Abstract
For the past several decades, humanity has been dealing with HIV. This disease is one of the biggest global health problems. Fortunately, modern antiretroviral therapy allows patients to manage the disease, improving their quality of life and their life expectancy. In addition, the use of these drugs makes it possible to reduce the risk of transmission of the virus to almost zero. Atherosclerosis is another serious pathology that leads to severe health problems, including disability and, often, the death of the patient. An effective treatment for atherosclerosis has not yet been developed. Both types of immune response, innate and adaptive, are important components of the pathogenesis of this disease. In this regard, the peculiarities of the development of atherosclerosis in HIV carriers are of particular scientific interest. In this review, we have tried to summarize the data on atherosclerosis and its development in HIV carriers. We also looked at the classic therapeutic methods and their features concerning the concomitant diagnosis.
Highlights
Atherosclerosis is a chronic inflammatory disease of the arterial wall, which quite often results in invalidity or fatal events
The erosion or breaking of atherosclerotic plaques leads to thrombotic events that can theoretically lead to death
Years of active research demonstrate that atherosclerosis is characterized by a tricky pathogenesis, the main aspects of which are lipid storage and chronic inflammation in the arterial wall
Summary
Atherosclerosis is a chronic inflammatory disease of the arterial wall, which quite often results in invalidity or fatal events. Circulating monocytes ‘stick’ to the affected section of the arterial wall and get inside, differentiating into macrophages that intensively participate in the lipid devourment through phagocytosis and generate the foam cells enriching atherosclerotic plaques [6,7]. Liable plaque erosion mechanisms require further study These processes are complicated to model in atherosclerotic animals. Inflammatory events, such as platelet-mediated local neutrophil enabling, myeloperoxidase release, toll-like receptor (TLR-2) signaling, and neutrophil-mediated damage, appear to be important in this process [13,14]. The lumen of the blood vessel narrows, resulting in both ischemia and metabolic changes in the alimented tissues. More dangerous is thrombogenesis, which occurs due to unstable plaques, and occasionally on the surface of intact plaques, which frequently leads to lethal consequences [15]
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