Association between lipid profile and clinical outcomes in COVID-19 patients.

High-density lipoprotein cholesterol (HDL-c) removes cholesterol, an essential component in lipid rafts, and this cholesterol removal can regulate protein attachment to lipid rafts, modulating their functionality in the immune cell response. Although severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can alter the lipid profile, there is little information on the role of HDL-c and other lipids in prognostic of the coronavirus disease 2019 (COVID-19) in Mexican population. This study aims to evaluate the predictive value of HDL-c and lipid profile on severity and survival of 102 patients infected with SARS-CoV-2 during the COVID-19 first wave. Our findings, derived from univariate and multivariate Cox proportional hazards regression models, highlighted age and hypertension as significant predictors of survival (HR = 1.04, p = 0.012; HR = 2.78, p = 0.027), while gender, diabetes, and obesity showed no significant impact. Triglycerides and HDL-c levels notably influenced mortality, with elevated triglycerides and lower HDL-c associated with higher mortality risk (p = 0.032). This study underscores the importance of lipid profiles alongside traditional risk factors in assessing COVID-19 risk and outcomes. It contributes to the understanding of COVID-19 patient management and emphasizes the need for further investigation into the role of dyslipidemia in influencing COVID-19 prognosis, potentially aiding in refined risk stratification and therapeutic strategies.

Vitamin D receptor gene polymorphisms role in COVID-19 severity: Results of a Mexican patients' cohort.

Vitamin D status has been involved with coronavirus disease 19 (COVID-19) severity. This may be mediated by vitamin D metabolism regulatory genes. Of interest is the vitamin D receptor (VDR) gene, which has been previously associated with other inflammatory and respiratory diseases. In order to investigate the role of VDR gene polymorphisms in COVID-19 severity and outcome, a total of 292 COVID-19 patients were classified according to severity in moderate (n = 56), severe (n = 89) and critical (n = 147) and, according to outcome in survivor (n = 163) and deceased (n = 129), and analysed for FokI and TaqI VDR gene polymorphisms by polymerase chain reaction-based restriction enzyme digestion. The FokI and TaqI single nucleotide polymorphisms (SNPs) were not associated with COVID-19 severity or mortality individually but when analysed by haplotype, TC was associated with an increased risk of presenting critical COVID-19. Additionally, FokI CT genotype was more frequent in COVID-19 patients with hypertension, and T allele carriers presented higher aspartate aminotransferase levels. Our results suggest a relationship between VDR FokI and TaqI SNPs and COVID-19 severity in Mexican population. Although there are some previous reports of VDR polymorphisms in COVID-19, this represents the first report in Latin American population. Further studies on other populations are encouraged.

Association of the HLA-G rs66554220 variant with non-segmental vitiligo and its clinical features in Northwestern Mexico population.

Introduction: The HLA-G molecule functions as a critical immunomodulatory checkpoint, its expression is significantly associated with pathological processes that may be responsible in part for autoimmune conditions such as non-segmental vitiligo (NS-V), characterized by chronic skin depigmentation. In this sense, the rs66554220 (14 bp ID) variant located in the 3'UTR, implicated in the regulation of HLA-G production, is associated with autoimmune diseases. Aim: To evaluate the role of the HLA-G rs66554220 variant in NS-V and its clinical features in Northwestern Mexicans. Material and methods: We genotyped the rs66554220 variant by SSP-PCR in 197 NS-V patients and 198 age-sex matched non-related healthy individuals (HI). Results: Del allele and genotype Del/Ins were the most prevalent in both study groups (NS-V/HI = 56%/55% and 46.70%/46.46%, respectively). Despite lacking association between the variant and NS-V, we found an association of the Ins allele in different inheritance models with familial clustering, onset of the illness, universal clinical subtype and Koebner's phenomenon. Conclusions: The rs66554220 (14 bp ID) variant is not a risk factor for NS-V in the Mexican population studied. To our knowledge, this is the first report about the topic in the Mexican population and worldwide that includes clinical features related with this HLA-G genetic variant.

