Backward bifurcation in within-host HIV models.

Area of Science:

• Immunology
• Mathematical Biology
• Virology

Background:

• Naive CD4 T cells activate and proliferate, generating helper T cells and increasing susceptibility to HIV.
• HIV dynamics can be influenced by the generation of new susceptible cell populations.

Purpose of the Study:

• To investigate the phenomenon of backward bifurcation in within-host HIV models.
• To determine the conditions under which bistability occurs in HIV infection.

Main Methods:

• Construction of a simple within-host HIV model incorporating key variables: healthy naive CD4 T cells, helper T cells, infected CD4 T cells, and virus.
• Theoretical and numerical analysis of the model, particularly concerning the viral basic reproduction number (R₀) and the threshold R_C.

Main Results:

• Bistability, characterized by backward bifurcation, can occur when R_C < R₀ < 1.
• The activation of healthy naive CD4 T cells into helper T cells contributes to the susceptible population and backward bifurcation.
• Backward bifurcation may persist even with latent infections and in extended models including CTL dynamics.

Conclusions:

• The generation of new susceptible cells through naive CD4 T cell activation can lead to bistability in HIV dynamics.
• Reducing the viral reproduction number below R_C is crucial for controlling within-host HIV spread.
• Therapeutic strategies may need to target the reduction of R₀ to below R_C to effectively manage HIV infection.