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Background Loss to follow-up (LTFU) remains a major challenge in achieving sustained HIV care. Understanding individual and structural factors influencing disengagement is essential to improve retention, particularly in low- and middle-income settings. This study aimed to identify predictors of LTFU among adults receiving antiretroviral therapy (ART) in western Mexico. Methods A case–control study was conducted among adults with HIV treated at a tertiary hospital. Cases met the national definition of LTFU (≥ 90 days beyond the expected clinic visit or pharmacy refill), while controls were retained patients during the same period. A total of 919 participants were included (148 LTFU, 771 retained). Multivariable logistic regression identified factors associated with LTFU. Results Median age was 42 years (IQR 34, 51) and 88% were male. The multivariable analysis identified that age was associated with lower risk of LTFU (adjusted odds ratio [aOR] per year, 0.94; 95% CI, 0.91–0.96). Secondary ART resistance (aOR, 4.03; 95% CI, 1.59–9.99), hard-drug use (aOR, 2.57; 95% CI, 1.68–3.93), psychiatric disorders (aOR, 3.58; 95% CI, 2.23–5.72), lower educational level (≥ upper secondary vs. no formal education/primary: aOR, 2.30; 95% CI, 1.34–3.94), emergency department visits (aOR, 2.63; 95% CI, 1.72–4.04), and years living with HIV (aOR per year, 1.06; 95% CI, 1.02–1.10) were associated with higher odds of LTFU. Conclusions These findings highlight the role of psychosocial and structural determinants of LTFU, underscoring the need for integrated interventions addressing education, mental health, and substance use to improve retention in HIV care in Mexico.

Prostate cancer remains largely refractory to immunotherapy, implying the existence of context-specific immune landscape programs that diverge between circulation and tumor. Here, we integrate bulk RNA sequencing from three cohorts (patient peripheral mononuclear cells, primary prostate tissue, and biochemical-recurrence tumors) with multiparameter flow cytometry, unsupervised UMAP/T-REX (Tracking Responders Expanding) mapping, and de novo discovery of long non-coding RNAs (lncRNAs) to characterize context-specific immunoregulation. Patient PBMCs revealed a coherent IL-1/TNF/IL-17 inflammatory architecture with strong chemotactic programs and an unexpected neutrophil-like signal despite density-gradient isolation, consistent with low-density PMN-MDSCs. In contrast, tumors broadly repressed chemokines and innate immune mediators, yet upregulated prostate cancer-associated lncRNAs, indicating local immune quiescence coupled with non-coding regulatory programs. Recurrent tumors acquired epithelial–mesenchymal transition and metabolic remodeling, accompanied by relapse-associated lncRNA signatures, whereas long-term nonrecurrent tumors preserved epithelial and stress-response networks. High-dimensional cytometry confirmed discrete, cancer-enriched myeloid clusters expressing CD47, SIRPα, PD-L1, CD73, and Galectin-9. Network analysis highlighted inflammatory hubs (CXCL2, PTGS2) in PBMCs and loss of mechanotransduction modules in tumors. Structural modeling uncovered a three-way junction and 3′ triple helix in lncRNA. Collectively, these data suggest that circulating inflammatory rewiring is associated with checkpoint-rich suppressor expansion and tumor immune quiescence, outlining integrated myeloid- and RNA-directed strategies for cancer research.

Inflammation is the immune system’s first biological response to infection, injury, or irritation. Evidence suggests that the anti-inflammatory effect is mediated by the regulation of various inflammatory cytokines, such as nitric oxide, interleukins, tumor necrosis factor alpha-α, interferon gamma-γ, as well as the non-cytokine mediator, prostaglandin E2. Currently, the mechanism of action and clinical usefulness of phytochemicals is known; their action on the activity of cytokines, free radicals, and oxidative stress. The latter are of great relevance in the development of diseases, such that the evidence collected demonstrates the beneficial effects of phytochemicals in maintaining health. Epidemiological evidence indicates that regular consumption of fruits and vegetables is related to a low risk of developing cancer and other chronic diseases.

