Abstract:
:There is growing literature on the subject of aneurysmal degeneration of arteries in patients who are infected with HIV. A patient recently seen at our medical center with an aneurysm of the carotid artery stimulated our interest in reviewing the mechanisms by which HIV may initiate or predispose to these pathologies. There are at least three major possibilities: (1) immunodeficiency allows bacteria that are known to cause mycotic aneurysms to proliferate without immune restraint; (2) one or more of the HIV envelope proteins sufficiently resemble one or more artery-specific-antigenic proteins (ASAPs) that may trigger an autoimmune response (molecular mimicry); and (3) the HIV virus itself infects arterial-resident cells that maintain the integrity of the load-bearing matrix. The computational searches reported here suggest that the ASAP, matrix cell adhesion molecule-1 (Mat-CAM-1), has a high degree of similarity to known ligands for HIV envelope proteins gp41 and gp120. No similarities of Mat-CAM-1 to the HIV envelope glycoproteins were detected. Accordingly, among the possibilities for explaining the HIV/aneurysm connection, direct infection of aortic fibroblasts by the HIV virus is more likely to be the pathogenetic mechanism than the process of molecular mimicry.
journal_name
Ann N Y Acad Scijournal_title
Annals of the New York Academy of Sciencesauthors
Tilson MD 3rd,Withers Ldoi
10.1196/annals.1383.018subject
Has Abstractpub_date
2006-11-01 00:00:00pages
387-91eissn
0077-8923issn
1749-6632pii
1085/1/387journal_volume
1085pub_type
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