Alberto Rizzo, Davide Moschese, Federica Salari, Andrea Giacomelli, Andrea Cavallo, Maria Vittoria Cossu, Loriana Morelli, Chiara Fusetti, Giorgia Carrozzo, Serena Reato, Valeria Micheli, Spinello Antinori, Alessandra Lombardi, Andrea Gori, Maria Rita Gismondo
The association between human papillomavirus (HPV) and other sexually transmitted infections (STIs) in anal lesions still remains unclear. Aim of the study was to evaluate the prevalence of simultaneous infection of HPV and Chlamydia trachomatis, Neisseria gonorrhoeae, Mycoplasma genitalium, and Trichomonas vaginalis in individuals screened for HPV anal infection. A total of 507 anal samples were tested for both anal HPV and STIs: 16% resulted positive for one or more non-HPV STIs. Specifically, C. trachomatis, M. genitalium, and N. gonorrhoeae were detected in 8%, 5%, and 4% of cases, respectively. Two groups were considered, including a positive STI group and a negative STI group. The prevalence of HPV was similar in patients in both groups: high risk (HR)-HPV and low risk (LR)-HPV were 67% and 53% versus 62% (p = 0.361) and 54% (p = 0.864) of patients, respectively. However, HPV 16, 18, 35, 51, 59, and 69 were significantly more frequent in patients tested positive for other STIs versus HPV infection alone (p < 0.05). No significant differences between the two groups were observed in vaccination coverage, 28% versus 32% (p = 0.463), and HIV status, 86% versus 84% (p = 0.658). The study shows that the overall HPV status is not directly correlated to other STIs in the investigated population, except for certain HPV types, including HR-HPV 16, reinforcing the urge for a greater vaccination coverage.
{"title":"Anal HPV prevalence in individuals with and without other concomitant sexually transmitted infections","authors":"Alberto Rizzo, Davide Moschese, Federica Salari, Andrea Giacomelli, Andrea Cavallo, Maria Vittoria Cossu, Loriana Morelli, Chiara Fusetti, Giorgia Carrozzo, Serena Reato, Valeria Micheli, Spinello Antinori, Alessandra Lombardi, Andrea Gori, Maria Rita Gismondo","doi":"10.1002/jmv.29852","DOIUrl":"https://doi.org/10.1002/jmv.29852","url":null,"abstract":"<p>The association between human papillomavirus (HPV) and other sexually transmitted infections (STIs) in anal lesions still remains unclear. Aim of the study was to evaluate the prevalence of simultaneous infection of HPV and <i>Chlamydia trachomatis</i>, <i>Neisseria gonorrhoeae</i>, <i>Mycoplasma genitalium</i>, and <i>Trichomonas vaginalis</i> in individuals screened for HPV anal infection. A total of 507 anal samples were tested for both anal HPV and STIs: 16% resulted positive for one or more non-HPV STIs. Specifically, <i>C. trachomatis</i>, <i>M. genitalium</i>, and <i>N. gonorrhoeae</i> were detected in 8%, 5%, and 4% of cases, respectively. Two groups were considered, including a positive STI group and a negative STI group. The prevalence of HPV was similar in patients in both groups: high risk (HR)-HPV and low risk (LR)-HPV were 67% and 53% versus 62% (<i>p</i> = 0.361) and 54% (<i>p</i> = 0.864) of patients, respectively. However, HPV 16, 18, 35, 51, 59, and 69 were significantly more frequent in patients tested positive for other STIs versus HPV infection alone (<i>p</i> < 0.05). No significant differences between the two groups were observed in vaccination coverage, 28% versus 32% (<i>p</i> = 0.463), and HIV status, 86% versus 84% (<i>p</i> = 0.658). The study shows that the overall HPV status is not directly correlated to other STIs in the investigated population, except for certain HPV types, including HR-HPV 16, reinforcing the urge for a greater vaccination coverage.</p>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":null,"pages":null},"PeriodicalIF":6.8,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.29852","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142013587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xinze Li, Qiaomiao Zhou, Zhe Lu, Renliang Huang, Dan Lin, Jing Xu, Xinhua Yu, Xuexia Li
Antigen presentation by HLA class II molecules to CD4+ T cells is an essential step for generating antibodies to hepatitis B antigens. In this study, we investigated the association between the HLA-DRB1 gene and the status of antibodies to hepatitis B surface and e antigens. Our results revealed a significant association between the status of anti-HBsAg and HLA-DRB1*04:03 (OR = 4.11, 95% CI = 1.50–10.84, p = 0.005, Padj. = 0.05) as well as HLA-DRB1*15:01 (OR = 1.74, 95% CI = 1.20–2.50, p = 0.002, Padj. = 0.045). MHC II binding predictions and in silico docking demonstrated strong binding affinity of HBsAg peptides to these two HLA-DRB1 molecules. Conversely, the status of anti-HBeAg was inversely associated with HLA-DRB1*14:54 (OR = 0.34, 95% CI = 0.18–0.64, p = 0.001, Padj. = 0.011), and in silico analysis revealed weak binding affinity of HBeAg peptides to HLA-DRB1*14:54. In conclusion, these findings support the involvement of HLA-DRB1 in humoral immunity against HBV infection.