Cardiovascular disease is a major cause of death among people living with HIV (PLH). Non-treated PLH show increased levels of inflammation and biomarkers of vascular activation, and arterial stiffness as a prognostic cardiovascular disease risk factor. We investigated the effect of one year of ART on treatment-naïve HIV(+) individuals on arterial stiffness and inflammatory and vascular cytokines. We cross-sectionally compared aortic stiffness via tonometry, inflammatory, and vascular serum cytokines on treatment-naïve (n = 20) and HIV (-) (n = 9) matched by age, sex, metabolic profile, and Framingham score. We subsequently followed young, treatment-naïve individuals after 1-year of ART and compared aortic stiffness, metabolic profile, and inflammatory and vascular serum biomarkers to baseline. Inflammatory biomarkers included: hs-CRP, D-Dimer, SAA, sCD163s, MCP-1, IL-8, IL-18, MRP8/14. Vascular cytokines included: myoglobin, NGAL, MPO, Cystatin C, ICAM-1, VCAM-1, and MMP9. Treatment-naïve individuals were 34.8 years old, mostly males (95%), and with high smoking prevalence (70%). Baseline T CD4+ was 512±324 cells/mcL. cfPWV was similar between HIV(-) and treatment-naïve (6.8 vs 7.3 m/s; p = 0.16) but significantly decreased after ART (-0.52 m/s; 95% CI -0.87 to -0.16; p0.006). Almost all the determined cytokines were significantly higher compared to controls, except for MCP-1, myoglobin, NGAL, cystatin C, and MMP-9. At follow-up, only total cholesterol and triglycerides increased and all inflammatory cytokines significantly decreased. Regarding vascular cytokines, MPO, ICAM-1, and VCAM-1 showed a reduction. D-Dimer tended to decrease (p = 0.06) and hs-CRP did not show a significant reduction (p = 0.17). One year of ART had a positive effect on reducing inflammatory and vascular cytokines and arterial stiffness.

Chronic periodontitis (CP), caused by bacteria and fungi, appears in up to 66% of HIV-patients. The impact and association of HIV-treatment (HAART) and itself has not been properly evaluated in the development and progression of CP. The immunopathogenesis is characterized by CD4 T-cells activation and the balance between the T-helper 1 (Th1) and T-helper 2 (Th2) or a mixed cytokine profile. Currently, the associated causes of an immune response in HIV-patients with CP is controversial. Our aims were the determination of spp. and cytokine profile in oral samples from HIV-positive patients with CP, considering the CD4 T cells levels and HAART use. From 500 HIV-positive patients evaluated, 228 patients were enrolled. Patients were separated in groups: (A) = 53 (≤200 CD4 T-cells on HAART); (B) = 57 (≤200 CD4 T-cells without HAART); (C) = 50 (>200 CD4 T-cells without HAART); (D) = 68 (>200 CD4 T-cells on HAART). spp. were isolated from the oral biofilm and crevicular fluid in CHROMagar and confirmed by endpoint PCR. Cytokine levels were measured by beads-based immunoassay in saliva by flow cytometry. 147 patients (64.5%) were positive to . and 204 strains were isolated; 138 (67.6%) were and the remaining species ( > > > . In this study, CHROMagar showed good sensitivity (95%) but poor specificity (68%); since of the 152 samples identified as , only 131 were confirmed by PCR; from the 10 samples identified as , only six were confirmed. Finally, of the 42 samples detected as , only five were confirmed. When evaluating spp. presence, group A and D had higher isolation, while group B had the highest species diversity. Whereas, group C had a significant reduction of spp. Despite the presence of and HAART, we found a Th1/Th2 hybrid profile in the saliva of patients with low CD4 T-cell count (group A). Abundance and diversity of the spp. detected in HIV-patients with CP could be related to HAART and low CD4 T-cells levels. Also, the immunosuppression might promote a local Th1/Th2 hybrid cytokine profile.

