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In this paper, we study the periodic and stable dynamics of an interactive wild and sterile mosquito population model with density-dependent survival probability. We find a release amount upper bound G ∗ , depending on the release waiting period T, such that the model has exactly two periodic solutions, with one stable and another unstable, provided that the release amount does not exceed G ∗ . A numerical example is also given to illustrate our results. [ABSTRACT FROM AUTHOR]

HIV can infect cells via virus-to-cell infection or cell-to-cell viral transmission. These two infection modes may occur in a synergistic way and facilitate viral spread within an infected individual. In this paper, we developed an HIV latent infection model including both modes of transmission and time delays between viral entry and integration or viral production. We analysed the model by defining the basic reproductive number, showing the existence, positivity and boundedness of the solution, and proving the local and global stability of the infection-free and infected steady states. Numerical simulations have been performed to illustrate the theoretical results and evaluate the effects of time delays and fractions of infection leading to latency on the virus dynamics. The estimates of the relative contributions to the HIV latent reservoir and the virus population from the two modes of transmission have also been provided. [ABSTRACT FROM PUBLISHER]

Time delays can affect the dynamics of HIV infection predicted by mathematical models. In this paper, we studied two mathematical models each with two time delays. In the first model with HIV latency, one delay is the time between viral entry into a cell and the establishment of HIV latency, and the other delay is the time between cell infection and viral production. We defined the basic reproductive number and showed the local and global stability of the steady states. Numerical simulations were performed to evaluate the influence of time delays on the dynamics. In the second model with HIV immune response, one delay is the time between cell infection and viral production, and the other delay is the time needed for the adaptive immune response to emerge to control viral replication. With two positive delays, we obtained the stability crossing curves for the model, which were shown to be a series of open-ended curves. [ABSTRACT FROM AUTHOR]