{"title":"Association of HLA-DRB1 alleles with status of antibodies to hepatitis B surface and e antigen","authors":"Xinze Li, Qiaomiao Zhou, Zhe Lu, Renliang Huang, Dan Lin, Jing Xu, Xinhua Yu, Xuexia Li","doi":"10.1002/jmv.29867","DOIUrl":"10.1002/jmv.29867","url":null,"abstract":"<p>Antigen presentation by HLA class II molecules to CD4<sup>+</sup> T cells is an essential step for generating antibodies to hepatitis B antigens. In this study, we investigated the association between the HLA-DRB1 gene and the status of antibodies to hepatitis B surface and e antigens. Our results revealed a significant association between the status of anti-HBsAg and HLA-DRB1*04:03 (OR = 4.11, 95% CI = 1.50–10.84, <i>p</i> = 0.005, <i>P</i><sub>adj.</sub> = 0.05) as well as HLA-DRB1*15:01 (OR = 1.74, 95% CI = 1.20–2.50, <i>p</i> = 0.002, <i>P</i><sub>adj.</sub> = 0.045). MHC II binding predictions and in silico docking demonstrated strong binding affinity of HBsAg peptides to these two HLA-DRB1 molecules. Conversely, the status of anti-HBeAg was inversely associated with HLA-DRB1*14:54 (OR = 0.34, 95% CI = 0.18–0.64, <i>p</i> = 0.001, <i>P</i><sub>adj.</sub> = 0.011), and in silico analysis revealed weak binding affinity of HBeAg peptides to HLA-DRB1*14:54. In conclusion, these findings support the involvement of HLA-DRB1 in humoral immunity against HBV infection.</p>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":null,"pages":null},"PeriodicalIF":6.8,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142017798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Emerging evidence shows increased humoral response post-omicron surge, but research on T cell responses is limited. This study investigated the durability, magnitude, and breadth of SARS-CoV-2-spike-specific T cell responses in 216 two-dose vaccinated individuals pre- and post-omicron surge. Post-surge samples showed enhanced T cell responses, indicating widespread asymptomatic exposure to omicron. Further analysis of 105 individuals with multiple exposures to SARS-CoV-2 through boosters or infections showed that post-omicron, two-dose vaccinated individuals had T cell responses comparable to those of COVID-19 convalescents or boosted individuals. Additionally, we report cross-reactive T cell responses against omicron sub-variants, including BA2.86, remained strong, with preserved frequencies of spike-specific stem-cell-like memory T cells. In silico prediction indicates that mutated epitopes of JN.1 and KP.2 retain over 95.6% of their HLA binding capability. Overall, our data suggests that T cell responses are sustained, enhanced, and cross-reactive against emerging SARS-CoV-2 variants following symptomatic or asymptomatic omicron infection.
