The Adventitial Angioproliferation in Human Immunodeficiency Virus Associated Large Artery Vasculopathy is Not a Manifestation of Kaposi Sarcoma

2015 
Introduction: Human immunodeficiency virus -associated large artery vasculopathy (HIV-vasculopathy) is characterized by distinctive transmural microanatomical alterations, including adventitial angioproliferation, similar to that described in early cutaneous Kaposi sarcoma (KS). Human herpesvirus -8 (HHV8), the etiological agent of KS, is identifiable in tissue sections. The aim of this study was to investigate, based on HHV8-latent nuclear antigen-1 (HHV8-LNA-1) immunohistochemical and HHV8 polymerase chain reaction (PCR) testing, whether KS is the cause of the angioproliferation. Materials and Methods: Sections from 20 large arteries, ten each with HIV-associated occlusive and aneurysmal vasculopathy and ten biopsies with early cutaneous KS from 30 anti-retroviral therapy naive patients were appraised microscopically and subjected to HHV8-LNA-1 immunostaining. Arterial sections were also subjected to HHV8 PCR investigation with appropriate positive and negative controls. Results: The microscopic large arterial adventitial alterations included a dissecting proliferation of capillary-caliber vasculature, surrounded by mixed inflammation, microhemorrhages, hemosiderin and vasa vasorum intimomedial fibrosis, and hypertrophy. Ten vessels also demonstrated adventitial leukocytoclastic and lymphocytic vasculitis. Immunohistochemical and PCR detection of HHV8 was consistently negative. Skin biopsies of KS shared the vascular adventitial alterations, but vasculitis and thrombosis were absent. Endothelial and dermal spindle cells were immunopositive for HHV8. Conclusion: The adventitial angioproliferation in large arteries with HIV-vasculopathy is not a manifestation of KS. The exact roles of HIV, including interaction with co-infective agents and cellular and subcellular responses in the induction of vasculopathic and vasa vasorum abnormalities, including adventitial angioinflammatory alterations, require accelerated investigation for improved disease understanding and patient management.
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