The Linear Array® (LA) genotyping test is one of the most used methodologies for Human papillomavirus (HPV) genotyping, in that it is able to detect 37 HPV genotypes and co-infections in the same sample. However, the assay is limited to a restricted number of HPV, and sequence variations in the detection region of the HPV probes could give false negatives results. Recently, 454 Next-Generation sequencing (NGS) technology has been efficiently used also for HPV genotyping; this methodology is based on massive sequencing of HPV fragments and is expected to be highly specific and sensitive. In this work, we studied HPV prevalence in cervixes of women in Western Mexico by LA and confirmed the genotypes found by NGS. Two hundred thirty three cervical samples from women Without cervical lesions (WCL, n = 48), with Cervical intraepithelial neoplasia grade 1 (CIN I, n = 98), or with Cervical cancer (CC, n = 87) were recruited, DNA was extracted, and HPV positivity was determined by PCR amplification using PGMY09/11 primers. All HPV- positive samples were genotyped individually by LA. Additionally, pools of amplicons from the PGMY-PCR products were sequenced using 454 NGS technology. Results obtained by NGS were compared with those of LA for each group of samples. We identified 35 HPV genotypes, among which 30 were identified by both technologies; in addition, the HPV genotypes 32, 44, 74, 102 and 114 were detected by NGS. These latter genotypes, to our knowledge, have not been previously reported in Mexican population. Furthermore, we found that LA did not detect, in some diagnosis groups, certain HPV genotypes included in the test, such as 6, 11, 16, 26, 35, 51, 58, 68, 73, and 89, which indicates possible variations at the species level. There are HPV genotypes in Mexican population that cannot be detected by LA, which is, at present, the most complete commercial genotyping test. More studies are necessary to determine the impact of HPV-44, 74, 102 and 114 on the risk of developing CC. A greater number of samples must be analyzed by NGS for the most accurate determination of Mexican HPV variants.

Pesticides are chemical substances used to control, prevent, or destroy agricultural, domestic, and livestock pests. These compounds produce adverse changes in health, and they have been associated with the development of multiple chronic diseases. This study aimed to present a detailed review of the effect of pesticides on the oral cavity and the oral microbiome. In the oral cavity, pesticides alter and/or modify tissues and the microbiome, thereby triggering imbalance in the ecosystem, generating an inflammatory response, and activating hydrolytic enzymes. In particular, the imbalance in the oral microbiome creates a dysbiosis that modifies the number, composition, and/or functions of the constituent microorganisms and the local response of the host. Pesticide exposure alters epithelial cells, and oral microbiota, and disrupts the homeostasis of the oral environment. The presence of pesticides in the oral cavity predisposes the appearance of pathologies such as caries, periodontal diseases, oral cancer, and odontogenic infections. In this study, we analyzed the effect of organochlorines, organophosphates, pyrethroids, carbamates, bipyridyls, and triazineson oral cavity health and ecosystems.

Purpose: This study aimed to analyze the association of the apolipoprotein E (ApoE) polymorphisms with type 2 diabetes mellitus (T2DM) among the admixed population of West Mexico. Patients and Methods: ApoE genotypes were determined in 168 T2DM patients and 449 non-diabetic control subjects from the general admixed population of West Mexico. The non-diabetic subjects were stratified according to body mass index (BMI) in normal weight (n=186), overweight (n=138), and obesity (n=125). ApoE genotypes were assessed by using a TaqMan allelic discrimination assay, insulin resistance (IR) by HOMA-IR, and biochemistry with a dry chemistry assay. Results: The rate of dyslipidemias and IR increased by BMI category among the control subjects. The greater shift in the prevalence of dyslipidemia was observed from normal weight (51.4%) to overweight (76.6%), p< 0.01. Normal weight or obese e4 allele carriers had a higher level of total cholesterol and hypercholesterolemia than non-e4 carriers. Among the T2DM patients, the e2 carriers had abnormal HOMA-IR value than the non-e2 carriers (p=0.002). Comparatively, between the T2DM patients vs non-diabetics, the e2e3 genotype or e2 allele conferred a higher risk for T2DM (adjusted OR= 2.36, 95% CI 1.28– 4.34, p=0.006 and adjusted OR=2.1, 95% Cl 1.20– 3.79, p=0.009, respectively). Conclusion: The ApoE e2 allele was associated with IR and the risk of T2DM in subjects from the general admixed population of West Mexico.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is closely associated with obesity and other cardiometabolic risk factors. MASLD has rapidly become the most common cause of liver disease worldwide, currently affecting 38% of the global population. Excess weight causes chronic inflammation and the activation of different pathways involved in liver damage. MASLD can progress from simple steatosis to steatohepatitis, giving way to its inflammatory component, metabolic dysfunction-associated steatohepatitis (MASH), previously recognized as non-alcoholic steatosis hepatitis (NASH). Chronic hepatitis C virus (HCV) infection remains a significant challenge to liver health as it triggers hepatic inflammation, metabolic disruption, and hepatic steatosis. The convergence of MASLD and chronic HCV infection can significantly alter the course of liver disease and accelerate the progression to severe liver damage. Currently, HCV treatment has a high cure rate. However, in patients who achieve a sustained virological response after treatment with direct-acting antivirals, weight gain, and excessive calorie intake may contribute to increased liver steatosis and a higher risk of liver disease progression. Therefore, the effective clinical and nutritional management of HCV patients, both before and after viral eradication, is crucial to reducing the risk of death from hepatocellular carcinoma. Understanding the complex interactions between MASLD and HCV infection is crucial for managing these patients appropriately. Herein, host and viral mechanisms inducing liver damage during the coexistence of MASLD and HCV infection are described, and their therapeutic and dietary management are discussed.

Genetic variation in PNPLA3 influences liver fat accumulation and hepatocellular injury in various liver diseases. However, the role of PNPLA3 intronic polymorphisms in hepatic damage among hepatitis C virus (HCV) patients remains unclear. This study aims to investigate the association of three intronic PNPLA3 polymorphisms (rs4823173, rs2896019, and rs2281135) with liver injury in HCV-infected patients with spontaneous HCV clearance (SC) and chronic hepatitis C (CHC). A total of 218 HCV-positive individuals were classified into SC (n = 64) or CHC (n = 154) groups. PNPLA3 genotypes were determined by qPCR using TaqMan probes and liver damage through serum markers, noninvasive index, and liver stiffness. Among SC patients, the genotypes AA-rs4823173, GG-rs2896019, and AA-rs2281135 were associated with higher AST, ALT, and APRI, as well as decreased platelet counts, compared with patients homozygous for the non-risk genotypes (p < 0.05). No associations were found in CHC patients. The three polymorphisms were in perfect linkage disequilibrium (r² = 1). The risk haplotype AGA was associated with higher AST and ALT, as well as lower platelet counts (p < 0.05) in SC patients. PNPLA3 intronic polymorphisms and their association with serum liver injury markers could help identify hepatic injury in HCV-negative patients.