新的证据显示,微粒激增后体液反应增强,但有关 T 细胞反应的研究却很有限。这项研究调查了216名接种两剂疫苗的人在奥米控激增前后SARS-CoV-2尖峰特异性T细胞反应的持久性、程度和广度。疫情激增后的样本显示 T 细胞反应增强,表明无症状暴露于奥米克龙的情况广泛存在。对通过加强剂或感染多次接触 SARS-CoV-2 的 105 人进行的进一步分析表明,接种奥米克龙后的两剂疫苗接种者的 T 细胞反应与 COVID-19 康复者或加强剂接种者相当。此外,我们还报告说,针对包括 BA2.86 在内的奥米克龙亚变体的交叉反应性 T 细胞反应仍然很强,尖峰特异性干细胞样记忆 T 细胞的频率保持不变。硅学预测表明,JN.1 和 KP.2 的突变表位保留了超过 95.6% 的 HLA 结合能力。总之,我们的数据表明,在无症状或无症状卵圆形感染后,T细胞对新出现的SARS-CoV-2变体的反应是持续的、增强的和交叉反应性的。
{"title":"Understanding the landscape of the SARS-CoV-2-specific T cells post-omicron surge","authors":"Akshay Binayke, Aymaan Zaheer, Siddhesh Vishwakarma, Priyanka Sharma, Jyotsna Dandotiya, Sreevatsan Raghavan, Mudita Gosain, Savita Singh, Souvick Chattopadhyay, Jyotsana Kaushal, Upasna Madan, Pallavi Kshetrapal, Gaurav Batra, Nitya Wadhwa, Anil Kumar Pandey, Shinjini Bhatnagar, Pramod Kumar Garg, Amit Awasthi","doi":"10.1002/jmv.29877","DOIUrl":"10.1002/jmv.29877","url":null,"abstract":"<p>Emerging evidence shows increased humoral response post-omicron surge, but research on T cell responses is limited. This study investigated the durability, magnitude, and breadth of SARS-CoV-2-spike-specific T cell responses in 216 two-dose vaccinated individuals pre- and post-omicron surge. Post-surge samples showed enhanced T cell responses, indicating widespread asymptomatic exposure to omicron. Further analysis of 105 individuals with multiple exposures to SARS-CoV-2 through boosters or infections showed that post-omicron, two-dose vaccinated individuals had T cell responses comparable to those of COVID-19 convalescents or boosted individuals. Additionally, we report cross-reactive T cell responses against omicron sub-variants, including BA2.86, remained strong, with preserved frequencies of spike-specific stem-cell-like memory T cells. In silico prediction indicates that mutated epitopes of JN.1 and KP.2 retain over 95.6% of their HLA binding capability. Overall, our data suggests that T cell responses are sustained, enhanced, and cross-reactive against emerging SARS-CoV-2 variants following symptomatic or asymptomatic omicron infection.</p>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":null,"pages":null},"PeriodicalIF":6.8,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142017800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Interferon regulatory factor 5 (IRF5) is a key transcription factor in inflammatory and immune responses, with its dysregulation linked to autoimmune diseases. Using bioinformatic approaches, including Basic Local Alignment Search Tool (BLAST) for sequence similarity searches, BLAST-Like Alignment Tool (BLAT) for genome-wide alignments, and several phylogenetics software, such as Multiple Alignment using Fast Fourier Transform (MAFFT), for phylogenetic analyses, we characterized the structure, origin, and evolutionary history of the human IRF5 pseudogene 1 (IRF5P1). Our analyses reveal that IRF5P1 is a chimeric processed pseudogene containing sequences derived from multiple sources, including IRF5-like sequences from disparate organisms. We find that IRF5P1 is specific to higher primates, likely originating through an ancient retroviral integration event approximately 60 million years ago. Interestingly, IRF5P1 resides within the triple QxxK/R motif-containing (TRIQK) gene, and its antisense strand is predominantly expressed as part of the TRIQK pre-messenger RNA (mRNA). Analysis of publicly available RNA-seq data suggests potential expression of antisense IRF5P1 RNA. We hypothesize that this antisense RNA may regulate IRF5 expression through complementary binding to IRF5 mRNA, with human genetic variants potentially modulating this interaction. The conservation of IRF5P1 in the primate lineage suggests its positive effects on primate evolution and innate immunity. This study highlights the importance of investigating pseudogenes and their potential regulatory roles in shaping lineage-specific immune adaptations.
