Background: This study examined the impact of age-adjusted cerebrospinal fluid (CSF) protein levels on clinical characteristics, disease severity, and outcomes in Guillain–Barré Syndrome (GBS) patients. Methods: This retrospective study included 71 GBS patients at UTMB Galveston. Albuminocytologic dissociation (ACD) was defined as CSF–total protein (CSF-TP) >0.45 g/L with a cell count of 0.45 g/L) and age-adjusted upper limits (URLs) for CSF-TP levels, comparing clinical, CSF, and electrophysiological characteristics across groups. Results: The mean age was 50 years (SD = 14.5). The mean age of patients with a CSF-TP > 45 g/L was higher (53 vs. 39 years, p = 0.000), whereas no such difference was noted using age-dependent URLs. Using age-adjusted CSF-TP URLs reduced the sensitivity for detecting ACD by 20%. CSF-TP > age-adjusted URLs were associated with lower MRC sum scores (39 vs. 47.43, p = 0.000), higher ICU admission rates (34% vs. 20%, p = 0.003), and the need for second-line treatment (41% vs. 17%, p = 0.049), and the trends were not observed with the conventional cutoff of 0.45 g/L. CSF-TP was an independent predictor of lower MRC sum scores (p = 0.009, 95% CI −0.058, −0.009) and higher GBS disability scores (p = 0.015, 95% CI 0.000, 0.004). Conclusions: ACD is a common finding in GBS, but normal protein levels do not exclude the diagnosis. Using age-adjusted URLs might improve specificity but reduce sensitivity for ACD detection, potentially increasing false negatives. CSF-TP levels exceeding age-adjusted URLs were more strongly associated with greater disease severity and poorer outcomes compared to the conventional cutoff of 0.45 g/L.

Respiratory syncytial virus (RSV) is a leading cause of lower respiratory tract infections in infants, young children, and immunocompromised individuals. Currently, FDA-approved monoclonal antibody therapies are limited to infants and young children with severe RSV disease. As a result, there is an urgent need for comprehensive studies of RSV pathogenesis to support the development of new therapeutic strategies. Exchange proteins directly activated by cAMP (EPAC) have recently emerged as key regulators in various viral infections. Our previous work identified EPAC isoform 2 (EPAC2) as a critical factor in RSV replication and host innate immune responses. However, the molecular mechanisms underlying EPAC2’s role in RSV infection remain unclear. In this study, we investigated EPAC2-mediated RSV infection by identifying EPAC2-interacting proteins. Proteomics and immunoprecipitation analyses revealed that junction plakoglobin (JUP) interacts with EPAC2 in both mock- and RSV-infected cells, with this interaction notably enhanced during RSV infection. To determine JUP’s role in RSV infection, we compared viral replication in JUP-deficient and control cells. JUP downregulation significantly reduced the production of infectious RSV particles, likely by impairing viral budding and viral gene transcription. Moreover, our findings indicate that JUP is essential for an effective cellular immune response to RSV infection. Together, these results suggest that EPAC2 and JUP may cooperatively regulate RSV replication and dissemination.