Interferon Inducible Guanylate Binding Protein 5 (GBP5) and Its Association With Oxidative Stress Markers in Regulating Dengue Severity: A Clinical and In Vitro Evaluation

View at publisher
Authors: Sanchita Chakraborty, Anand Kasirajan, A R Sunil, Aman Kumar Mohanty, Siva Ranganathan Green, Joshy Maducolil Easow, Agieshkumar Balakrishna Pillai
Cited by: 1
References: 50

Abstract

Human guanylate-binding proteins (GBPs), induced by interferon in endothelial cells, are being explored as therapeutic targets for viral and metabolic diseases. However, their role in dengue pathogenesis, particularly regarding endothelial leakage in severe cases, remains unclear. To shed some light, the current study assessed mRNA and plasma GBP5 levels in 26 patients with severe dengue (SD), 15 with warning signs (DWW), 15 without warning signs (DWOW), and 10 healthy controls, using RT-PCR and ELISA, respectively. Correlation between plasma GBP5 levels and oxidative stress markers, such as plasma lipid peroxidation, Protein oxidation, and DNA oxidation, was further investigated. GBP5 knockdown was assessed for its effects on oxidative stress and endothelial integrity in the HUVEC model. During the early febrile phase, GBP5 level was significantly elevated in all dengue cases compared to HC; towards the critical phase, there was a sharp decline observed in SD (p < 0.001) and DWW (p < 0.05) cases, which is accompanied by an increased oxidative stress marker, indicating its plausible association with dengue severity. Interferon stimulation of HUVEC cells significantly increased GBP5 expression (p < 0.05) and sustained oxidative stress levels, while GBP5 silencing raised oxidative stress and lowered endothelial integrity. Our findings highlight the potential of GBP5 as a prognostic marker and therapeutic target in the management of dengue.

Fields of Study & Subjects

Mosquito-borne diseases and control Malaria Research and Control Invertebrate Immune Response Mechanisms

Publication details

Journal / source
Journal of Medical Virology
Publisher
Wiley
Volume
98
Issue
4
Pages
e70891–e70891
Publication date
1 April 2026
Language
EN