{"title":"The primate-specific presence of interferon regulatory factor-5 pseudogene 1","authors":"Avery Marquis, Vanessa Hubing, Chanasei Ziemann, Etsuko N. Moriyama, Luwen Zhang","doi":"10.1002/jmv.29879","DOIUrl":"10.1002/jmv.29879","url":null,"abstract":"<p>Interferon regulatory factor 5 (IRF5) is a key transcription factor in inflammatory and immune responses, with its dysregulation linked to autoimmune diseases. Using bioinformatic approaches, including Basic Local Alignment Search Tool (BLAST) for sequence similarity searches, BLAST-Like Alignment Tool (BLAT) for genome-wide alignments, and several phylogenetics software, such as Multiple Alignment using Fast Fourier Transform (MAFFT), for phylogenetic analyses, we characterized the structure, origin, and evolutionary history of the human IRF5 pseudogene 1 (IRF5P1). Our analyses reveal that IRF5P1 is a chimeric processed pseudogene containing sequences derived from multiple sources, including IRF5-like sequences from disparate organisms. We find that IRF5P1 is specific to higher primates, likely originating through an ancient retroviral integration event approximately 60 million years ago. Interestingly, IRF5P1 resides within the triple QxxK/R motif-containing (TRIQK) gene, and its antisense strand is predominantly expressed as part of the TRIQK pre-messenger RNA (mRNA). Analysis of publicly available RNA-seq data suggests potential expression of antisense IRF5P1 RNA. We hypothesize that this antisense RNA may regulate IRF5 expression through complementary binding to IRF5 mRNA, with human genetic variants potentially modulating this interaction. The conservation of IRF5P1 in the primate lineage suggests its positive effects on primate evolution and innate immunity. This study highlights the importance of investigating pseudogenes and their potential regulatory roles in shaping lineage-specific immune adaptations.</p>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":null,"pages":null},"PeriodicalIF":6.8,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.29879","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142017799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Epstein–Barr virus (EBV) is a highly successful pathogen that infects ~95% of the adult population and is associated with diverse cancers and autoimmune diseases. The most abundant viral factor in latently infected cells is not a protein but a noncoding RNA called EBV-encoded RNA 1 (EBER1). Even though EBER1 is highly abundant and was discovered over forty years ago, the function of EBER1 has remained elusive. EBER1 interacts with the ribosomal protein L22, which normally suppresses the expression of its paralog L22-like 1 (L22L1). Here we show that when L22 binds EBER1, it cannot suppress L22L1, resulting in L22L1 being expressed and incorporated into ribosomes. We further show that L22L1-containing ribosomes preferentially translate mRNAs involved in the oxidative phosphorylation pathway. Moreover, upregulation of L22L1 is indispensable for growth transformation and immortalization of resting B cells upon EBV infection. Taken together, our results suggest that the function of EBER1 is to modulate host gene expression at the translational level, thus bypassing the need for dysregulating host gene transcription.
