A delayed HIV-1 model with cell-to-cell spread and virus waning

Area of Science:

• Mathematical Biology
• Virology
• Epidemiology

Background:

• Human Immunodeficiency Virus type 1 (HIV-1) infection involves complex transmission dynamics.
• Understanding the role of intracellular delays and different transmission routes is crucial for modeling viral spread.
• Virus waning is a key factor influencing viral load and disease progression.

Purpose of the Study:

• To propose and analyze a mathematical model for HIV-1 infection incorporating delays, viral and cellular transmissions, and virus waning.
• To investigate the threshold dynamics and stability of the proposed HIV-1 model.
• To assess the impact of intracellular delays and transmission routes on HIV-1 infection dynamics.

Main Methods:

• Development of a delayed mathematical model for HIV-1 infection.
• Analysis of the basic reproduction number ($$) to determine disease persistence.
• Investigation of stability switches due to intracellular delays using analytical and numerical methods.

Main Results:

• The basic reproduction number ($$) characterizes the infection threshold.
• Positive intracellular delays can induce stability switches in the infected steady state.
• Ignoring cell-to-cell transmission leads to underestimation of HIV-1 infection risk.
• Models without virus waning show higher viral loads compared to those with virus waning.

Conclusions:

• Cell-to-cell transmission and virus waning are critical factors in HIV-1 infection dynamics.
• Intracellular delays play a significant role in the stability of infected states.
• Accurate modeling of HIV-1 transmission requires consideration of multiple factors, including delays and varied transmission routes.