Human herpesvirus 6 (HHV-6), a widely distributed member of the Herpesviridae family, establishes lifelong latency in monocytes and macrophages. The persistence of HHV-6 under immunosuppressive conditions, such as chronic alcohol consumption, may potentiate liver inflammation and exacerbate tissue damage by synergising with the hepatotoxic effects of ethanol. This interaction could raise significant concerns in the context of infectious diseases, as it poses a heightened risk to individuals with a history of heavy alcohol use, particularly those with underlying comorbidities or compromised immune function. The transcription factor NF-κB, essential for transactivating target genes involved in immune and inflammatory responses and CD163, expressed on anti-inflammatory macrophages, provides valuable insights into tissue damage during the presence of HHV- 6 infection.
Fifty-four liver tissue specimens were collected from the following groups: control (n=11), young alcohol users (n=15), and chronic alcohol users (n=28). Specimens were immunohistochemically stained with anti-CD163, anti-NF-κB, and anti-HHV-6 antibodies and analysed via light microscopy. HHV-6- and CD163-positive cells were counted quantitatively, while both the intensity and distribution of NF-κB expression were analysed semi-quantitatively. Statistical analysis was performed using SPSS 28.0.
HHV-6-positive liver lobules were identified in 48.75% of the controls, 63.89% of young alcohol users, and 72.04% of chronic alcohol users. The mean CD163-positive cell count in the lobular area increased significantly in young alcohol users (mean=135 ± 43 SEM) and chronic alcohol users (mean=226 ± 38 SEM) compared to the controls (mean=59 ± 14 SEM). NF-κB expression intensity in the lobular area was significantly higher in young alcohol users (p<0.005), and both intensity and distribution were notably increased in chronic alcoholics (p<0.001, p=0.02) compared to the controls.
Chronic alcohol consumption increases liver inflammation and damage, potentially exacerbated by HHV‑6 persistence. Further studies are needed to confirm these interactions and explore the mechanisms driving the synergistic effects of HHV-6 and ethanol on liver tissue damage.