Background The study of stool microbiota has taken great relevance in the last years, given its role in the maintenance of the intestinal metabolic, physiological, and immunological homeostasis, as well as, its effect over HIV biomarkers levels such as CD4/CD8 ratio, high sensitivity C-Reactive Protein (hs-CRP), related to poor outcomes (rapid progression to AIDS). Several efforts have been made to characterize the gut microbiome. In HIV infection, most of the studies report the presence of a dysbiotic pattern; however, few of them have made an approach in elderly HIV-positive subjects despite the fact that nowadays this subgroup is rising. In this study, we compared the composition of faecal microbiota, Short Chain Fatty Acids (SCFAs), and systemic biomarkers between elderly HIV-positive and HIV-negative subjects. Methods A cross-sectional study with 18 HIV-negative controls and 20 HIV-positive patients. The quantification of Bacteroidetes, Firmicutes, Proteobacteria, Actinobacteria, Lactobacillus , Enterobacteriaceae, Bifidobacterium , Escherichia coli, Clostridium leptum, Clostridium coccoides was performed in faecal samples by qPCR. The analysis was performed by calculating the ΔCq of each microorganism using 16S rDNA as a reference gene. Faecal SCFAs were measured by HPLC. The hs-CRP and sCD14 were performed by ELISA. Results An increase in the Firmicutes/Bacteroidetes ratio, coupled with a significant increase in the proteobacteria phylum was detected in HIV-positive subjects. In contrast, a decrease in the Clostridium leptum group was observed . Nevertheless, these elderly HIV-positive patients showed higher levels of total SCFAs mainly by an augmented propionic acid values, compared to HIV-negative subjects. Whereas high levels of hs-CRP were positively correlated with sCD14 in the HIV-positive group. Conclusions Alterations in bacterial communities reveals a dysbiotic state related to an unbalance of faecal SCFAs. Therefore, these intestinal conditions might drive an increase of poor prognostic biomarkers in elderly HIV-positive subjects.

Background The CKD in PLHIV is highly prevalent in Jalisco. Despite its control with ART, HIV is characterized by generating low-grade inflammation events that contribute to the development and progression of CKD. Considering the importance of hs-CRP in the context of CKD, various genetic predisposition studies have been conducted to search for variants of the CRP gene, among which the SNV rs2808630 has been associated with serum hs-CRP concentrations and progression of CKD. Due to the above, there is interest in studying this SNV, addressing the limited information available on this topic in Mexico. Methods The case-control study included 163 patients with CKD, 102 PLHIV with CKD under ART with undetectable viral loads from the Hospital Civil of Guadalajara “Fray Antonio Alcalde” and 115 controls. Clinical assessment and general laboratory studies were carried out. Also, serum quantification of inflammatory biomarkers was performed by ELISA method. The determination of CRP SNV rs2808630 by qPCR and the association with inflammatory biomarkers was evaluated. Statistical analysis was carried out considering significant values p  < 0.05. Results Lower prevalence of CC genotype was shown in our population. Of the 358 samples, 221 (61.7%) present the wild-type genotype. The results analyzed correspond with what has been reported worldwide in studies of CRP SNV rs2808630 in the development of CKD without having a relationship with inflammatory and kidney function biomarkers. However, higher creatinine and IL-6 concentrations were observed in the group with the CC genotype. A significant correlation between IL-6 and eGFR was identified in CKD patients, but not for PLHIV with CKD, highlighting a potential difference in inflammatory dynamics between these groups. Importantly, in PLHIV with CKD, we found a strong correlation between hs-CRP and IL-8, suggesting a possible association with a higher proportion of the inflammatory isoform of hs-CRP, which may have implications for disease progression and cardiovascular risk. Conclusions The presence of the CRP SNV does not appear to contribute to the development of CKD and has no association with inflammatory biomarkers. Though, genetically independent manner, hs-CRP levels are slightly different between groups and are underrated when related to the CKD stage in PLHIV. Also, high IL-6 concentrations are related to CKD progression, while IL-8 seems to have a better relation to CKD in PLHIV.

