Sodium taurocholate hydrate inhibits influenza virus replication and suppresses influenza a Virus-triggered inflammation in vitro and in vivo

• DOI: 10.1016/j.intimp.2023.110544
• Publication Date: 2023-06-29T17:06:03Z
• Authors: Xiaolu Sun; Xiaotong Hu; Qiang Zhang; Li Zhao; Xiaomei Sun; Li Yang; Meilin Jin
• Keywords: Taurocholic Acid; Inflammation; Influenza A Virus, H5N1 Subtype; Influenza A Virus, H3N2 Subtype; NF-kappa B; Virus Replication; Antiviral Agents; 3. Good health; Mice; Influenza A Virus, H1N1 Subtype; Influenza, Human; Influenza A Virus, H9N2 Subtype; Humans; Animals

Influenza A virus is an important respiratory pathogen that poses serious threats to human health. Owing to the high mutation rate of viral genes, weaker cross-protection of vaccines, and rapid emergence of drug resistance, there is an urgent need to develop new antiviral drugs against influenza viruses. Taurocholic acid is a primary bile acid that promotes digestion, absorption, and excretion of dietary lipids. Here, we demonstrate that sodium taurocholate hydrate (STH) exhibits broad-spectrum antiviral activity against influenza strains H5N6, H1N1, H3N2, H5N1, and H9N2 in vitro. STH significantly inhibited the early stages of influenza A virus replication. The levels of influenza virus viral RNA (vRNA), complementary RNA (cRNA), and mRNA were specifically reduced in virus-infected cells following STH treatment. In vivo, STH treatment of infected mice alleviated clinical signs and reduced weight loss and mortality. STH also reduced TNF-α, IL-1β, and IL-6 overexpression. STH significantly inhibited the upregulation of TLR4 and the NF-kB family member p65, both in vivo and in vitro. These results suggest that STH exerts a protective effect against influenza infection via suppression of the NF-kB pathway, highlighting the potential use of STH as a drug for treating influenza infection.