Analysis of the heat shock protein 70 (HSP70) genetic variants in nonsegmental vitiligo patients.

BACKGROUND: Vitiligo is an autoimmune disease that courses with skin depigmentation because of the destruction of melanocytes. Vitiliginous melanocyte is prone to damage because of oxidative stress which activates cellular stress response and the release of heat shock proteins such as HSP70 promoting immune activation against the melanocyte. Variants in HSP70 genes (HSPA) might alter their expression and thus modulate vitiligo susceptibility. Therefore, we sought to evaluate the role of the 5' untranslated region HSPA1A G/C (rs1043618) and the exonic HSPA1B A/G (rs1061581) and HSPA1L T/C (rs2227956) gene variants in nonsegmental vitiligo. METHODS: A total of 200 nonsegmental vitiligo patients and 208 age/gender-matched healthy subjects were genotyped for rs1043618, rs1061581, and rs2227956 variants by PCR-RFLP. RESULTS: Variants rs1043618 and rs1061581 were not associated with vitiligo susceptibility. On the other hand, the rs2227956 C allele and TC genotype were associated with protection against vitiligo. A similar effect was observed for the GAC haplotype. Any of the aforementioned HSP70 gene variants were associated with the clinical characteristics of vitiligo. CONCLUSION: Our findings suggest that the HSPA1L rs2227956 gene variant might influence the susceptibility to vitiligo. Being the first study of HSP70 gene variants in vitiligo, further research is encouraged to corroborate these results.

Genetic Polymorphisms of Tumor Necrosis Factor Alpha and Susceptibility to Dengue Virus Infection in a Mexican Population.

To evaluate the association of the -308 and -238 tumor necrosis factor alpha (TNF-α) gene polymorphisms with clinical manifestations of dengue and TNF-α serum levels in a northwestern Mexican population. The study populations included dengue fever (DF) and dengue hemorrhagic fever (DHF) patients, and a group of healthy controls (HCs) without history of dengue. Polymerase chain reaction-restriction fragment length polymorphism and Enzyme-Linked Immunosorbent Assay were performed to determine genotypes and serum concentration of TNF-α, respectively. There were no significant differences in alleles, genotypes, and haplotype frequencies between patients and HCs. However, when patients were separated into DF and DHF, there was an increased prevalence of the -308 GA genotype in HCs compared to DHF (odds ratio [OR] = 0.129, 95% confidence interval [CI] = 0.018-0.945, p = 0.025), as well as the GG haplotype (OR = 0.49, 95% CI = 0.273-0.880, p = 0.01757) in DF. The genotypes of both polymorphisms were not associated with hematologic manifestations. Serum TNF-α levels were significantly higher in patients than in HCs (p = 0.004). Our results suggest a minimal effect of the -308 and -238 TNF-α gene polymorphisms in dengue patients and that their increased serum levels of TNF-α are independent of genotypes.

Stromal Cell-Derived Factor-1-3'A Polymorphism Favors HIV-1 Infection in Mexican Women.

OBJECTIVE: To evaluate the association of the stromal cell-derived factor-1 (SDF1)-3'A polymorphism to HIV-1 infection, CD4+ T-lymphocyte counts, and viral load levels in a northwestern Mexican population. METHODS: We investigated allele and genotype frequencies of the SDF1-3'A polymorphism in 634 mestizo individuals from Northwest Mexico (204 HIV-1 infected persons, 256 uninfected blood donors, and 174 uninfected female sex workers) by the PCR- RFLP method and compared them using a x(2) test. We also searched for correlations between the polymorphism and CD4+ T lymphocyte and viral load counts. RESULTS: No differences were observed in the frequencies of alleles and genotypes between patients and controls. However, in female patients we found a significantly increased prevalence of both the A allele and GA heterozygous genotype compared to male patients, female blood donors, and female sex workers. CONCLUSION: Here we describe the association of the SDF1-3'A polymorphism with HIV-1 infection only in women, but not to CD4+ T-lymphocyte categories, viral load levels in patients with HIV-1/AIDS, or to exposure levels in female sex workers.