{"title":"Epstein–Barr virus noncoding RNA EBER1 promotes the expression of a ribosomal protein paralog to boost oxidative phosphorylation","authors":"Sita Paudel, Nara Lee","doi":"10.1002/jmv.29869","DOIUrl":"10.1002/jmv.29869","url":null,"abstract":"<p>Epstein–Barr virus (EBV) is a highly successful pathogen that infects ~95% of the adult population and is associated with diverse cancers and autoimmune diseases. The most abundant viral factor in latently infected cells is not a protein but a noncoding RNA called EBV-encoded RNA 1 (EBER1). Even though EBER1 is highly abundant and was discovered over forty years ago, the function of EBER1 has remained elusive. EBER1 interacts with the ribosomal protein L22, which normally suppresses the expression of its paralog L22-like 1 (L22L1). Here we show that when L22 binds EBER1, it cannot suppress L22L1, resulting in L22L1 being expressed and incorporated into ribosomes. We further show that L22L1-containing ribosomes preferentially translate mRNAs involved in the oxidative phosphorylation pathway. Moreover, upregulation of L22L1 is indispensable for growth transformation and immortalization of resting B cells upon EBV infection. Taken together, our results suggest that the function of EBER1 is to modulate host gene expression at the translational level, thus bypassing the need for dysregulating host gene transcription.</p>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":null,"pages":null},"PeriodicalIF":6.8,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.29869","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rui Su, Lihua Yan, Bei Jiang, Jia Li, Ping Li, Yonggang Liu, Jing Miao, Cuiying Chen, Liang Xu, Li Ren, Yuqiang Mi
This study aimed to establish a novel noninvasive model based on the serum N-glycan spectrum for providing an objective value for determining the stage of liver necroinflammation related to chronic hepatitis B (CHB) patients. N-glycan profiles of the sera of 295 treatment-naïve CHB patients were analyzed. N-glycan profiles were tested for different liver necroinflammation stages using DNA sequence-assisted fluorophore-assisted carbohydrate electrophoresis. A serum N-glycan model named N-glycan-LI (NGLI) using support vector machine was selected to evaluate the classification of liver necroinflammation (G < 2 and G ≥ 2). The area under the receiver operating characteristic curves (AUROCs) was 0.898 (training set, n = 236) and 0.911 (validation set, n = 59) regardless of the stage of liver fibrosis (AUROC = 0.886 and 0.926, respectively, in S < 2 and S ≥ 2 group). The NGLI correspondingly had the highest specificity (SP) of 90.79% and negative predictive value of 92.00% in an inactive stage (including immune-tolerant [IT] and inactive-carrier [IC] stage), had the highest positive predictive value of 95.18% in stage immune-active, and had the highest SP of 93.94% in grey zone IT + IC. N-glycan profiles appear to correlate well with hepatic necroinflammation in CHB when compared with liver biopsy. The newly developed model appears to reliably predict liver damage in naïve-treatment patients with CHB.
{"title":"A novel model based on serum N-glycan markers for evaluating stage of liver necroinflammation in treatment-naïve chronic hepatitis B patients","authors":"Rui Su, Lihua Yan, Bei Jiang, Jia Li, Ping Li, Yonggang Liu, Jing Miao, Cuiying Chen, Liang Xu, Li Ren, Yuqiang Mi","doi":"10.1002/jmv.29863","DOIUrl":"10.1002/jmv.29863","url":null,"abstract":"<p>This study aimed to establish a novel noninvasive model based on the serum N-glycan spectrum for providing an objective value for determining the stage of liver necroinflammation related to chronic hepatitis B (CHB) patients. N-glycan profiles of the sera of 295 treatment-naïve CHB patients were analyzed. N-glycan profiles were tested for different liver necroinflammation stages using DNA sequence-assisted fluorophore-assisted carbohydrate electrophoresis. A serum N-glycan model named N-glycan-LI (NGLI) using support vector machine was selected to evaluate the classification of liver necroinflammation (G < 2 and G ≥ 2). The area under the receiver operating characteristic curves (AUROCs) was 0.898 (training set, <i>n</i> = 236) and 0.911 (validation set, <i>n</i> = 59) regardless of the stage of liver fibrosis (AUROC = 0.886 and 0.926, respectively, in S < 2 and S ≥ 2 group). The NGLI correspondingly had the highest specificity (SP) of 90.79% and negative predictive value of 92.00% in an inactive stage (including immune-tolerant [IT] and inactive-carrier [IC] stage), had the highest positive predictive value of 95.18% in stage immune-active, and had the highest SP of 93.94% in grey zone IT + IC. N-glycan profiles appear to correlate well with hepatic necroinflammation in CHB when compared with liver biopsy. The newly developed model appears to reliably predict liver damage in naïve-treatment patients with CHB.