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Objectives: Patients in cognitive behavioural therapy (CBT) who are high in interpersonal sensitivity may have difficulty fully engaging in treatment because therapy sessions require intimate interpersonal interactions that are especially uncomfortable for these individuals. The current study tests the hypotheses that patients who are high in interpersonal sensitivity benefit less from CBT for symptoms of depression and anxiety, show a slower rate of change in those symptoms, and are more likely to drop out of treatment. Methods: Participants were 832 outpatients who received naturalistic CBT. We assessed interpersonal sensitivity before treatment began and depression and anxiety symptoms at every therapy session. We assessed early, premature, and uncollaborative termination after treatment ended. We constructed multilevel linear regression models and logistic regression models to assess the effects of baseline interpersonal sensitivity on the treatment outcome, the slope of change in depression and anxiety symptoms, and each type of dropout. Results: Higher baseline interpersonal sensitivity was associated with a slower rate of change and less overall change in anxiety but not depressive symptoms. Baseline interpersonal sensitivity was not a predictor of dropout. Conclusions: Interpersonal sensitivity at baseline predicts less change and a slower rate of change in anxiety symptoms. Early detection of elevated interpersonal sensitivity can help therapists take action to address these barriers to successful treatment and help scientists build decision support tools that accurately predict the trajectory of change in anxiety symptoms for these patients. [ABSTRACT FROM AUTHOR]

Nipah virus (NiV) is a highly lethal zoonotic virus with a potential large-scale outbreak, which poses a great threat to world health and security. In order to explore more potential factors associated with NiV, a proximity labeling method was applied to investigate the F, G, and host protein interactions systematically. We screened 1996 and 1524 high-confidence host proteins that interacted with the NiV fusion (F) glycoprotein and attachment (G) glycoprotein in HEK293T cells by proximity labeling technology, and 863 of them interacted with both F and G. The results of GO and KEGG enrichment analysis showed that most of these host proteins were involved in cellular processes, molecular binding, endocytosis, tight junction, and other functions. Cytoscape software (v3.9.1) was used for visual analysis, and the results showed that Cortactin (CTTN), Serpine mRNA binding protein 1 (SERBP1), and stathmin 1 (STMN1) were the top 20 proteins and interacted with F and G, and were selected for further validation. We observed colocalization of F-CTTN, F-SERBP1, F-STMN1, G-CTTN, G-SERBP1, and G-STMN1 using confocal fluorescence microscopy, and the results showed that CTTN, SERBP1, and STMN1 overlapped with NiV F and NiV G in HEK293T cells. Further studies found that CTTN can significantly inhibit the infection of the Nipah pseudovirus (NiVpv) into host cells, while SERBP1 and STMN1 had no significant effect on pseudovirus infection. In addition, CTTN can also inhibit the infection of the Hendra pseudovirus (HeVpv) in 293T cells. In summary, this study revealed that the potential host proteins interacted with NiV F and G and demonstrated that CTTN could inhibit NiVpv and HeVpv infection, providing new evidence and targets for the study of drugs against these diseases. [ABSTRACT FROM AUTHOR]

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging tick‐borne hemorrhagic fever disease with high fatality rate of 10%–20%. Vaccines or specific therapeutic measures remain lacking. Human interferon inducible transmembrane protein 3 (hIFITM3) is a broad‐spectrum antiviral factor targeting viral entry. However, the antiviral activity of hIFITM3 against SFTS virus (SFTSV) and the functional mechanism of IFITM3 remains unclear. Here we demonstrate that endogenous IFITM3 provides protection against SFTSV infection and participates in the anti‐SFTSV effect of type Ⅰ and Ⅲ interferons (IFNs). IFITM3 overexpression exhibits anti‐SFTSV function by blocking Gn/Gc‐mediated viral entry and fusion. Further studies showed that IFITM3 binds SFTSV Gc directly and its intramembrane domain (IMD) is responsible for this interaction and restriction of SFTSV entry. Mutation of two neighboring cysteines on IMD weakens IFITM3‐Gc interaction and attenuates the antiviral activity of IFITM3, suggesting that IFITM3‐Gc interaction may partly mediate the inhibition of SFTSV entry. Overall, our data demonstrate for the first time that hIFITM3 plays a critical role in the IFNs‐mediated anti‐SFTSV response, and uncover a novel mechanism of IFITM3 restriction of SFTSV infection, highlighting the potential of clinical intervention on SFTS disease. [ABSTRACT FROM AUTHOR]