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Hindi Review Article
Sources for Inflammation and Accelerated Aging in Well Controlled HIV Patients on Antiretroviral Therapy
| Gnoni ML1*, Friedstrom S2, Blatt S2, Fernandez H2 and Ramirez JA3 | |
| 1Department of Medicine, Louisville, Kentucky; GoodSamaritan Hospital (Trihealth system) Department of Internal Medicine, Cincinnati, USA | |
| 2Department of Medicine, Division of Infectious Diseases, GoodSamaritan Hospital, Cincinnati, USA | |
| 3Division of Infectious Diseases, University of Louisville, Kentucky, USA | |
| Corresponding Author : | Gnoni ML Department of Medicine, Louisville Kentucky; GoodSamaritan Hospital (Trihealth system) Department of Internal Medicine, Cincinnati, USA Tel: 5025483525 E-mail: Martin_Gnoni@trihealth.com |
| Received: September 1, 2015 Accepted: September 28, 2015 Published: September 30, 2015 | |
| Citation: Gnoni ML, Friedstrom S, Blatt S, Fernandez H, Ramirez JA (2015) Sources for Inflammation and Accelerated Aging in Well Controlled HIV Patients on Antiretroviral Therapy. J Infect Dis Ther 3:239. doi:10.4172/2332-0877.1000239 | |
| Copyright: © 2015 Gnoni et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. | |
| Related article at Pubmed, Scholar Google | |
Abstract
After the introduction of highly active antiretroviral therapy (HAART) in the middle 1990, the mortality and morbidity of HIV has decreased dramatically. However, even well controlled patients on HAART are now suffering from “accelerated aging” with increased incidence of cardiovascular, respiratory, neurologic, metabolic, renal, and liver disease. Persistent low-level replication, coinfections, deposition of collagen in lymphoid tissue, microbial translocation in the GI and respiratory mucosa, overproduction of cellular debris, and immune-senescence may all contribute to its pathogenicity. Further exploration of these possible mechanisms will help us to define optimal trials to decrease the accelerated aging in HIV patients.