</p>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":null,"pages":null},"PeriodicalIF":6.8,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.29863","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Phu Nguyen Trong Tran, Noppachai Siranart, Theerapon Sukmark, Umaporn Limothai, Sasipha Tachaboon, Terapong Tantawichien, Chule Thisyakorn, Usa Thisyakorn, Nattachai Srisawat
Dengue shock syndrome (DSS) substantially worsens the prognosis of children with dengue infection. This study aimed to develop a simple clinical tool to predict the risk of DSS. A cohort of 2221 Thai children with a confirmed dengue infection who were admitted to King Chulalongkorn Memorial Hospital between 1987 and 2007 was conducted. Another data set from a previous publication comprising 2,301 Vietnamese children with dengue infection was employed to create a pooled data set, which was randomly split into training (n = 3182), testing (n = 697) and validating (n = 643) datasets. Logistic regression was compared to alternative machine learning algorithms to derive the most predictive model for DSS. 4522 children, including 899 DSS cases (758 Thai and 143 Vietnamese children) with a mean age of 9.8 ± 3.4 years, were analyzed. Among the 12 candidate clinical parameters, the Bayesian Model Averaging algorithm retained the most predictive subset of five covariates, including body weight, history of vomiting, liver size, hematocrit levels, and platelet counts. At an Area Under the Curve (AUC) value of 0.85 (95% CI: 0.81–0.90) in testing data set, logistic regression outperformed random forest, XGBoost and support vector machine algorithms, with AUC values being 0.82 (0.77–0.88), 0.82 (0.76–0.88), and 0.848 (0.81–0.89), respectively. At its optimal threshold, this model had a sensitivity of 0.71 (0.62–0.80), a specificity of 0.84 (0.81–0.88), and an accuracy of 0.82 (0.78–0.85) on validating data set with consistent performance across subgroup analyses by age and gender. A logistic regression-based nomogram was developed to facilitate the application of this model. This work introduces a simple and robust clinical model for DSS prediction that is well-tailored for children in resource-limited settings.
{"title":"A simple nomogram to predict dengue shock syndrome: A study of 4522 south east Asian children","authors":"Phu Nguyen Trong Tran, Noppachai Siranart, Theerapon Sukmark, Umaporn Limothai, Sasipha Tachaboon, Terapong Tantawichien, Chule Thisyakorn, Usa Thisyakorn, Nattachai Srisawat","doi":"10.1002/jmv.29874","DOIUrl":"10.1002/jmv.29874","url":null,"abstract":"<p>Dengue shock syndrome (DSS) substantially worsens the prognosis of children with dengue infection. This study aimed to develop a simple clinical tool to predict the risk of DSS. A cohort of 2221 Thai children with a confirmed dengue infection who were admitted to King Chulalongkorn Memorial Hospital between 1987 and 2007 was conducted. Another data set from a previous publication comprising 2,301 Vietnamese children with dengue infection was employed to create a pooled data set, which was randomly split into training (<i>n</i> = 3182), testing (<i>n</i> = 697) and validating (<i>n</i> = 643) datasets. Logistic regression was compared to alternative machine learning algorithms to derive the most predictive model for DSS. 4522 children, including 899 DSS cases (758 Thai and 143 Vietnamese children) with a mean age of 9.8 ± 3.4 years, were analyzed. Among the 12 candidate clinical parameters, the Bayesian Model Averaging algorithm retained the most predictive subset of five covariates, including body weight, history of vomiting, liver size, hematocrit levels, and platelet counts. At an Area Under the Curve (AUC) value of 0.85 (95% CI: 0.81–0.90) in testing data set, logistic regression outperformed random forest, XGBoost and support vector machine algorithms, with AUC values being 0.82 (0.77–0.88), 0.82 (0.76–0.88), and 0.848 (0.81–0.89), respectively. At its optimal threshold, this model had a sensitivity of 0.71 (0.62–0.80), a specificity of 0.84 (0.81–0.88), and an accuracy of 0.82 (0.78–0.85) on validating data set with consistent performance across subgroup analyses by age and gender. A logistic regression-based nomogram was developed to facilitate the application of this model. This work introduces a simple and robust clinical model for DSS prediction that is well-tailored for children in resource-limited settings.