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Sexual trauma is common. Consequences of sexual trauma can include deterioration of mental and physical health and it can also affect future romantic and sexual relationships. Previous studies have identified common healthy and destructive coping mechanisms to recover after experiencing sexual trauma, but few studies have investigated useful strategies to move into a healthy sexual relationship focused on resilience. In-depth semi-structured interviews were conducted with 41 women with a history of sexual trauma who were in a healthy sexual relationship at the time of participation. Participants provided strategies that helped them move beyond the sexually traumatic event(s) toward a healthy sexual relationship. Reflexive thematic analysis identified 5 effective and 6 ineffective strategies reported by the participants. Rich examples of resilience and empowerment were overarching in the effective strategies used for moving toward healthy sexual relationships. Women were also able to reflect on the strategies that were ineffective for them with kindness and understanding for their coping at that time, a normalizing theme for women working through sexual trauma. The results of this study will help therapists and researchers working with women who have experienced sexual trauma learn from their experiences in working beyond trauma toward a healthy sexual relationship., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2023 Mark et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Gastroenteritis caused by bacterial and viral pathogens constitutes a major public health threat in the United States accounting for 35% of hospitalizations. In particular, Salmonella enterica and noroviruses cause the majority of gastroenteritis infections, with emergence of sporadic outbreaks and incidence of increased infections. Although mechanisms underlying infections by these pathogens have been individually studied, little is known about the mechanisms regulating co-infection by these pathogens. In this study, we utilized RAW 264.7 murine macrophage cells to investigate the mechanisms governing co-infection with S. enterica serovar Heidelberg and murine norovirus (MNV). We demonstrate that infection of RAW 264.7 cells with S. enterica reduces the replication of MNV, in part by blocking virus entry early in the virus life cycle, and inducing antiviral cytokines later in the infection cycle. In particular, bacterial infection prior to, or during MNV infection affected virus entry, whereas MNV entry remained unaltered when the virus infection preceded bacterial invasion. This block in virus entry resulted in reduced virus replication, with the highest impact on replication observed during conditions of co-infection. In contrast, bacterial replication showed a threefold increase in MNV-infected cells, despite the presence of antibiotic in the medium. Most importantly, we present evidence that the infection of MNV-infected macrophages by S. enterica blocked MNV-induced apoptosis, despite allowing efficient virus replication. This apoptosis blockade was evidenced by reduction in DNA fragmentation and absence of poly-ADP ribose polymerase (PARP), caspase 3 and caspase 9 cleavage events. Our study suggests a novel mechanism of pathogenesis whereby initial co-infection with these pathogens could result in prolonged infection by either of these pathogens or both together.