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The interplay between Aspergillus fumigatus and the host immune response in lung infection has been subject of studies over the last years due to its importance in immunocompromised patients. The multifactorial virulence factors of A. fumigatus are related to the fungus biological characteristics, for example, structure, ability to grow and adapt to high temperatures and stress conditions, besides capability of evading the immune system and causing damage to the host. In this context, the fungus recognition by the host innate immunity occurs when the pathogen disrupts the natural and chemical barriers followed by the activation of acquired immunity. It seems clear that a Th1 response has a protective role, whereas Th2 reactions are often associated with higher fungal burden, and Th17 response is still controversial. Furthermore, a fine regulation of the effector immunity is required to avoid excessive tissue damage associated with fungal clearance, and this role could be attributed to regulatory T cells. Finally, in this work we reviewed the aspects involved in the complex interplay between the host immune response and the pathogen virulence factors, highlighting the immunological issues and the importance of its better understanding to the development of novel therapeutic approaches for invasive lung aspergillosis.
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http://dx.doi.org/10.1155/2013/693023 | DOI Listing |
Turkiye Parazitol Derg
September 2025
Ege University Faculty of Medicine, Department of Parasitology, İzmir, Türkiye.
Objective: Leishmaniasis, caused by protozoan parasites of the spp., presents significant global health challenges, with visceral leishmaniasis (VL) and cutaneous leishmaniasis forms causing severe morbidity and mortality. Macrophages serve as primary host cells, where spp.
View Article and Find Full Text PDFPLoS Pathog
September 2025
Institute of Medical Virology, University of Zurich, Zurich, Switzerland.
SUMO-modified Tripartite Motif Protein 28 (TRIM28; KAP1) plays a crucial role in repressing endogenous retroelement (ERE) transcription. We previously provided evidence that loss of SUMO-modified TRIM28 triggered by influenza A virus (IAV) infection promotes activation of host antiviral immunity via a mechanism involving derepression of EREs and production of immunostimulatory RNAs. While the IAV NS1 protein might limit consequences of such activation via its dsRNA-binding activity, we hypothesized that other human pathogenic viruses could have evolved more direct strategies to counteract this potential ERE-based defense system.
View Article and Find Full Text PDFJ Virol
September 2025
Laboratory of Virology, Wageningen University & Research, Wageningen, the Netherlands.
Vertebrate animals and many small DNA and single-stranded RNA viruses that infect vertebrates have evolved to suppress genomic CpG dinucleotides. All organisms and most viruses additionally suppress UpA dinucleotides in protein-coding RNA. Synonymously recoding viral genomes to introduce CpG or UpA dinucleotides has emerged as an approach for viral attenuation and vaccine development.
View Article and Find Full Text PDFAdv Sci (Weinh)
September 2025
State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University, Yangling, Shaanxi, 712100, P. R. China.
Mounting evidence indicates that viruses exploit elevated reactive oxygen species (ROS) levels to promote replication and pathogenesis, yet the mechanistic underpinnings of this viral strategy remain elusive for many viral systems. This study uncovers a sophisticated viral counter-defense mechanism in the Cryphonectria hypovirus 1 (CHV1)-Fusarium graminearum system, where the viral p29 protein subverts host redox homeostasis to overcome antiviral responses. That p29 directly interacts with and inhibits the enzymatic activity of fungal NAD(P)H-dependent FMN reductase 1 (FMR1), leading to increased ROS accumulation and subsequent autophagy activation is demonstrated.
View Article and Find Full Text PDFFront Cell Dev Biol
August 2025
Department of Epidemiology, Preclinical Research and Advanced Diagnostics, National Institute for Infectious Diseases IRCCS "L. Spallanzani", Rome, Italy.
The human microbiota is composed of a complex community of microorganisms essential for maintaining host homeostasis, especially in the gastrointestinal tract. Emerging evidence suggests that dysbiosis is linked to various cancers, including colorectal cancer (CRC). The microbiota contributes to CRC development and progression by influencing inflammation, genotoxic stress, and key cell growth, proliferation, and differentiation pathways.
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