Mathematical models of the interrelated dynamics of hepatitis D and B

•We develop models for HBV and HDV dynamics in vivo.•Inefficacy of lamivudine for chronic coinfection provides empirical test for models.•We compare models with and without infected hepatocyte proliferation.•Results imply need for infected cell proliferation to sustain chronic coinfection.

The hepatitis delta virus (HDV) is a rarest form of viral hepatitis, but has the worst outcomes for patients. It is a subviral satellite dependent on coinfection with hepatitis B (HBV) to replicate within the host liver. To date, there has been little to no modeling effort for HDV. Deriving and analyzing such a mathematical model poses difficulty as it requires the inclusion of (HBV). Here we begin with a well-studied HBV model from the literature and expand it to incorporate HDV. We investigate two models, one with and one without infected hepatocyte replication. Additionally, we consider treatment by the drug lamivudine. Comparison of model simulations with experimental results of lamivudine treatment indicate that infected cell proliferation may play a significant role in chronic HDV infection. Our results also shed light on several questions surrounding HDV and illustrate the need for more data.