Viviane Schuch

Black and African American women in the United States experience disproportionately high rates of maternal and infant mortality and morbidity, including placenta-mediated complications such as preeclampsia, preterm birth, and miscarriage. These inequities arise from the interaction of social and environmental conditions with biological pathways that become embedded over the life course, with the placenta serving as a central mediator. In this review, we examine how placental biology integrates genetic variation, epigenetic regulation, paternal contributions, immune processes, and lived social context to shape pregnancy outcomes. We synthesize evidence showing that placental dysfunction, particularly immune dysregulation driven by infectious, environmental, and psychosocial stressors, contributes to placenta-mediated complications with disproportionate impacts among African American women. We highlight how reliance on racial categories in U.S. biomedical research can obscure biological inference and argue for ancestry-informed approaches, alongside self-identified ethnicity, to disentangle inherited genetic variation from socially patterned exposures. Surveying published genome-wide association studies, we show that underrepresentation of African-ancestry populations remains a major constraint on discovery and translation in pregnancy genomic research. We further describe how placental epigenetic mechanisms link socioeconomic and environmental exposures to fetal development, placental aging, and long-term maternal–child health. Finally, we discuss how pregnancy and placental datasets remain sparse and fragmented, and consider how machine-learning approaches may improve pregnancy risk prediction when designed with equity in mind, by integrating placental multi-omics, ancestry-aware genomics, clinical data, and social determinants. Together, this review positions the placenta as a critical interface through which structural inequities shape maternal–fetal health and identifies priorities for more inclusive and equitable research and health care.

Viral infections continue to pose significant global health challenges, with pathogens like Dengue Virus (DENV), Chikungunya Virus (CHIKV), Yellow Fever Virus (YFV), Human Immunodeficiency Virus (HIV), and Influenza Virus (FLU) contributing to widespread morbidity and mortality. A comprehensive understanding of the host immune response to these infections is crucial for developing more effective diagnostics, treatments, and vaccines. In this study, we conducted a meta-analysis of transcriptomic datasets from whole blood and peripheral blood mononuclear cell (PBMC) samples of individuals infected with DENV, CHIKV, YFV, HIV, and FLU. Utilizing a systems biology approach, we identified both shared and virus-specific molecular mechanisms underlying immune responses to these infections. Several key genes, including OAS2, MX1, and IFI44L, were consistently up-regulated across multiple viral infections, highlighting their roles in antiviral defense, immune modulation, and cellular stress responses. Additionally, virus-specific genes such as TNFSF10 and NT5C3A were found to be uniquely up-regulated in arboviruses, underscoring the distinct immune pathways activated by different viral families. Our co-expression network analysis revealed coordinated gene expression patterns across different viral infections, offering insights into conserved molecular networks that could inform the development of broad-spectrum antiviral therapies. Despite challenges related to biological heterogeneity and variations in study design, this meta-analysis provides a foundation for future research aimed at unraveling the complex immune mechanisms that govern host-pathogen interactions.

Chikungunya virus (CHIKV) has become a significant public health concern due to the increasing number of outbreaks worldwide and the associated comorbidities. Despite substantial efforts, there is no specific treatment or licensed vaccine against CHIKV to date. The E2 glycoprotein of CHIKV is a promising vaccine candidate as it is a major target of neutralizing antibodies during infection. In this study, we evaluated the immunogenicity of two DNA vaccines (a non-targeted and a dendritic cell-targeted vaccine) encoding a consensus sequence of E2_CHIKV and a recombinant protein (E2*_CHIKV). Mice were immunized with different homologous and heterologous DNAprime-E2* protein boost strategies, and the specific humoral and cellular immune responses were accessed. We found that mice immunized with heterologous non-targeted DNA prime- E2*_CHIKV protein boost developed high levels of neutralizing antibodies, as well as specific IFN-γ producing cells and polyfunctional CD4⁺ and CD8⁺ T cells. We also identified 14 potential epitopes along the E2_CHIKV protein. Furthermore, immunization with recombinant E2*_CHIKV combined with the adjuvant AS03 presented the highest humoral response with neutralizing capacity. Finally, we show that the heterologous prime-boost strategy with the non-targeted pVAX-E2 DNA vaccine as the prime followed by E2* protein + AS03 boost is a promising combination to elicit a broad humoral and cellular immune response. Together, our data highlights the importance of E2_CHIKV for the development of a CHIKV vaccine.