Antiretroviral therapies (ART) are strongly associated with weight gain and metabolic syndrome (MetS) development in HIV-infected patients. Few studies have evaluated the association between gut microbiota and integrase strand transfer inhibitor (INSTI)-based and protease inhibitor (PI)-based regimens in HIV-infected patients with MetS. To assess this, fecal samples were obtained from HIV-infected patients treated with different regimens (16 PI + MetS or 30 INSTI + MetS) and 18 healthy controls (HCs). The microbial composition was characterized using 16S rRNA amplicon sequencing. The INSTI-based and PI-based regimens were associated with a significant decrease in α-diversity compared to HCs. The INSTI + MetS group showed the lowest α-diversity between both regimens. A significant increase in the abundance of short-chain fatty acid (SCFA)-producing genera (Roseburia, Dorea, Ruminococcus torques, and Coprococcus) was observed in the PI + MetS group, while Prevotella, Fusobacterium, and Succinivibrio were significantly increased in the INSTI + MetS group. Moreover, the Proteobacteria/Firmicutes ratio was overrepresented, and functional pathways related to the biosynthesis of LPS components were increased in the INSTI + MetS group. The gut microbiota of patients receiving INSTIs showed a more pronounced dysbiosis orchestrated by decreased bacterial richness and diversity, with an almost complete absence of SCFA-producing bacteria and alterations in gut microbiota functional pathways. These findings have not been previously observed.

Acute pancreatitis (AP) is one of the gastrointestinal pathologies that most frequently requires hospital admission; about half of all deaths occur within the first two weeks and are caused by multi-organ failure. Predicting the degree of severity of AP before 48 h is a challenge. Background/Objectives: Having an early marker, before 48 h after admission, could be useful to avoid or diagnose early complications such as organ failure (OF). A few sentences could place the question addressed in a broader context and highlight the purpose of the study. Methods: A retrospective study conducted in a third-level hospital, during the period from August 2019 to June 2021. Patients aged >18 years, with a diagnosis of PA, who had a complete clinical history and complete biochemical and imaging data were included. The scores of the APACHE II, BISAP, revised Atlanta classification, and modified Marshall scales were recorded. Results: Of the 103 patients included, 60% were women, the mean age was 47.76 years, and the hospital stay was 8 days (IQR 6–12); the most frequent etiology was biliary in 46 (44.7%) patients; the most frequent BMI was overweight with 34 (33%) patients; and 38 (36.9%) patients had a systemic inflammatory response at admission. Hypoalbuminemia was observed in 34 (33%) of the 103 patients at admission; of these, 42 (40.8%) had an APACHE II score > 8 points, 17 (16.3%) a BISAP score > 2, 57 (54.8%) patients were classified as moderate AP according to the revised Atlanta classification, and 54 patients had a score according to the modified Marshall score > 2. A statistically significant difference in the development of death was observed between patients with hypoalbuminemia versus those with normal serum albumin levels. Conclusions: In this study, we show the usefulness of hipoalbuminemia (<3.5 g/dL) at hospital admission in patients with AP, as a severity and mortality indicator. With the results obtained, we conclude that low albumin levels are a good predictor of severity and are useful for establishing timely treatment and close follow-up.

Background HIV subjects have several kidney pathologies, like HIV-associated nephropathy or antiretroviral therapy injury, among others. The global prevalence of Chronic Kidney Disease (CKD) is 8–16%; however, in HIV subjects, the prevalence varies between geographic regions (2–38%). The aim was to determine the prevalence of CKD and identify the associated risk factors. Methods A longitudinal descriptive study was carried out at the 'Hospital Civil de Guadalajara' Feb'18 – Jan'19. Basal clinical, demographic, opportunistic infections (OI), and laboratory data were obtained at months 0 and 3; inclusion criteria were ≥ 18 years old, naïve HIV + , urine albumin/creatinine ratio, serum creatinine & urine test, and signed informed consent. Descriptive and multiple logistic regression statistical analyses were made. Results One hundred twenty subjects were included; 92.5% were male, 33 ± 9.5 years, 60% consumed tobacco, 73% alcohol, and 59% some type of drug. The CKD prevalence was 15.8%. CKD patients had a higher risk of hepatitis C virus coinfection, Relative Risk (RR):5.9; HCV infection, RR:4.3; ≥ 30 years old, RR:3.9; C clinical-stage, RR:3.5; CD4 +  T cells count < 200 cells/μL, RR: 2.4; and HIV-1 viral load ≥ 100,000 cop/mL, RR: 2.7. Conclusions Our study showed a higher CKD prevalence in patients with HIV; higher CKD development with coinfections as Hepatitis C Virus and Mycobacterium tuberculosis . The identification and prompt management of CKD and coinfections should be considered to avoid the progression and to delay renal replacement therapy as long as possible.