LL-37 · research summary

HBV pgRNA induces chronic inflammation in an IL-1β-dependent manner.

Frontiers in immunology · 2026. Summary drawn from the study's full text. Each statement is followed by the exact sentence it comes from. This is a research summary, not medical advice.

Study type

Observational study with in vitro experimental validation involving transcriptomic analysis and cell stimulation assays.
“The aim of this study was to investigate the transcriptomic profile of pgRNA-positive patients with CHB in comparison to pgRNA-negative patients and to evaluate its role in innate immunity.”

Subjects

Patients with chronic hepatitis B (CHB) receiving nucleoside analogs, specifically HBeAg-negative individuals, along with healthy controls and HBV-related HCC samples from a database.
“A total of 88 patients with CHB who were receiving nucleoside analogs (NAs) were enrolled in this study.”

Sample size

88 CHB patients were enrolled for plasma analysis, with a subset of 8 patients (4 pgRNA-positive, 4 pgRNA-negative) undergoing RNA sequencing.
“A total of 88 patients with CHB who were receiving nucleoside analogs (NAs) were enrolled in this study.”

Duration

Plasma samples were collected between January 2022 and August 2023.
“In this study, we examined 88 plasma samples collected between January 2022 and August 2023 in the hepatology outpatient clinic of the First Department of Internal Medicine.”

Reported findings

HBV pgRNA-positive serum activated platelets in an autophagy-dependent manner, characterized by elevated LC3-B and BECLIN-1 levels and downregulated P62.
“This study demonstrated that HBV pgRNA activates platelets in an autophagy-dependent manner.”
The platelet-neutrophil axis resulted in a proinflammatory phenotype in neutrophils characterized by high levels of IL-1β without significant NET formation.
“Moreover, the platelet–neutrophil axis is responsible for a proinflammatory phenotype in which IL-1β is overexpressed.”
Transcriptomic analysis identified common differentially expressed genes involved in platelet activation and neutrophil degranulation pathways in CHB patients.
“With respect to the transcriptomic analysis, which was performed via two distinct analyses, we identified common differentially expressed (DE) genes involved in platelet activation and neutrophil degranulation pathways.”

Limitations stated by the authors

The study was limited by a small sample size for transcriptome analysis, preventing analysis of different disease phenotypes, and limited biopsy availability prevented verification of results on the side of infection.
“Initially, we performed transcriptome analysis in a small group of patients. Consequently, we were unable to perform analyses with different disease phenotypes.”

Source: PubMed 42440489 · DOI 10.3389/fimmu.2026.1812831 · all study summaries

Study type

Observational study with in vitro experimental validation involving transcriptomic analysis and cell stimulation assays.

“The aim of this study was to investigate the transcriptomic profile of pgRNA-positive patients with CHB in comparison to pgRNA-negative patients and to evaluate its role in innate immunity.”

Reported findings

HBV pgRNA-positive serum activated platelets in an autophagy-dependent manner, characterized by elevated LC3-B and BECLIN-1 levels and downregulated P62.

“This study demonstrated that HBV pgRNA activates platelets in an autophagy-dependent manner.”

The platelet-neutrophil axis resulted in a proinflammatory phenotype in neutrophils characterized by high levels of IL-1β without significant NET formation.

“Moreover, the platelet–neutrophil axis is responsible for a proinflammatory phenotype in which IL-1β is overexpressed.”

Transcriptomic analysis identified common differentially expressed genes involved in platelet activation and neutrophil degranulation pathways in CHB patients.

“With respect to the transcriptomic analysis, which was performed via two distinct analyses, we identified common differentially expressed (DE) genes involved in platelet activation and neutrophil degranulation pathways.”

Limitations stated by the authors

The study was limited by a small sample size for transcriptome analysis, preventing analysis of different disease phenotypes, and limited biopsy availability prevented verification of results on the side of infection.

“Initially, we performed transcriptome analysis in a small group of patients. Consequently, we were unable to perform analyses with different disease phenotypes.”