Background: Helicobacter pylori is a globally prevalent pathogen and a major contributor to gastric diseases, including chronic gastritis, peptic ulcer disease, and gastric cancer. This study investigates the prevalence, distribution, and clinical relevance of its key virulence genes, vacA and cagA, in a Peruvian patient cohort. Materials and Methods: Fifty-one gastric biopsies were collected from patients with a presumptive diagnosis of H. pylori-induced gastritis at Hospital Carlos Alberto Seguín Escobedo in Arequipa, Peru, in March 2024. Two biopsies per patient—one from the antrum and one from the gastric body—were obtained during endoscopy. DNA extraction was performed using the Quick-DNA Fungal/Bacterial Kit (Zymo Research, USA). Molecular identification of H. pylori was conducted via PCR targeting the glmM gene, while the vacA and cagA virulence genes were detected using specific primers. Statistical analyses, including Pearson’s chi-square and Mann–Whitney tests, were applied to assess associations between virulence gene presence and clinical or histopathological variables. Results: Among the gastric biopsies, the vacA gene was detected in 37.3% of samples, while cagA was present in 17.6%. Statistical analysis revealed significant associations between vacA and specific clinical and endoscopic features, including erythematous gastropathy, nodular gastritis, and emetic syndrome, suggesting its localized role in disease pathogenesis. Additionally, the presence of cagA was significantly linked to moderate inflammatory intensity in gastric body biopsies, indicating its association with more severe histopathological outcomes. Chronic gastritis was the most common histopathological finding, with moderate intensity correlating strongly with the presence of virulence genes. Conclusions: These findings highlight substantial regional variability in the distribution and pathogenicity of H. pylori genotypes. This study underscores the importance of incorporating molecular diagnostics into routine clinical practice to improve diagnostic accuracy and inform region-specific therapeutic strategies. This is particularly crucial in endemic regions like Peru, where unique environmental and genetic factors may influence infection dynamics and disease outcomes.

Tuberculosis (TB) remains a major public health challenge in Peru, where interindividual variability in treatment response and drug-induced hepatotoxicity may be influenced by host genetic background. This study aimed to characterize clinically relevant polymorphisms in NAT2, CYP2E1, and SLCO1B1 in a cohort of TB patients from Southern Peru, a genetically underrepresented Andean population. Thirty-five adults receiving first-line therapy (isoniazid and rifampicin) underwent targeted Sanger sequencing of key functional variants among these three genes. NAT2 acetylator phenotypes were predominantly intermediate (68.6%), followed by rapid (20%) and slow (11.4%) profiles, with high minor allele frequencies for rs1041983 and rs1801280. CYP2E1 functional promoter variants were infrequent, whereas SLCO1B1 exhibited notable allelic heterogeneity, suggesting potential variability in rifampicin transport. Comparative analysis with previously reported Peruvian data revealed regional differences in acetylator distribution, supporting population-specific pharmacogenomic stratification. Although clinical toxicity outcomes were not evaluated, the high prevalence of reduced acetylation genotypes suggests a substantial proportion of patients may benefit from genotype-informed isoniazid dosing strategies. These findings provide foundational data for implementing precision medicine approaches using affordable and targeted technologies in TB management within Andean populations and support the integration of pharmacogenomics into national TB control programs.

Bacterial self-healing concrete has emerged as a bio-based strategy to enhance the durability of cementitious materials and reduce the environmental impact associated with premature infrastructure deterioration. Its functional principle relies on microbially induced calcium carbonate precipitation (MICP), through which bacterial metabolism promotes CaCO₃ deposition within cracks. However, self-healing efficiency cannot be explained solely by mineral precipitation capacity. Concrete is a restrictive microbial environment characterized by alkalinity, desiccation, osmotic stress, nutrient limitation and physical confinement. Therefore, effective crack sealing requires a coordinated sequence involving bacterial survival, sporulation, germination, metabolic reactivation, biofilm-associated mineral nucleation and localized biomineralization. This integrative narrative review synthesizes mechanistic, material and biosafety evidence on bacterial self-healing concrete, focusing on spore-forming bacteria such as Bacillus subtilis and related taxa, including Paenibacillus. The evidence indicates that stress tolerance, germination signaling, calcium handling, biofilm establishment and stability, and encapsulation-mediated microenvironmental control are key determinants of performance, but remain insufficiently integrated into materials-oriented studies. Large-scale implementation also requires preventive assessment of strain persistence, genetic stability, horizontal gene transfer, environmental microbiome interactions and life-cycle exposure scenarios. Bacterial self-healing concrete should therefore be understood as a living or bioactive material system whose responsible development depends on the integration of microbiology, molecular biology, materials science, civil engineering, environmental risk assessment, occupational health, and public health.