Aug 2026· Proceedings of the National Academy of Sciences of the United States of America· Vol 123· 0 citations· 18 references
Medicine
TL;DR
It is shown that DENV-4 infection induces significant DNA damage and suppresses the transcription of genes involved in DNA repair and select mutagenic translesion synthesis (TLS) polymerases, indicating that DENV-4-dependent pathobiology leaves durable biological “scars” that incrementally increase chronic disease risk, including carcinogenesis and postdengue syndromes.
Abstract
The molecular mechanisms behind Dengue virus-dependent host pathogenesis, especially genome instability, remain largely unclear. This RNA virus causes a debilitating disease during active infection and presents future risks of postdengue syndromes, leukemia, and DNA damage in the blood cells of infected patients, with the underlying mechanisms unknown. In this study, we show that DENV-4 infection induces significant DNA damage and suppresses the transcription of genes involved in DNA repair and select mutagenic translesion synthesis (TLS) polymerases, indicating that DENV-4-dependent pathobiology leaves durable biological “scars” that incrementally increase chronic disease risk, including carcinogenesis and postdengue syndromes.
The DNA damage response (DDR) network maintains genomic integrity, functions as a signaling hub that viruses exploit to drive pathogenesis, and constitutes a central interface between viral infection and host cell fate. This review discusses the molecular mechanisms by which viruses subvert host DDR pathways, with an e...
Zika virus (ZIKV) infection triggers cellular stress well before the full establishment of interferon-stimulated gene expression. Intrinsic cellular mechanisms, including adaptive processes such as antioxidant defenses, the unfolded protein response (UPR), autophagy and programmed cell death (PCD) pathways, act early t...
Grégorie Lebeau, Jonathan Turpin, É. Frumence et al.· Virology· 0 citations
Investigation of a diverse panel of 16 SIV Vpr isolates shows that 13 out of 16 are capable of significantly activating DDR signaling compared to control infected cells, and hijacking of DDR responses to promote remodeling of the nuclear environment is a broadly conserved Vpr function.
Zaddock Williford, Emily Leavitt, Nicholas Saladino et al.· bioRxiv· 0 citations
Epstein–Barr Virus (EBV) is an oncogenic gammaherpesvirus present in >95% of the adult population. EBV is responsible for nearly 2% of the global cancer burden and is a contributing factor in the development and progression of both epithelial and lymphoid malignancies. Throughout its lifecycle, EBV manipulates the DNA...
Emily DiMaulo-Milk, B. Damania· Viruses· 0 citations
Significance Cells mount antiviral responses when they detect infection by a virus, and viruses have evolved mechanisms to resist the host responses. In this study, we have discovered a new form of host response. Upon entry of viruses that occurs by fusion of the viral envelope with the plasma membrane, nuclear DNA is...
Nicolás Romero, H. Oh, Max E. Mertens et al.· Proceedings of the National...· 0 citations
