Virology Journal最新文献

Background: Herpes zoster(HZ), a severe complication following hematopoietic stem cell transplantation (HSCT), is associated with significant morbidity. The effect of herpes zoster vaccine(HZV) for preventing HZ on patients after HSCT is unclear. We conducted a systematic review and meta-analysis investigating the efficacy and safety of HZV in HSCT recipients.

Methods: The databases Pubmed, Embase, and Cochrane Library were searched to identify relevant studies. Random-effects models were used to calculate risk ratios (RRs) and 95% confidence intervals (CIs) for HZ infection and related events.

Results: A total of 3048 individuals from five studies (four randomized controlled trials and one retrospective cohort study) were included. The overall incidence of HZ in the HZV group and control group was 6.4% and 18.3% respectively, resulting in a pooled RR of 0.36 (95%CI, 0.29-0.45; P < 0.001), indicating no heterogeneity (P = 0.88,I² = 0). HZV demonstrated a reduction in the risk of PHN (RR, 0.40; 95% CI, 0.15-1.11), although statistical significance was not reached (P = 0.08). Furthermore, through two independent RCTs, HZV showed a decrease in the incidence of HZ-related complications compared to placebo administration. The overall incidence of adverse events in the HZV group and control group was found to be 63.6% and 60.2% respectively, with a pooled RR of 1.02 (95% CI, 0.97-1.06, P = 0.51), indicating no heterogeneity (P = 0.66, I² = 0).

Conclusion: The HZV group demonstrated a significant reduction in the risk of HZ among HSCT recipients, without an increase in adverse events. This highlights the positive impact of HZV on decreasing the incidence of PHN and complications associated with HZ. Furthermore, our findings support the effectiveness and tolerability of HZV as a preventive measure against HZ for HSCT recipients.

Direct skin-to-skin contact during intimate sexual contact with a human papillomavirus (HPV)-positive individual is often the cause of HPV infection. In addition, many studies have been written up to date that look at the role of HPV in the growth of other types of tumors. Not all urological cancers are associated with HPV. However, penile cancer (PC) is often caused by HPV, especially high-risk types. HPV-16 has been the most frequent (68.3%), followed by HPV-6 (8.1%) and HPV-18 (6.9%). An increased risk of getting certain types of urinary cancers like prostate, bladder, testicular, and kidney has also been linked to these infections. Additionally, HPV may play a part in continuous inflammation and cancer progression in different organs and tissues. So, making HPV vaccine programs available to more people of the male sex around the world could significantly lower the number of urinary cancers caused by HPV. The critical effects of HPV on different types of urologic cancers (UCs), such as testicular, prostate, penile, and kidney cancer, and the importance of HPV vaccination have been seen in this study.

Objective: This study aims to develop a dynamic nomogram model using machine learning to improve short-term prognosis prediction and identify patients who would benefit from intravenous immunoglobulin (IVIG) therapy.

Methods: A multicenter retrospective study was conducted on 396 patients diagnosed with SFTS. Univariate and multivariate Cox regression analyses identified significant predictors of mortality. Machine learning models, including Random Survival Forest, Stepwise Cox Modeling, and Lasso Cox Regression, were compared for their predictive performance. The optimal model, incorporating consciousness, LDH, AST, and age, was used to construct a dynamic nomogram. The nomogram's performance was validated in training, validation, and external test sets. Additionally, the impact of IVIG therapy on survival was assessed within high-risk groups identified by the nomogram.

Results: The dynamic nomogram demonstrated excellent predictive performance with an AUC of 0.903 in the training set, 0.933 in the validation set, and 0.852 in the test set, outperforming SOFA and APACHE II scores. Calibration curves confirmed the model's accuracy. In the high-risk group, the hazard ratio (HR) for death for those who injected immunoglobulin versus those who did not was 0.569 (95% CI 0.330-0.982) in the nomogram model.

Conclusion: The dynamic nomogram effectively predicts short-term prognosis and identifies the population that benefits from IVIG therapy in patients with novel bunyavirus sepsis. This tool can aid clinicians in risk stratification and personalized treatment decisions, potentially improving patient outcomes.

Viral hemorrhagic Lassa fever (LF), caused by Lassa virus (LASV), is a significant public health concern endemic in West Africa with high morbidity and mortality rates, limited treatment options, and potential for international spread. Despite advances in interrogating its epidemiology and clinical manifestations, the molecular mechanisms driving pathogenesis of LASV and other arenaviruses remain incompletely understood. This review synthesizes current knowledge regarding the role of LASV host-virus interactions in mediating the pathogenesis of LF, with emphasis on interactions between viral and host proteins. Through investigation of these critical protein-protein interactions, we identify potential therapeutic targets and discuss their implications for development of medical countermeasures including antiviral drugs. This review provides an update in recent literature of significant LASV host-virus interactions important in informing the development of targeted therapies and improving clinical outcomes for LF patients. Knowledge gaps are highlighted as opportunities for future research efforts that would advance the field of LASV and arenavirus pathogenesis.

