**5.4 Other postulated mechanisms involved in the pathogenesis of HIV related vasculopathy**

Direct invasion by HIV of vascular endothelium and toxicities related to highly active antiretroviral therapy (HAART) have been postulated as possible additional mechanisms resulting in endothelial injury [17].

**71**

*Human Immunodeficiency Virus Associated Large Artery Disease*

*DOI: http://dx.doi.org/10.5772/intechopen.85956*

**5.5 HIV-associated aortopathy**

**5.6 Other forms of HIV related vasculopathy**

possible manifestation of HIV vasculopathy.

disrupted internal elastic lamina and calcification.

HIV disease [5].

**Figure 4.**

**vasculopathy**

HIV-associated aortopathy may present as aneurysmal disease of the ascending and the descending aorta (**Figure 4a**–**d**). Bacterial infections have been implicated in the pathogenesis of aortic aneurysms [5, 6]. A few case reports have reported the presence of *Salmonella*-related mycotic aneurysmal disease in HIV-positive patients. These aneurysms have been reported in immunosuppressed patients with advanced

*Two and three dimensional long axis trans-oesophageal images of an enlarged ascending aorta in a patient* 

*with HIV associated aortopathy (arrow) (a, b) and a normal aorta in a control (arrow) (c, d).*

HIV may affect femoral, carotid and popliteal arteries [5]. It may manifest as aneurysmal or occlusive disease as well as present as arterio-venous fistula and as arterial dissection. Since the advent of HAART, atherosclerotic disease is also a

Large vessel vasculopathy related to HIV is characterised by involvement of all three layers of the vessel wall [5]. There is infiltration of the vasa vasorum, periadventitial vessels and the adventitia by leucocytes. The media demonstrates fibrosis, muscle damage and elastin fragmentation. The intima also is characterised by

Intracranial aneurysms due to HIV have been reported in children [5]. Overall histopathological studies have shown similar microscopic characteristics as previously described. Some studies, however, have shown distinct tissue characteristics in arteries of patients with intracranial aneurysms. These include variable absence of internal elastic lamina fragmentation, medial thickening with sub-intimal SMC deposition, presence of viral protein gp41 within the

**6. Histopathological features of HIV associated large vessel** 

*Human Immunodeficiency Virus Associated Large Artery Disease DOI: http://dx.doi.org/10.5772/intechopen.85956*

#### **Figure 4.**

*Aortic Aneurysm and Aortic Dissection*

**5.1 Inflammation and endothelial injury**

pro-inflammatory pathways in HIV related vasculitis.

additional mechanism of endothelial dysfunction [17].

**5.2 Smooth muscle cell proliferation and migration**

mechanisms resulting in endothelial injury [17].

Endothelial cell dysfunction as a result of increase in inflammatory mediators to viral proteins has been implicated in the pathogenesis of HIV related vasculitis [5]. The inflammatory mediators include interleukins 1, 6 and 8, and tumour necrosis factor-alpha. The aforementioned argument is supported by a study by Nieuwhof et al., in the setting of cerebral vasculitis, whereby, they found an increased CD25 positive receptor positive T-cells. HIV envelope surface glycoprotein 120 and a transactivator transcription protein that have been implicated in the stimulation of

*Pathogenesis of HIV associated vasculopathy. (Reproduced from Ref. [5]. Permission obtained from B Pillay).*

Increased oxidative stress in HIV in animal studies has been proposed as an

Smooth muscle cells, an important component of the muscularis media, possess important surface receptors such as CD4, CCR5 and CXCR4 [5]. These receptors mediate the entry of HIV virus into the cell resulting in invasion and disruption of tunica media, and activation of tissue factor 2 with resultant stimulation of pro-

It is theorised that the arterial wall possesses receptors known as matrix adhe-

**5.4 Other postulated mechanisms involved in the pathogenesis of HIV related** 

Direct invasion by HIV of vascular endothelium and toxicities related to highly active antiretroviral therapy (HAART) have been postulated as possible additional

sion molecule-1 which may share ligands with similar deoxyribonucleic acid sequences to those present in the viral envelope glycoprotein, GP41 and GP120 [5]. This may result in an autoimmune response within the host and cell damage.

**70**

coagulant pathways.

**Figure 3.**

**5.3 Molecular mimicry**

**vasculopathy**

*Two and three dimensional long axis trans-oesophageal images of an enlarged ascending aorta in a patient with HIV associated aortopathy (arrow) (a, b) and a normal aorta in a control (arrow) (c, d).*

#### **5.5 HIV-associated aortopathy**

HIV-associated aortopathy may present as aneurysmal disease of the ascending and the descending aorta (**Figure 4a**–**d**). Bacterial infections have been implicated in the pathogenesis of aortic aneurysms [5, 6]. A few case reports have reported the presence of *Salmonella*-related mycotic aneurysmal disease in HIV-positive patients. These aneurysms have been reported in immunosuppressed patients with advanced HIV disease [5].

#### **5.6 Other forms of HIV related vasculopathy**

HIV may affect femoral, carotid and popliteal arteries [5]. It may manifest as aneurysmal or occlusive disease as well as present as arterio-venous fistula and as arterial dissection. Since the advent of HAART, atherosclerotic disease is also a possible manifestation of HIV vasculopathy.
