Anti-HAV VP1 Recombinant Antibody (K2-4F2) (CAT#: MRO-539LC)

Belkaya, Serkan, et al. "Inherited IL-18BP deficiency in human fulminant viral hepatitis." Journal of Experimental Medicine 216.8 (2019): 1777-1790. https://doi.org/10.1084/jem.20190669

This research explores a rare genetic cause of fulminant viral hepatitis (FVH), a severe condition that occurs in otherwise healthy individuals during primary infection with common liver-tropic viruses. The study identifies a homozygous 40-nucleotide deletion in the IL18BP gene, which encodes the IL-18 binding protein (IL-18BP), in a child who died from FVH after hepatitis A virus infection. Through detailed genetic and functional analyses, the researchers demonstrate that this mutation results in complete IL-18BP deficiency, preventing the neutralization of IL-18, a cytokine that can activate natural killer (NK) cells. In vitro experiments reveal that excessive IL-18 activity in the absence of IL-18BP leads to uncontrolled NK cell-mediated killing of hepatocytes. This discovery provides the first proof that FVH can be caused by a single-gene inborn error that selectively disrupts liver-specific immunity.
Creative Biolabs provided mouse anti-HAV VP1 antibody (K2-4F2) that was used for immunostaining hepatitis A virus in infected hepatocytes. This antibody enabled researchers to detect and visualize HAV infection in hepatocyte cell culture models, which was crucial for studying the mechanisms of IL-18/IL-18BP-mediated hepatotoxicity in the context of viral infection. The ability to specifically identify HAV-infected cells helped establish that IL-18-activated NK cells kill both infected and uninfected hepatocytes, and that this cytotoxicity could be reversed by the addition of IL-18BP, supporting the central hypothesis about the role of IL-18BP deficiency in FVH pathogenesis.