Fig. 1.

Schematic of the model.

Our mathematical model (Eq. 1) incorporates the viral dynamics of HBV-positive HDV-naïve target cells (T), two types of HDV-infected cells (I₁ and I₂), HDV virions (V), ALT (A), and HBsAg (H). Target cells become infected and convert to I₁ at rate β₁ and to I₂ at rate β₂. Virions are cleared at rate c_V. I₁ and I₂ under non-cytolytic clearance to become target cells at rates q₁ and q₂, and die at rate δ. Infected cells produce virions at rate p. Target cells are produced at rate p_T and die at rate δ_T. ALT is produced by target cell death at rate φ and by infected cell death at rate σ. ALT is cleared from blood at rate c_A. HBsAg is produced by target cells and HDV-infected cells at rate p_H and cleared from blood at rate c_H. BLV blocks infection with efficacy η and may reduce viral clearance with efficacy θ as shown with the green symbols. Blocking of HDV production by IFN, LNF or NAPs is shown using red symbols (parameter ε). Secondary effects of IFN in increasing cell death are reflected by κ >1 and NAPs efficacy in blocking HBsAg production is shown with parameter ε_H. ALT, alanine aminotransferase; BLV, bulevirtide; HBsAg, hepatitis surface antigen; HBV, hepatitis B virus; HDV, hepatitis D virus; IFN, interferon-α/λ; LNF, lonafarnib; NAPs, nucleic acid polymers.