Dengue (DENV) and Chikungunya (CHIKV) viruses can be transmitted simultaneously by Aedes mosquitoes, and there may be co-infections in humans. However, how the adaptive immune response is modified in the host has yet to be known entirely. In this study, we analyzed the cross-reactivity and neutralizing activity of IgG antibodies against DENV and CHIKV in sera of patients from the Mexican Institute of Social Security in Veracruz, Mexico, collected in 2013 and 2015 and using IgG antibodies of BALB/c mice inoculated with DENV and/or CHIKV. Mice first inoculated with DENV and then with CHIKV produced IgG antibodies that neutralized both viruses. Mice were inoculated with CHIKV, and then with DENV; they had IgG antibodies with more significant anti-CHIKV IgG antibody neutralizing activity. However, the inoculation only with CHIKV resulted in better neutralization of DENV2. In sera obtained from patients in 2013, significant cross-reactivity and low anti-CHIKV IgG antibody neutralizing activity were observed. In CHIKV-positive 2015 sera, the anti-DENV IgG antibody neutralizing activity was high. These results suggest that CHIKV stimulates DENV2-induced memory responses and vice versa. Furthermore, cross-reactivity between the two viruses generated neutralizing antibodies, but exchanging CHIKV for DENV2 generated a better anti-CHIKV neutralizing response.

Chikungunya fever (CHIKV) has reemerged as a serious global health problem worldwide. Currently, no antiviral drugs are available for the prevention or treatment of CHIKV infection. Therefore, this study aimed to analyze the anti-CHIKV potential of the alga Spirulina maxima. Extracts were obtained by maceration using solvents of different polarities (hexane, dichloromethane, and methanol). The cytotoxic activity of the extracts was evaluated using the MTT assay, which demonstrated that none of the extracts had a cytotoxic effect on VERO and BJ cell lines. The anti-CHIKV effect was evaluated using a plate assay with VERO, HepG2, and BJ cell lines. The results showed that the methanol extract had the best anti-CHIKV effect, completely inhibiting viral replication at a concentration of 15 µg/mL in all three cell lines. Furthermore, the addition time assay suggested that the mechanism of action is related to the inhibition of some processes at the beginning of the infection, such as the entry or early replication of the virus. In conclusion, SP contains molecules that could provide a basis for future research on the development of new drug therapies against CHIKV.

Cancer remains one of the leading causes of morbidity and mortality globally, driven by genetic alterations, uncontrolled cell proliferation, and metabolic reprogramming. The tumor microenvironment (TME) is a highly dynamic and heterogeneous system composed of tumor cells, immune cells, stromal cells, and extracellular matrix (ECM) components, which influence cancer progression. Tumor-associated macrophages (TAMs), especially those polarized into the M2 phenotype, play a critical role in modulating this environment. M2 macrophages promote tumor progression through mechanisms such as immune suppression, angiogenesis, and metastasis. This polarization is heavily influenced by the altered metabolic landscape of tumors, where the Warburg effect leads to excessive lactate production, which in turn drives M2 polarization through G protein-coupled receptor 132 (GPR132). M2 macrophages secrete cytokines like IL-10, transforming growth factor β (TGF-β), and vascular endothelial growth factor (VEGF), which contribute to immune escape, tumor growth, and metastasis. The metabolic shifts within TAMs, especially the transition from oxidative phosphorylation to glycolysis, further support the pro-tumoral functions of these cells. This review explores the intricate relationship between M2 macrophage polarization bias, tumor metabolism, and the resulting impact on cancer progression, highlighting the potential of targeting these pathways for therapeutic strategies. The findings suggest that M2 macrophage polarization could serve as a key prognostic factor for cancer outcomes and provide a basis for future research into therapeutic interventions that target macrophage polarization and the tumor metabolic milieu.

One of the greatest challenges in the study of coronavirus disease 2019 (COVID-19) has been to establish the determining factors in the severity of the disease. Through extensive research efforts, a crucial factor responsible for disease control or exacerbation in COVID-19 has been identified—the regulation of the immune response. The abnormal release of interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-α) has been extensively studied in the context of the altered immune response observed in severe cases of COVID-19. However, recent attention has turned towards the excessive release of IL-17 and the increased presence of T helper 17 (Th17) cells, the main secretory cells of this cytokine. These factors have garnered interest due to their potential involvement in the cytokine storm observed in severe cases of COVID-19. In this review, it will be delved into the intricate mechanisms by which IL-6 contributes to the differentiation of Th17 cells, resulting in an increase in the population of Th17 cells. Moreover, it will be explored the proportional relationship between the increase of these lymphocytes and the release of IL-17 and other chemokines, which all together play a key role in promoting the chemotaxis and activation of neutrophils. Ultimately, this cascade of events culminates in the generation of tissue damage by neutrophils. Additionally, therapeutic options targeting these lymphocytes and cytokines are explored, providing insights into potential avenues for intervention.