Apoptosis has been shown to be induced and downregulated by the Hantaan virus (HTNV) nucleocapsid (N) protein. To address these conflicting data, expression of the p53 protein, one of the key molecules involved in apoptosis, was assessed in the presence of the N protein in A549 and HeLa cells. The amount of p53, increased by drug treatment, was reduced when cells were infected with HTNV or transfected with an expression vector of the HTNV N protein. When cells were treated with a proteasome inhibitor (MG132) or an MDM2 antagonist (Nutlin-3), p53 expression was not reduced in N protein-overexpressed cells. We concluded that the HTNV N protein ubiquitinates and degrades p53 MDM2-dependently. Here we report downregulation of p53 expression through a post-translational mechanism: MDM2-dependent ubiquitination and degradation by the HTNV N protein. These results indicate that N protein-dependent p53 degradation through the ubiquitin proteasome system is one of the anti-apoptotic mechanisms employed by HTNV.
State Key Laboratory of Virology/ Institute of Medical Virology, School of Basic Medical Sciences, Wuhan University, 185 Donghu Road, Wuhan, 430071, Hubei Province, China. Electronic address:
Hantaan virus (HTNV) infection in humans can cause hemorrhagic fever and renal syndrome (HFRS). Understanding host responses to HTNV infection is crucial for developing effective disease intervention strategies. Previous RNA-sequencing studies have investigated the role of microRNAs (miRNAs) in the post-transcriptional regulation of host genes in response to HTNV infection.
* SAB-163 is a new therapeutic treatment developed from transchromosomic bovine plasma, showing strong effectiveness against multiple hantavirus strains and extended bioavailability in animal models.
* The treatment has demonstrated protective effects in hamsters when administered around the time of exposure and is now ready for phase 1 clinical trials after passing safety and efficacy tests.
Hantavirus causes severe diseases with high mortality rates, and current treatments are lacking; however, Type I interferon has shown promise when administered early.
The study reveals that Hantaan virus (HTNV) increases the expression of the enzyme cholesterol 25-hydroxylase (CH25H), which then helps inhibit HTNV infection through cholesterol regulation.
It suggests that 25-hydroxycholesterol (25HC) and cholesterol-lowering statins could be repurposed as effective antiviral treatments against hantavirus infections, highlighting the potential of targeting cholesterol metabolism in developing new therapies.
Vaccines has long been the focus of antiviral immunotherapy research. Viral epitopes are thought to be useful biomarkers for immunotherapy (both antibody-based and cellular). In this study, we designed a novel vaccine molecule, the Hantaan virus (HTNV) glycoprotein (GP) tandem Th epitope molecule (named the Gnc molecule), in silico.
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