Abstract:Dyslipidemia has been frequently observed among individuals infected with human immunodeficiency virus type 1 (HIV-1), and factors related to HIV-1, the host, and antiretroviral therapy (ART) are involved in this phenomenon. This study reviews the roles of genetic polymorphisms, HIV-1 infection, and highly active antiretroviral therapy (HAART) in lipid metabolism. Lipid abnormalities can vary according to the HAART regimen, such as those with protease inhibitors (PIs). However, genetic factors may also be invo… Show more
“…It has been suggested that host genetic polymorphisms influence the risk of developing numerous diseases in HIV-infected people. [16][17][18] Estrogene hormone is well known to play an essential role in the growth and development during childhood and estrogen receptors (ERs) mediate much estrogen action.…”
Background: Estrogen plays a key role in human physiological processes. Polymorphisms of estrogen receptors have been implicated in the development of numerous diseases. The aim of this study was to evaluate the frequency of ERα gene Pvull and Xbal polymorphisms and assessing their association with CD4+ T-cell counts in HIV-infected children on highly active antiretroviral therapy. Methods: CD4+ T cell counts were determined using the FACS count system. ERα PvuII and XbaI polymorphisms were analyzed by PCR-RFLP. Results: This study enrolled 34 HIV-infected children on HAART. The frequencies of the PvuII and XbaI gene polymorphisms were PP 41,2%, Pp 26,5%, pp 32,4% and XX 35,3%, Xx 17,6%, xx 47,1% respectively. CD4+ T-cell counts were significantly associated with XbaI polymorphisms (p<0.05), but not PvuII polymorphisms (p>0.01). Discussion: Host genetic factor polymorphism is an important determinant of HIV disease progression and treatment response. The ERα Pvull and Xbal polymorphisms can increase risk for the development of HIV-related complication, including oral diseases. Conclusion: The ERα gene XbaI polymorphism was significantly associated with CD4+ T-cell counts. It may explain the role of estrogen in the regulation of HIV replication. Studying human genetic variation in HIV-infected individuals is important to guide a new therapeutic approach.
“…It has been suggested that host genetic polymorphisms influence the risk of developing numerous diseases in HIV-infected people. [16][17][18] Estrogene hormone is well known to play an essential role in the growth and development during childhood and estrogen receptors (ERs) mediate much estrogen action.…”
Background: Estrogen plays a key role in human physiological processes. Polymorphisms of estrogen receptors have been implicated in the development of numerous diseases. The aim of this study was to evaluate the frequency of ERα gene Pvull and Xbal polymorphisms and assessing their association with CD4+ T-cell counts in HIV-infected children on highly active antiretroviral therapy. Methods: CD4+ T cell counts were determined using the FACS count system. ERα PvuII and XbaI polymorphisms were analyzed by PCR-RFLP. Results: This study enrolled 34 HIV-infected children on HAART. The frequencies of the PvuII and XbaI gene polymorphisms were PP 41,2%, Pp 26,5%, pp 32,4% and XX 35,3%, Xx 17,6%, xx 47,1% respectively. CD4+ T-cell counts were significantly associated with XbaI polymorphisms (p<0.05), but not PvuII polymorphisms (p>0.01). Discussion: Host genetic factor polymorphism is an important determinant of HIV disease progression and treatment response. The ERα Pvull and Xbal polymorphisms can increase risk for the development of HIV-related complication, including oral diseases. Conclusion: The ERα gene XbaI polymorphism was significantly associated with CD4+ T-cell counts. It may explain the role of estrogen in the regulation of HIV replication. Studying human genetic variation in HIV-infected individuals is important to guide a new therapeutic approach.
“…The main genes studied are those that encode proteins, receptors, and enzymes related to lipid metabolism and regulation. Polymorphisms in LDLR, apoE, apo B, apo A-I, apo C-III, apo A-V, PCSK9, CETP, and LP genes have been associated with changes in lipid profile [45]. Regarding the LDLR gene, over 1,288 different variants have been implicated in the etiology of dslipidemia [46].…”
Section: Discussionmentioning
confidence: 99%
“…Because gene polymorphisms cause dyslipidemia, they should be investigated in these patients to identify individuals with an increased risk of developing dyslipidemia when on HAART, especially those containing PIs. This knowledge could guide individualized treatment decisions and lead to new therapeutic targets for the treatment of dyslipidemia [45].…”
“…The degree of inflammatory and metabolic response to ischemic stroke may be variable and the extent variability in genes coding for proteins of pathways involved in the inflammation (Waterer and Wunderink 2003) and in the metabolism (de Almeida et al 2013), considered the main pathophysiologic pathways of ischemic stroke, limits the generalization of previous results to the Brazilian population, considered one of the most genetically heterogeneous worldwide, as result of a great miscegenation (Pena et al 2011;Brazil 2013b).…”
The aim of this study was to evaluate the association between inflammatory and metabolic markers and short-time outcome with acute ischemic stroke subtypes. A total of 121 patients was classified according to TOAST criteria, such as large artery atherosclerosis (LAAS), lacunar infarct (LAC), cardioembolic infarct (CEI), other determined etiology (ODE), and undetermined etiology (UDE). The functional impairment was evaluated within the first eight hours of stroke and the outcome after three-month follow-up using the modified Rankin Scale. Blood samples were obtained up to 24 h of stroke. Compared with 96 controls, patients with LAAS, CEI, and LAC subtypes showed higher levels of white blood cells, high-sensitivity C-reactive protein (hsCRP), interleukin 6 (IL-6), metalloproteinase 9 (MMP-9), glucose, and iron (p < 0.05); and lower high-density lipoprotein cholesterol (HDL-C) (p < 0.0001); platelets, insulin, insulin resistance, and homocysteine were higher in LAC (p < 0.0001); ferritin was higher in LAAS (p < 0.0001); and total cholesterol (TC) was lower in LAAS and CEI (p < 0.01). When stroke subtypes were compared, insulin was higher in LAAS vs. LAC and in LAC vs. CEI (p < 0.05); and TC was lower in LAAS vs. LAC (p < 0.05). Outcome and rate of mortality after three-month were higher in LAAS vs. LAC (p < 0.001 and p = 0.0391 respectively). The results underscored the important role of the inflammatory response and metabolic changes in the pathogenesis of ischemic stroke subtypes that might be considered on the initial evaluation of stroke patients to identify those that could benefit with individualized therapeutic strategies that taken into account these markers after acute ischemic event.
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