TLR signalling in the liver in the setting of HIV-HBV coinfection. HIV infection results in a significant increase in circulating LPS, potentially triggering an inflammatory response via activation of TLR4. ssHIV RNA can also activate TLR7 or 8 leading to an increase in NF-κB which can drive both HIV replication and production of proinflammatory cytokines and chemokines. HBV binds to and inhibits signalling through Mal/TIRAP which would inhibit proinflammatory responses in the coinfected liver. Increased LPS and/or increased hepatic apoptosis in the coinfected liver could also activate TLR9 resulting in further inflammation and HIV replication.