</p>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":null,"pages":null},"PeriodicalIF":6.8,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron subvariants raises concerns regarding the effectiveness of immunity acquired from previous Omicron subvariants breakthrough infections (BTIs) or reinfections (RIs) against the current circulating Omicron subvariants. In this study, we prospectively investigate the dynamic changes of virus-specific antibody and T cell responses among 77 adolescents following Omicron BA.2.3 BTI with or without subsequent Omicron BA.5 RI. Notably, the neutralizing antibodies (NAbs) titers against various detected SARS-CoV-2 variants, especially the emerging Omicron CH.1.1, XBB.1.5, XBB.1.16, EG.5.1, and JN.1 subvariants, exhibited a significant decrease along the time. A lower level of IgG and NAbs titers post-BTI was found to be closely associated with subsequent RI. Elevated NAbs levels and shortened antigenic distances were observed following Omicron BA.5 RI. Robust T cell responses against both Omicron BA.2- and CH.1.1-spike peptides were observed at each point visited. The exposure to Omicron BA.5 promoted phenotypic differentiation of virus-specific memory T cells, even among the non-seroconversion adolescents. Therefore, updated vaccines are needed to provide effective protection against newly emerging SARS-CoV-2 variants among adolescents.
{"title":"SARS-CoV-2 reinfection broadens the antibody responses and promotes the phenotypic differentiation of virus-specific memory T cells in adolescents","authors":"Xin-Jing Zhao, Xiao-Lin Liu, Hong-Jing Gu, Ti Liu, De-Yu Li, Sheng Zhang, Jie Wu, Kai-Ge Du, Shen Tian, Jin-Jin Chen, Qiang Xu, Chen-Long Lv, Bao-Gui Jiang, Hui Wang, Zeng-Qiang Kou, Guo-Lin Wang, Li-Qun Fang","doi":"10.1002/jmv.29873","DOIUrl":"10.1002/jmv.29873","url":null,"abstract":"<p>The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron subvariants raises concerns regarding the effectiveness of immunity acquired from previous Omicron subvariants breakthrough infections (BTIs) or reinfections (RIs) against the current circulating Omicron subvariants. In this study, we prospectively investigate the dynamic changes of virus-specific antibody and T cell responses among 77 adolescents following Omicron BA.2.3 BTI with or without subsequent Omicron BA.5 RI. Notably, the neutralizing antibodies (NAbs) titers against various detected SARS-CoV-2 variants, especially the emerging Omicron CH.1.1, XBB.1.5, XBB.1.16, EG.5.1, and JN.1 subvariants, exhibited a significant decrease along the time. A lower level of IgG and NAbs titers post-BTI was found to be closely associated with subsequent RI. Elevated NAbs levels and shortened antigenic distances were observed following Omicron BA.5 RI. Robust T cell responses against both Omicron BA.2- and CH.1.1-spike peptides were observed at each point visited. The exposure to Omicron BA.5 promoted phenotypic differentiation of virus-specific memory T cells, even among the non-seroconversion adolescents. Therefore, updated vaccines are needed to provide effective protection against newly emerging SARS-CoV-2 variants among adolescents.</p>","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":null,"pages":null},"PeriodicalIF":6.8,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.29873","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Antonio E. Pontiroli, Ivan Zanoni, Elisabetta Tanzi, Elena Tagliabue, Lucia La Sala
{"title":"Effect of influenza vaccination on SARS-CoV-2 infection: Relationship between SARS-CoV-2 infection rates and effects of influenza vaccination","authors":"Antonio E. Pontiroli, Ivan Zanoni, Elisabetta Tanzi, Elena Tagliabue, Lucia La Sala","doi":"10.1002/jmv.29868","DOIUrl":"10.1002/jmv.29868","url":null,"abstract":"","PeriodicalId":16354,"journal":{"name":"Journal of Medical Virology","volume":null,"pages":null},"PeriodicalIF":6.8,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}