Human papillomavirus (HPV), particularly strains 16 and 18, contributes to oropharyngeal squamous cell carcinoma (OPSCC), even in non-smokers and non-drinkers. This study investigated gene expression variations in HPV-positive OPSCCs according to the virus genotype. An RNA sequencing analysis of 36 p16-positive OPSCC patients revealed distinct expression patterns between tumors with only E6/E7 transcripts (E6E7) and those with additional E5 transcripts (E5-added). The E6E7 group displayed activation of FOS-related pathways and the NF-κB signaling pathway. Notably, the genes associated with tumor growth and cancer antigens differed between the groups. These findings suggest that the presence of HPV E5 might influence the transformation stages and gene expression, potentially affecting patient outcomes. The E5-added group expressed multiple cancer-associated antigens, presenting potential targets for personalized immunotherapy approaches for HPV-positive OPSCC.
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http://dx.doi.org/10.1016/j.cancergen.2025.02.010 | DOI Listing |
Virology
March 2025
ICMR-National Institute of Virology, 20-A, Dr. Ambedkar Road, Pune 411001, India.
H5N1 viruses belonging to clade 2.3.4.
View Article and Find Full Text PDFJ Immunol
January 2025
Institute of Virology and Immunology, Mittelhäusern, Switzerland.
While several African swine fever virus (ASFV)-encoded proteins potently interfere with the cGAS-STING (cyclic GMP-AMP synthetase-stimulator of interferon genes) pathway at different levels to suppress interferon (IFN) type I production in infected macrophages, systemic IFN-α is induced during the early stages of AFSV infection in pigs. The present study elucidates a mechanism by which such responses can be triggered, at least in vitro. We demonstrate that infection of monocyte-derived macrophages (MDMs) by ASFV genotype 2 strains is highly efficient but immunologically silent with respect to IFN type I, IFN-stimulated gene induction, and tumor necrosis factor production.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
March 2025
Department of Hepatobiliary and Pancreatic Surgery and Zhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China.
Chronic infections with hepatitis E virus (HEV), especially those of genotype 3 (G3), frequently lead to liver fibrosis and cirrhosis in patients. However, the causation and mechanism of liver fibrosis triggered by chronic HEV infection remain poorly understood. Here, we found that the viral multiple-domain replicase (ORF1) undergoes unique ubiquitin-proteasomal processing leading to formation of the EV-erived MAD ctivator (HDSA), a viral polypeptide lacking putative helicase and RNA polymerase domains.
View Article and Find Full Text PDFJ Epidemiol Glob Health
March 2025
Department of Public Health, College of Public Health and Health Informatics, King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia.
Introduction: Viral hepatitis stands accountable for approximately 1.34 million deaths worldwide, with the number of fatalities steadily growing with time. This is partly due to the various genotypes of hepatitis C virus and having no vaccination developed yet.
View Article and Find Full Text PDFStat Med
March 2025
Vaccine and Infectious Disease and Public Health Sciences Divisions, Fred Hutchinson Cancer Center, Seattle, Washington, USA.
Based on data from a randomized, controlled vaccine efficacy trial, this article develops statistical methods for assessing vaccine efficacy (VE) to prevent COVID-19 infections by a discrete set of genetic strains of SARS-CoV-2. Strain-specific VE adjusting for possibly time-varying covariates is estimated using augmented inverse probability weighting to address missing viral genotypes under a competing risks model that allows separate baseline hazards for different risk groups. Hypothesis tests are developed to assess whether the vaccine provides at least a specified level of VE against some viral genotypes and whether VE varies across genotypes.
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