Laura I. Levi

Historically, women have been shown to underestimate their abilities, while men often assess themselves more accurately or overestimate. This study aims to determine self-assessment accuracy during online Objective Structured Clinical Examinations (OSCEs) according to gender. A prospective study was conducted among fourth-year medical students at Paris Cité University during faculty training OSCEs, utilizing Zoom® software for remote participation. Students and evaluators assessed performances using 5-point Likert scales for medical knowledge, interpersonal skills, and overall performance. Additionally, students predicted their grade out of twenty. The assessment covered three independent stations. This study included 259 medical students (177 women, 81 men, one non-binary (excluded from further analyses)) evaluated by 130 physicians. Evaluator scores did not differ according to students’ gender (total score out of 20: men: 10.25 ± 3.45, women: 10.23 ± 3.44 p = 0.817) nor students’ self-assessments (total score out of 20: men: 11.22 ± 3.02, women: 11.00 ± 3.03; p = 0.466) whatever the domains and stations (all p > 0.05). The difference (delta) between self-assessment and evaluator scores for medical knowledge (men: 0.73 ± 1.00, women: 0.64 ± 1.02; p = 0.296), interpersonal skills (men: 1.02 ± 1.06, women: 0.93 ± 1.09; p = 0.296), and total score (men: 0.98 ± 3.41, women: 0.68 ± 3.42; p = 0.296) showed no gender differences. Further analysis categorized students based on their self-assessment accuracy, revealing that both men and women displayed a high ratio of accurate self-assessments (78.1% for overall performance across all stations), with minimal overestimation observed in both genders (20.9% for overall performance across all stations). Instances of overestimation or underestimation were rare and not consistent over the 3 stations, indicating that such misjudgments are likely situational rather than inherent traits. This study reveals similar self-assessment accuracy according to gender in online training OSCEs suggesting a shift towards gender-equitable self-perceptions among medical students compared to previous studies. Research remains necessary to corroborate these results and explore the underlying factors contributing to this shift in self-perception.

Chikungunya virus (CHIKV) is a mosquito-borne RNA virus that poses an emerging threat to humans. In a manner similar to other RNA viruses, CHIKV encodes an error-prone RNA polymerase which, in addition to producing full-length genomes, gives rise to truncated, non-functional genomes, which have been coined defective viral genomes (DVGs). DVGs have been intensively studied in the context of therapy, as they can inhibit viral replication and dissemination in their hosts. In this work, we interrogate the influence of viral RNA secondary structures on the production of CHIKV DVGs. We experimentally map RNA secondary structures of the CHIKV genome using selective 2′-hydroxyl acylation analyzed by primer extension and mutational profiling (SHAPE-MaP), which couples chemical labelling with next-generation sequencing. We correlate the inferred secondary structure with preferred deletion sites of CHIKV DVGs. We document an increased probability of DVG generation with truncations at unpaired nucleotides within the secondary structure. We then generated a CHIKV mutant bearing synonymous changes at the nucleotide level to disrupt the existing RNA secondary structure (CHIKV-D2S). We show that CHIKV-D2S presents altered DVG generation compared to wild-type virus, correlating with the change in RNA secondary structure obtained by SHAPE-MaP. Our work thus demonstrates that RNA secondary structure impacts CHIKV DVG production during replication.

Chikungunya virus (CHIKV) is a mosquito borne RNA virus that poses an emerging threat to humans. As other RNA viruses, CHIKV encodes an error-prone RNA polymerase which, in addition to full-length genomes, gives rise to truncated, non-functional genomes coined defective viral genomes (DVGs). DVGs have been intensively studied in the context of therapy, as they can inhibit viral replication and dissemination in their hosts. In this work, we interrogate the influence of viral RNA secondary structures on the production of CHIKV DVGs. We experimentally map RNA secondary structures of CHIKV genome using selective 2′-hydroxyl acylation analyzed by primer extension and mutational profiling (SHAPE-MaP), which couples chemical labelling with next-generation sequencing. We correlate the inferred secondary structure with preferred deletion sites of CHIKV DVGs. We document an increased probability of DVG generation with truncations at unpaired nucleotides within the secondary structure. We then generated a CHIKV mutant bearing synonymous changes at the nucleotide level to disrupt existing RNA secondary structure (CHIKV-D2S). We show that CHIKV-D2S presents altered DVG generation compared to wild-type virus, correlating with its change in RNA secondary structure obtained by SHAPE-MaP. Our work thus demonstrates that RNA secondary structure impacts CHIKV DVG production during replication.

We describe a case of healthcare-associated bloodstream infection due to Mycobacterium fortuitum. Whole-genome sequencing showed that the same strain was isolated from the shared shower water of the unit. Nontuberculous mycobacteria frequently contaminate hospital water networks. Preventative actions are needed to reduce the exposure risk for immunocompromised patients.

Cytomegalovirus (CMV) viremia in persons with human immunodeficiency virus (HIV) reflects the level of immunodeficiency. In the absence of CMV end-organ disease, early start of effective antiretroviral therapy is the only treatment required and is most often sufficient to control CMV replication.

Objective: The aim of this study was to assess the prevalence of cytomegalovirus (CMV) viremia in HIV-positive patients starting antiretroviral therapy (ART) and to evaluate its impact on clinical outcomes. Design: A retrospective analysis of four clinical trials (INSIGHT FIRST, SMART, START, and ANRS REFLATE TB). Methods: Stored plasma samples from participants were used to measure CMV viremia at baseline prior to initiating ART and at visits through 1 year of follow-up after ART initiation. CMV viremia was measured centrally using a quantitative PCR assay. Within FIRST, associations of CMV viremia at baseline and through 8 months of ART were examined with a composite clinical outcome of AIDS, serious non-AIDS events, or death using Cox proportional hazards regression. Results: Samples from a total of 3176 participants, 1169 from FIRST, 137 from ANRS REFLATE TB, 54 from SMART, and 1816 from START were available with baseline CMV viremia prevalence of 17, 26, 0, and 1%, respectively. Pooled across trials, baseline CMV viremia was associated with low CD4⁺ T-cell counts and high HIV RNA levels. In FIRST, CMV viremia was detected in only 5% of participants between baseline and month 8. After adjustment for CD4⁺ T-cell count and HIV RNA levels, hazard ratios for risk of clinical outcomes was 1.15 (0.86–1.54) and 2.58 (1.68–3.98) in FIRST participants with baseline and follow-up CMV viremia, respectively. Conclusion: Baseline CMV viremia in HIV-positive patients starting ART is associated with advanced infection and only persistent CMV viremia after ART initiation is associated with a higher risk of morbidity and mortality.

Arthropod-borne viruses pose a major threat to global public health. Thus, innovative strategies for their control and prevention are urgently needed. Here, we exploit the natural capacity of viruses to generate defective viral genomes (DVGs) to their detriment. While DVGs have been described for most viruses, identifying which, if any, can be used as therapeutic agents remains a challenge. We present a combined experimental evolution and computational approach to triage DVG sequence space and pinpoint the fittest deletions, using Zika virus as an arbovirus model. This approach identifies fit DVGs that optimally interfere with wild-type virus infection. We show that the most fit DVGs conserve the open reading frame to maintain the translation of the remaining non-structural proteins, a characteristic that is fundamental across the flavivirus genus. Finally, we demonstrate that the high fitness DVG is antiviral in vivo both in the mammalian host and the mosquito vector, reducing transmission in the latter by up to 90%. Our approach establishes the method to interrogate the DVG fitness landscape, and enables the systematic identification of DVGs that show promise as human therapeutics and vector control strategies to mitigate arbovirus transmission and disease.