Background: Mothers with an undetectable viral load pose no risk of transmitting the Human Immunodeficiency Virus (HIV) to their fetuses. However, there is limited information on the HIV viral suppression status (≤ 1000 RNA copies/mL) among pregnant mothers at the national level. This study aimed to assess the HIV viral load suppression status among pregnant women and identify factors associated with unsuppressed maternal viral levels (> 1000 RNA copies/mL).

Methods: We conducted a cross-sectional study using secondary data from the national HIV viral load data repository. The study included all pregnant women who initiated antiretroviral therapy (ART) and underwent routine HIV viral load testing. Data were collected from July 2022 to June 2023 (2015 Ethiopian Fiscal Year (EFY)). Analysis was performed using STATA v.17, with descriptive statistics (frequency, percentage, mean, and standard deviation) calculated. A mixed-effects logistic regression model was used to quantify the strength of associations between variables and HIV viral load status (suppressed vs. unsuppressed), expressed through odds ratios.Variables showing a significant association with the outcome (p < 0.02) were selected for further analysis using multiple logistic regression models.

Results: The analysis included a total of 13,000 mothers with complete data from viral load tests conducted on pregnant women. The HIV viral suppression rate among these women before delivery was 96.8%. Among those with suppressed results, 96.5% had an undetectable HIV viral load. Multiple binary logistic regression analysis indicated that individuals aged 19-29 had 3.17 times higher odds (AOR 3.17, 95% CI 1.17-5.17, p = 0.002) of having an unsuppressed viral load compared to those under 19. Additionally, individuals with poor adherence to treatment had 12.6 times higher odds of experiencing unsuppressed viral loads (AOR 12.64, 95% CI 10.74-14.54, p = 0.001). However, no significant association was found between the timing of viral load testing and unsuppressed maternal HIV viral load.

Conclusion: The findings indicate that while the overall rates of HIV viral suppression among pregnant women are high, specific demographic factors such as age and treatment adherence play crucial roles in achieving undetectable viral loads. The data suggests a need for targeted interventions focusing on mothers age from 19 to 30 years and strategies to improve adherence to treatment regimens to enhance outcomes further.The results have significant implications for policy and clinical practices aimed at improving health outcomes for mothers and newborns affected by HIV/AIDS.

Background: Rash is a common childhood infection, mainly caused by viruses. Hand, foot, and mouth disease (HFMD), a common viral rash infection, has become one of the most common infectious diseases in Asian countries and caused outbreaks in children and adults worldwide. Following the introduction of enterovirus A71 (EVA71) vaccines, Coxsackievirus A6 (CVA6) has recently emerged. However, the disease is not commonly reported in Africa, where studies are scarce.

Methods: In the current study, we focused on the HFMD outbreak that occurred in Cape Verde in July 2023 during field investigations around a cluster of patients with rash and fever. Samples collected from patients were tested using Measles and Rubella-specific immunoglobulin M and quantitative reverse transcription PCR (qRT-PCR) of a panel of viruses causing rashes and subjected to genome sequencing followed by phylogenetic analysis.

Results: Eighteen out of the 22 samples were tested positive for CVA6 RNA by real-time RT-PCR, of which two tested also positive for EVA71 and Coxsackievirus A16 (CVA16). Subsequent sequencing revealed that all CVA6 sequences belonged to the D genotype, particularly the D3 sub-genotype recently described in China.

Conclusion: Our study uncovers the first-ever reported outbreak of CVA6 associated with atypical HFMD in children from Cape Verde and highlights thus the need to implement an active hospital-based HFMD surveillance in Africa.

Background: Orf virus (ORFV) is gaining attention as a promising viral vector for cancer therapy because of its unique properties. Recent studies have shown that ORFV could be effective against various cancers, particularly nasopharyngeal carcinoma. This research explores the ability of wild-type ORFV and recombinant ORFVs, which lack specific virulence factors, to kill NPC cells and modulate the immune response.

Methods: Two NPC cell lines, HK1 (from Hong Kong) and TW02 (from Taiwan), were infected with wild-type ORFV and two recombinant ORFVs lacking either vascular endothelial growth factor (VEGF) or chemokine binding protein (CBP) virulence factors. The oncolytic effects were evaluated by assessing cell death pathways, particularly pyroptosis, which was monitored through the cleavage of gasdermin E (GSDME). The activation of survival pathways, such as focal adhesion kinase (FAK) and AKT, was also analyzed. In addition, the influence of ORFV infection on natural killer (NK) cell recruitment and cytotoxicity was investigated. In vivo experiments were conducted in a xenograft mouse model in which HK1 tumors were used to evaluate the antitumor activity of wild-type ORFV and two deletion-mutant ORFVs.

Results: Wild-type ORFV effectively killed NPC cells, especially HK1 cells. The recombinant ORFVs, despite being attenuated by the loss of VEGF or CBP, retained the ability to infect and cause NPC cell death, with the CBP-deleted virus showing notable effectiveness in HK1 cells. Early ORFV infection led to pyroptosis via GSDME cleavage, causing cell detachment and a reduction in FAK and AKT activation. ORFV also enhanced NK cell recruitment and boosted NK cell-mediated cytotoxicity in infected NPC cells. In the HK1 xenograft model, CBP-deleted ORFV significantly inhibited tumor growth.

