|Year : 2015 | Volume
| Issue : 4 | Page : 146-147
Human Immunodeficiency Virus Vasculopathy: A Mystery Wrapped in an Enigma
Anshul Kumar Gupta1, Ramesh K Tripathi2
1 Department of Cardiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bengaluru, Karnataka, India
2 Burjeel Vascular Center, Abu Dhabi, UAE
|Date of Web Publication||13-Apr-2016|
Anshul Kumar Gupta
Department of Cardiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bengaluru, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Gupta AK, Tripathi RK. Human Immunodeficiency Virus Vasculopathy: A Mystery Wrapped in an Enigma. Indian J Vasc Endovasc Surg 2015;2:146-7
"The world has halted and reversed the spread of human immunodeficiency virus (HIV). The epidemic has been forced into decline. New HIV infections and AIDS-related deaths have fallen dramatically since the peak of the epidemic. Now, the response is going one step further - ending the AIDS epidemic by 2030.0" 
Over the last three decades, HIV has surprised and troubled every clinician around the world with its myriad manifestations and the extreme pace with which it has emerged into a global pandemic, afflicting about 36.9 million people around the world by the end of 2014.  The battle between the virus and mankind had been tilted toward the former, until recently, when UNAIDS declared that we have crossed the peak of the pandemic and new HIV infections are declining around the world thus exceeding the Millennium Development Goal-6 (halting the rise of HIV cases by 2015) set forth 15 years back in 2000. This new echelon of success inspired the UNAIDS to advance from Millennium Development Goal to Sustainable Development Goal of ending the AIDS epidemic by 2030. At the same time, even though new HIV infections have declined, there are still an unacceptably high number of new HIV infections and AIDS-related deaths occurring each year. In 2014, around 2 million people were newly infected with HIV and 1.2 million people died of AIDS-related illnesses. 
HIV is implicated in a multisystem disease process and the cardiovascular system is no exception. Many patients present with vascular complications, especially in advanced disease. HIV-related vascular disease has remained an enigma since its initial report in 1987 as small- and medium-sized arteriopathy described during autopsy of children with AIDS.  Since then, the involvement of small, medium, as well as large vessels has been reported. The pathogenesis of HIV vasculopathy has been believed to be an intricate interplay between inflammation caused by virus per se, the role of opportunistic infections and elements of atherosclerosis and prothrombotic factors. The spectrum of manifestations of vascular involvement in HIV is quite wide and includes aneurysms, occlusive lesions, spontaneous arteriovenous fistulas, arterial dissection, atherosclerosis, infectious agents, and drug-related vasculitides. The exact pathological basis for such varied manifestations is lacking, and many hypotheses have been put forth and tested in small studies.
It is in this context that in this issue of the journal, Pillay et al.  report the findings of their pathological study on HIV vasculopathy specimens to test the hypothesis that the angioproliferation of adventitial layer in patients with HIV large vessel vasculopathy may be a manifestation of Kaposi sarcoma (KS). The study was conducted on 20 arterial specimens (10 with aneurysmal disease and another 10 with occlusive disease) from antiretroviral therapy naïve adult HIV vasculopathy patients and comparison was done with 10 samples from patients with HIV and KS. Interestingly, the microscopic sections of all HIV vasculopathy specimens showed characteristic adventitial angioproliferative and inflammatory changes similar to the dermal changes seen in KS. However, while all KS samples showed the sine quo non presence of HHV-8 LNA-1 antigen, the same was cogently absent in all HIV vasculopathy samples (aneurysm as well as occlusive disease) as demonstrated by Immunohistochemical staining and Polymerase chain reaction (PCR) for HHV-8.
The study convincingly disproves the role of HHV8 in the pathogenesis of HIV vasculopathy which if proven would have opened novel frontiers in its management in the form of systemic therapy against HHV8. At present, a single unified pathological hypothesis to explain the spectrum of HIV vasculopathy does not seem likely, further studies will definitely unravel the mysterious mechanisms underpinning the varied manifestations of HIV vasculopathy. Further elucidation of the underlying pathological processes will definitely add to our armamentarium of highly active antiretroviral therapy (HAART) to battle this unique complication of HIV/AIDS. Until then, HAART will remain the cornerstone of management of patients with HIV-related vasculopathy.
We would like to thank Dr. Himanshu Verma for his help in preparing the manuscript.
| References|| |
Joshi VV, Pawel B, Connor E, Sharer L, Oleske JM, Morrison S, et al.
Arteriopathy in children with acquired immune deficiency syndrome. Pediatr Pathol 1987;7:261-75.
Pillay B, Ramdial PK, Ramburan A, Nargan K, Naidoo DP. The adventitial angioproliferation in human immunodefi ciency virus associated large artery vasculopathy is not a manifestation of Kaposi sarcoma. Indian J Vasc Endovasc Surg 2016 ;2:139-45.