Research Progress on Metabolic Syndrome (MS) in HIV/AIDS Patients

MS includes metabolic disorders, from belly fat to diabetes, hypertension and dyslipidemia, that influence individuals' psychological and physical health. That's because MS is more common in HIV/AIDS patients than in non-HIV individuals, and because diagnostic criteria and sample sizes are different, as are clinical features and pathophysiology. Here we summarize the current research on MS in HIV/AIDS patients to offer and advise recommendations for early detection and management of MS in HIV/AIDS patients. HIV/AIDS patients are, as we all know, more at risk for some non-communicable disease than non-HIV individuals. As lives were prolonged for HIV/AIDS patients, metabolic syndrome, cardiovascular disease, tumors, chronic kidney disease and other NAD grew in frequency, and today outstrip AIDS, and now constitute a larger share of the lives and survival of HIV/AIDS patients. The literature tells us that HIV/AIDS patients will have chronic non-communicable disease 15–16 years before the general population, and twice as many cardiovascular events as the general population. As a major cause of cardiovascular disease, MS can make life and health of HIV/AIDS patients hellish. There is a 16.7 to 31.3% MS incidence of HIV/AIDS patients worldwide according to the study. MS in HIV/AIDS patients is increasing and becoming more common – as several studies in recent years have shown.

Figure 1. The interplay between HIV infection and host metabolism. (Sources: Kang S, et al.; 2020)

HIV Infection Promotes MS

HIV infection can also foster MS. The HPA axis also bears on the prevalence of MS in HIV/AIDS patients. The previous literature reported that even in HIV/AIDS patients on cART, between 14 and 46 per cent continue to exhibit HPA axis disorders – predominantly through the elevated basal glucocorticoid level. This attribute could be one of the primary causes of MS in HIV/AIDS patients HIV can influence lipid transport and blood lipid levels in infected cells. – The transport protein adenosine triphosphate binding cassette transporter A1 (ABCA1) keeps cholesterol homeostasis in check by controlling cholesterol's transportation throughout the cell and its extracellular environment. The HIV Nef protein expressed in HIV-infected cells can lower cholesterol efflux and ABCA1 in recent years. On the basis of the above process, cells infected with HIV will also exhibit lipid transport disruptions and accumulate lipids within their bodies. HIV Tat protein can also make more cholesterol and lead to dyslipidemia. There are HIV-associated proteins associated with hypertension. HIV Nef and Tat proteins can lead to hypertension by vascular oxidative stress, smooth muscle cell growth and migration, and endothelial dysfunction. HIV also raises blood pressure directly by directly attacking the renin-angiotensin-aldosterone system (RAAS). Yet there's not much known about the use of RAAS in HIV/AIDS patients. The disease of amino acid metabolism is what can make HIV cause abnormal blood sugar. One report determined by targeted metabolomics analysis that amino acid metabolites kynurenine, ornithine and homocysteine had been linked with increased fasting blood sugar and insulin resistance. Therefore, HIV can foster MS. Given the disease structure of MS is highly complex and its abnormal metabolic elements interact with each other, there are still many studies to complete to explain how HIV acts in the long-term effects of MS and how the abnormal metabolic elements of MS interact with each other in HIV/AIDS patients.

HIV-1 gp24 Antibody

HIV-1 gp24 Antigens