Conclusion: ORFV, particularly the wild-type and CBP-deleted variants, has significant potential as an oncolytic viral vector for NPC therapy. It induces cell death via pyroptosis and enhances immune-mediated tumor cell destruction through NK cells. The attenuated CBP-deleted ORFV offers a safer and effective option for cancer treatment, making it a promising candidate for future therapeutic applications.

SARS-CoV-2 infection widely induces antibody response targeting diverse viral proteins, including typical representative N-terminal domain (NTD), receptor-binding domain (RBD), and S2 subunit of spike. A lot of NTD-, RBD-, and S2-specific monoclonal antibodies (mAbs) have been isolated from COVID-19 convalescents, some of which displaying potent activities to inhibit viral infection. However, a small portion of NTD-specific mAbs elicited by wild-type (WT) SARS-CoV-2 primary infection could facilitate the virus entry into target cells in vitro, so called NTD-targeting infection-enhancing antibodies (NIEAs). To date, SARS-CoV-2 has evolved to massive variants carrying various NTD mutations, especially recent Omicron BA.2.86 and JN.1. In this study, we investigated whether these WT-NIEAs could still enhance the infectivity of emerging Omicron variants. Nine novel WT-NIEAs with diverse germline gene usage were identified from 3 individuals, effectively enlarging available antibody panel of NIEAs. Bivalent binding of NIEAs to inter-spike contributed to their infection-enhancing activities. WT-NIEAs could enhance the infectivity of SARS-CoV-2 variants emerged before Omicron, but ineffective to Omicron variants including BA.2.86 and JN.1, which was because of their changed antigenicity of NTDs. Overall, these data clearly demonstrated the cross-reactivity of these pre-existed WT-NIEAs to a series of SARS-CoV-2 variants, helping to evaluate the risk of enhanced infection of emerging variants in future.

Background: Activating Transcription Factor 3 (ATF3) is known for its tumor-suppressive properties in cervical cancer, particularly through its role in stress response and interactions with human papillomavirus (HPV) oncogenes. This study investigates ATF3's regulatory impact on metastasis-related genes, oxidative stress, and DNA damage in HPV-positive cervical cancer cells.

Methods: HeLa and Ca Ski cell lines were transfected with ATF3-expressing vectors. Western blotting and quantitative reverse transcription polymerase chain reaction (RT-qPCR) were used to confirm ATF3 overexpression following transfection. ROS assays and Comet assays assessed the impact of ATF3 on oxidative stress and DNA damage, while RT-qPCR was used to evaluate changes in HPV E6/E7, SHARP1, and MMP1 gene expression.

Results: ATF3 overexpression led to elevated ROS levels (p < 0.02), resulting in oxidative DNA damage. These results demonstrate ATF3's cytotoxic impact on cervical cancer cells through oxidative stress and DNA damage. Additionally, ATF3 overexpression significantly decreased MMP1 expression (p < 0.03), indicating a potential anti-metastatic effect, while SHARP1 and HPV E6/E7 expression levels were not significantly altered, indicating selective gene modulation by ATF3.

Conclusion: These findings reveal that ATF3 contributes to tumor suppression in cervical cancer by modulating oxidative stress and DNA damage, selectively targeting genes involved in metastasis. These findings supports ATF3's role in regulating key pathways in HPV-positive cervical cancer cells, providing a basis for further exploration of ATF3 as a target in therapeutic strategies aimed at improving outcomes in cervical cancer.

Background: Cervical cancer poses a substantial global health challenge. Estrogen-related receptor alpha (ERRα) is a central regulator of cellular energy metabolism associated with poor cancer prognosis. However, the effect of ERRα expression on cervical cancer prognosis and immune infiltration has not been explored. This study aims to clarify the expression pattern and role of ERRα in cervical cancer.

Methods: We analyzed ERRα expression and its clinical prognosis in cervical cancer using multiple databases, including The Cancer Genome Atlas (TCGA) and Tumor Immune Estimation Resource (TIMER). The results were further validated through immunohistochemistry (IHC) on 221 cervical cancer tissue samples. Furthermore, Kaplan-Meier and Cox regression analyses were used to assess the clinical significance of ERRα in cervical cancer patients. All calculations were performed using the R package.

Results: ERRα expression was significantly higher in cervical cancer tissues compared to normal tissues. High ERRα expression was associated with poor overall survival (OS), disease-specific survival (DSS), and progression-free survival (PFS). Multivariate Cox regression analysis confirmed ERRα as an independent prognostic factor. Additionally, ERRα expression correlated with various immune cell types and immune checkpoints, indicating its role in the tumor immune microenvironment.

Conclusions: ERRα emerges as a promising prognostic biomarker in cervical cancer, influencing immune cell infiltration and potentially guiding personalized therapeutic approaches. Future investigations are warranted to delineate the mechanistic pathways through which ERRα contributes to cervical cancer progression and to assess its viability as a target for innovative immunotherapy strategies.