction development. Although animal models have limitations and can never completely mimic HIV-1 infection of humans or the physiological relevance of a single protein product in the human microenvironment, they start to provide proof of concept for a general vascular dysregulation operated by HIV-1 and its products. Altogether, these data show that a microenvironment

Recognizing the interaction of some HIV-1 protein products with their receptors as the key events in sustaining endothelial aberrant functioning could help us to identify new thera-

peutic strategies in combating and/or preventing HIV-1-related vascular disease.

patients have a high risk of endothelial dysfunction in the absence and in

patients under combination antiretroviral therapy (cART) occurs following

Pietro Mazzuca, Arnaldo Caruso and Francesca Caccuri\*

\*Address all correspondence to: francesca.caccuri@unibs.it

Department of Molecular and Translational Medicine, University of Brescia Medical School, Brescia, Italy
