Journal of Medical Virology最新文献

Hepatic encephalopathy (HE) is an independent risk factor for mortality in patients with hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF). We aim to assess the effectiveness of 3D deep learning based on CT imaging in predicting HE in HBV-ACLF patients. A retrospective study was conducted on 222 HBV-ACLF patients who underwent CT scans at two medical centers. The cohort from Huashan Hospital, consisting of 146 patients, was randomly divided into a training cohort (n = 102) and a validation cohort (n = 44). An external test cohort (n = 76) was sourced from Shanghai Public Health Clinical Center. We employed two architectures, ResNet50 and DenseNet201, to extract 3D deep learning features related to HE. Classical radiomics features were extracted from liver CT images and modeled using three machine learning algorithms. Clinical features associated with HE were analyzed via multivariate logistic regression. The 3D deep learning model demonstrated strong performance in predicting HE in ACLF patients, particularly the ResNet50 model, which achieved AUC values of 0.844 (95% CI: 0.752-0.936) in the training cohort, 0.833 (95% CI: 0.671-0.996) in the validation cohort, and 0.833 (95% CI: 0.686-0.981) in the test cohort. Classical radiomics also demonstrated predictive potential, where XGBoost outperformed other algorithms. INR and ammonia levels were independently associated with HE. The nomogram model integrating 3D deep learning, radiomics features, and clinical predictors achieved the highest predictive accuracy across all cohorts. 3D deep learning performed excellently in predicting HE in ACLF patients, and its combination with radiomics and clinical features further enhanced predictive performance.

BK polyomavirus (BKPyV) can establish persistent infections in 90% of the healthy adult population, and its reactivation is associated with graft failure in kidney transplant patients. Ischemic injury (IS) increases the risk of viral reactivation, making BKPyV a primary cause of allograft failure. However, the detailed molecular mechanisms of IS that promote BKPyV replication are not well characterized. The aim of the study was to identify the critical pathways and hub genes involved in IS's promotion of polyomavirus replication based on single-cell RNA-seq and bulk RNA-seq data. We found that IS could activate the DNA damage response pathway to promote polyomavirus replication. Additionally, we identified CDK1 as a hub gene according to the conservation of gene expression pattern and key pathways in mice and humans. Subsequently, using siRNA experiments, we demonstrated that CDK1 knockdown inhibits BKPyV replication. Together, the present study found that IS could regulate the expression of CDK1 via the "DNA damage response" pathway to promote polyomavirus replication.

EXPRESSION OF CONCERN: P. Colson, P. Gautret, J. Delerce, H. Chaudet, P. Pontarotti, P. Forterre, R. Tola, M. Bedotto, L. Delorme, W. Bader, A. Levasseur, J.-C. Lagier, M. Million, N. Yahi, J. Fantini, B. La Scola, P.-E. Fournier, and D. Raoult, “The Emergence, Spread and Vanishing of a French SARS-CoV-2 Variant Exemplifies the Fate of RNA Virus Epidemics and Obeys the Mistigri Rule,” Journal of Medical Virology 95, no. 1 (2023): e28102, https://doi.org/10.1002/jmv.28102.

This Expression of Concern is for the above article, published online on 28 August 2022 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Hinh Ly; and Wiley Periodicals, LLC. The Expression of Concern has been agreed due to questions raised about the study's adherence to French legal and ethical requirements for research involving human subjects. The investigation into these concerns is ongoing. Therefore, the journal has decided to issue an Expression of Concern to inform and alert readers.

HTLV-1 infection is a chronic condition associated with the development of malignancies, inflammatory, and neurological disorders. In this study, the causes of hospitalization and mortality were assessed in a cohort of 508 individuals living with HTLV-1 followed over a 30-year period. Overall mortality was 8.5% in this population and increased to 15% among patients with HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a major neurological syndrome characterized by motor, sensory, and urinary dysfunction. Hospitalization was required by 147 participants of the cohort (28.9%), and this increased to 40.2% (121 of 301) among those with HAM/TSP. Patients were admitted at least once, with a mean of two admissions per patient. Hospitalization was associated with HAM/TSP, particularly the degree of motor disability and HIV coinfection. Infectious diseases were the leading cause of both hospitalization (66.7%) and death (69%), most commonly urinary tract infections, pneumonia, and infected pressure ulcers. In addition, mortality was also directly related to the intensity of motor impairment and the number of hospitalizations. HAM/TSP was associated with an increased risk of hospitalization and readmission. Additionally, greater motor impairment was linked to higher risks of both hospitalization and mortality, while elevated HTLV-1 PVL was found to contribute to an increased risk of death. In conclusion, these findings highlight the importance of prevention and timely management of secondary infections to reduce morbidity and mortality in individuals living with HTLV-1, particularly those affected by HAM/TSP, which frequently present urinary dysfunction and pressure ulcers.

EXPRESSION OF CONCERN: P. Colson, J. Delerce, P. Pontarotti, C. Devaux, B. La Scola, J. Fantini, and D. Raoult, “Resistance-Associated Mutations to the Anti-SARS-CoV-2 Agent Nirmatrelvir: Selection Not Induction,” Journal of Medical Virology 96, no. 2 (2024): e29462, https://doi.org/10.1002/jmv.29462.

This Expression of Concern is for the above article, published online on 16 February 2024 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Hinh Ly; and Wiley Periodicals, LLC. The Expression of Concern has been agreed due to questions raised about the study's adherence to French legal and ethical requirements for research involving human subjects. The investigation into these concerns is ongoing. Therefore, the journal has decided to issue an Expression of Concern to inform and alert readers.

Torquetenovirus load has been proposed as an immunomodulated biomarker of host immune status, yet its behavior in situ within HPV-infected mucosa remains poorly defined. We conducted a retrospective cross-sectional study of 220 patients undergoing HPV screening (181 cervical swabs, 39 anal brushings). HPV was genotyped with Allplex™ HPV28, and TTV load was quantified by in-house RT-qPCR and expressed as log₁₀ copies per 20 ng total DNA. Analyses included nonparametric group comparisons (Mann-Whitney) and site-stratified logistic regression to estimate the TTV-HPV association. Genotype co-occurrence was summarized by heatmaps and network analysis and formally tested with Fisher's exact test with Benjamini-Hochberg FDR correction. TTV load was higher in HPV-positive subjects (p < 0.01), with a significant difference in BR and a trend in CS. In a binary logistic model, each 1-log₁₀ increase in TTV was associated with a 60% increase in the odds of HPV positivity (OR = 1.60, 95% CI 1.07–2.39; p = 0.022), with consistent results across CS and BR. TTV load increased with greater genotypic complexity in co-infections (genotype richness) and was also higher in infections sustained exclusively by HR genotypes than by LR genotypes (p < 0.01). The co-occurrence map and network analysis highlighted recurrent genotype combinations (e.g., 16/53, 53/68, 42/53) and central nodes (16, 31, 51, 56, 68, 53). In situ quantification of TTV is associated with HPV positivity and with genotype complexity/risk class, offering local predictive power. The co-occurrence evidence remains exploratory but supports TTV as an indirect indicator of mucosal immunocompetence.