Aditya Bhalerao1, Luca Cucullo1,2. 1. Department of Pharmaceutical Sciences, Texas Tech University Health Sciences Center, Amarillo, TX 79106, USA. 2. Center for Blood Brain Barrier Research, Texas Tech University Health Sciences Center, Amarillo, TX 79106, USA.
Abstract
AIM: With the advent of highly active and combination antiretroviral therapy have substantially increased the life expectancy of patients infected with human immunodeficiency virus (HIV). However, this has brought into sharp contrast the incidence of several 'Non-acquired immunodeficiency syndrome (AIDS) diseases such as NeuroAIDS which identifies a group of neurological disorders caused primarily by HIV-mediated damage to the central and peripheral nervous systems. Given the patients depleted immune condition, the use and abuse of drug and addictive substances such as tobacco smoking can further deteriorates their overall health and accelerate the progression and severity of the disease. In this review we detail the pathogenesis, progression and characteristics of HIV and the impact of tobacco smoking as a risk factor for the progression of the disease to NeuroAIDS. This is a poorly understood aspect of HIV-related complications that needs to be addressed. SUBJECTS AND METHODS: Review of theoretical approaches and knowledge synthesis. RESULTS: Tobacco smoking is highly prevalent in HIV patients when compared to the general population. The oxidative damage and inflammatory stress caused by chronic smoking on the cerebrovascular system have been well established. Considering that HIV patients have an impaired immune system and smokers per se are more susceptible to viral and bacterial inflammatory neuropathologies than non-smokers, it is conceivable that tobacco smoking as a risk factor for the progression of HIV into NeuroAIDS and related neurological impairments. CONCLUSION: Tobacco smoke (TS) may bring about a synergistic effect in the context of persistent inflammatory state and cerebrovascular damage which facilitate HIV infection and progression to NeuroAIDS when compared to non-smokers.
AIM: With the advent of highly active and combination antiretroviral therapy have substantially increased the life expectancy of patients infected with human immunodeficiency virus (HIV). However, this has brought into sharp contrast the incidence of several 'Non-acquired immunodeficiency syndrome (AIDS) diseases such as NeuroAIDS which identifies a group of neurological disorders caused primarily by HIV-mediated damage to the central and peripheral nervous systems. Given the patients depleted immune condition, the use and abuse of drug and addictive substances such as tobacco smoking can further deteriorates their overall health and accelerate the progression and severity of the disease. In this review we detail the pathogenesis, progression and characteristics of HIV and the impact of tobacco smoking as a risk factor for the progression of the disease to NeuroAIDS. This is a poorly understood aspect of HIV-related complications that needs to be addressed. SUBJECTS AND METHODS: Review of theoretical approaches and knowledge synthesis. RESULTS: Tobacco smoking is highly prevalent in HIV patients when compared to the general population. The oxidative damage and inflammatory stress caused by chronic smoking on the cerebrovascular system have been well established. Considering that HIV patients have an impaired immune system and smokers per se are more susceptible to viral and bacterial inflammatory neuropathologies than non-smokers, it is conceivable that tobacco smoking as a risk factor for the progression of HIV into NeuroAIDS and related neurological impairments. CONCLUSION: Tobacco smoke (TS) may bring about a synergistic effect in the context of persistent inflammatory state and cerebrovascular damage which facilitate HIV infection and progression to NeuroAIDS when compared to non-smokers.
Authors: D N Burns; D Hillman; J D Neaton; R Sherer; T Mitchell; L Capps; W G Vallier; M D Thurnherr; F M Gordin Journal: J Acquir Immune Defic Syndr Hum Retrovirol Date: 1996-12-01
Authors: Mohammad A Kaisar; Heidi Villalba; Shikha Prasad; Taylor Liles; Ali Ehsan Sifat; Ravi K Sajja; Thomas J Abbruscato; Luca Cucullo Journal: Redox Biol Date: 2017-06-17 Impact factor: 11.799