**1. Introduction**

Human immunodeficiency virus (HIV) is a global disease. According to global HIV and acquired immunodeficiency syndrome (AIDS) statistics in 2017, there were 36.9

#### **Figure 2.**

*Diagram illustrating HIV replication. (A) The virus glycoprotein receptors bind to host cell CD4 and a co-receptor CCR5. (B) Fusion of the virus with the host cell membrane results in viral uncoating and the release of the viral nucleocapsid into the cytoplasm. (C) The enzyme reverse transcriptase converts the single stranded RNA into double stranded DNA. (D) The viral DNA is transported to the host nucleus where it is integrated into the host's DNA. (E) Viral DNA is transcribed and translated using host cell machinery and then cleaved by viral protease into functional viral proteins. (F) Viral RNA and proteins assemble at the cell surface and bud off the cellular membrane. (Reproduced from Ref. [2]. Permission obtained from Michael S Pepper).*

million [31.1–43.9 million] people living with HIV, of whom 35.1 million [29.6–41.7 million] adults. The majority of these individuals reside in the developing world [1].

HIV infection involves multiple systems including the cardiovascular system. A structure of the HIV virus and its replication in a cell are depicted in **Figures 1** and **2**. A large number of these patients present with vascular pathology [3, 4]. HIV afflicts the vascular system in multiple ways. Patients may present with a diverse array of aneurysms, occlusive disease, spontaneous arteriovenous fistulae and dissections. The precise pathogenesis of HIV related vasculitis remains poorly understood, a few recent studies have tried to address this issue [5].

In this chapter we will review the current knowledge pertaining to the important entity of HIV associated vasculopathy with an emphasis on effects of HIV on the aorta.

#### **2. Definition and broad overview of aortic aneurysms**

An aortic aneurysm is a dilation of a segment of the aortic wall, which may undergo further expansion and rupture [6]. It is defined as at least a 50% increase in diameter compared with the expected normal diameter of the vessel. They may occur in the ascending or the descending thoracic or abdominal aorta.

It may be fusiform or saccular in morphology [6]. A fusiform aneurysm is characterised by a uniform symmetric enlargement of the entire circumference of the aortic wall. A saccular aneurysm involves dilation of a localised portion of the aortic wall.

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*Human Immunodeficiency Virus Associated Large Artery Disease*

These are true aneurysms as opposed to false aneurysms, as they involve all three

There are multiple aetiologies implicated in the pathogenesis of aortic aneurysms [6].

2.Genetic diseases, such as Marfan syndrome, Loeys-Dietz syndrome, Ehlers-Danlos syndrome, familial thoracic aortic aneurysms, bicuspid aortic valve disease, Turner syndrome and aortopathy associated with congenital heart disease.

3.Inflammatory diseases, such as Takayasu's disease and giant cell arteritis.

4.Infectious diseases, including bacterial infections (the most common organisms implicated are *Staphylococcus aureus*, *Salmonella* species, *Escherichia coli*, *Streptococcus* species, *Neisseria* species and gram-negative bacilli) and fungi. Recently, HIV has been implicated in the pathogenesis of aortic aneurysms.

The true incidence and prevalence of aortic aneurysms is difficult to ascertain due to the silent nature of this disease [7]. In a computed chest tomography (CT) study the prevalence of asymptomatic thoracic ascending aneurysm was 0.16% [8]. In a different study the prevalence was noted to be 0.34% [9]. The incidence and prevalence of aneurysms tend to differ between studies due to different aortic dimension cut-offs. The majority of studies did not include aortas between 4 and 5 cm [7]. The annual incidence according to two studies was estimated to be in the range of 5.6 and 10.4 cases per 100,000 patient-years [10, 11]. Thoracic aneurysms

Abdominal aortic aneurysm is predominantly a disease of men [12–15]. The incidence rises with age. In screening studies its prevalence is estimated at 4–8%. The incidence of new cases of abdominal aortic aneurysms in the western popula-

The true incidence and prevalence of HIV associated aneurysms remains understudied. The incidence of symptomatic vasculitis in HIV-infected patients is

The pathogenesis of HIV associated vasculopathy is multifactorial (**Figure 3**)

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

1.Degenerative or atherosclerotic diseases.

Infected aortic aneurysms have a high mortality.

are more common in men greater than 60 years of age [7].

**5. Pathogenesis of HIV associated vasculopathy**

• Smooth muscle cell proliferation and migration

• Inflammation and endothelial injury

[5]. Three pathophysiological processes have been implicated:

tion is estimated at 0.4–0.67% [7].

reported to be 1% [16].

• Molecular mimicry

layers of the aortic wall.

These include:

**4. Epidemiology**

**3. Aetiology**

These are true aneurysms as opposed to false aneurysms, as they involve all three layers of the aortic wall.
