To study the impact of media coverage on spread and control of infectious diseases, we use a susceptible-exposed-infective (SEI) model, including individuals' behavior changes in their contacts due to the influences of media coverage, and fully investigate the model dynamics. We define the basic reproductive number ?0 for the model, and show that the modeled disease dies out regardless of initial infections when ?0< 1, and becomes uniformly persistently endemic if ?0>1. When the disease is endemic and the influence of the media coverage is less than or equal to a critical number, there exists a unique endemic equilibrium which is asymptotical stable provided ?0 is greater than and near one. However, if ?0 is larger than a critical number, the model can undergo Hopf bifurcation such that multiple endemic equilibria are bifurcated from the unique endemic equilibrium as the influence of the media coverage is increased to a threshold value. Using numerical simulations we obtain results on the effects of media coverage on the endemic that the media coverage may decrease the peak value of the infectives or the average number of the infectives in different cases. We show, however, that given larger ?0, the influence of the media coverage may as well result in increasing the average number of the infectives, which brings challenges to the control and prevention of infectious diseases.

In this paper, we propose and analyze a delayed HIV-1 model with CTL immune response and virus waning. The two discrete delays stand for the time for infected cells to produce viruses after viral entry and for the time for CD8+ T cell immune response to emerge to control viral replication. We obtain the positiveness and boundedness of solutions and find the basic reproduction number R0. If R0 < 1, then the infection-free steady state is globally asymptotically stable and the infection is cleared from the T-cell population; whereas if R0 > 1, then the system is uniformly persistent and the viral concentration maintains at some constant level. The global dynamics when R0 > 1 is complicated. We establish the local stability of the infected steady state and show that Hopf bifurcation can occur. Both analytical and numerical results indicate that if, in the initial infection stage, the effect of delays on HIV-1 infection is ignored, then the risk of HIV-1 infection (if persists) will be underestimated. Moreover, the viral load differs from that without virus waning. These results highlight the important role of delays and virus waning on HIV-1 infection.

In this paper, we include two time delays in a mathematical model for the CD8+ cytotoxic T lymphocytes (CTLs) response to the Human T-cell leukaemia virus type I (HTLV-I) infection, where one is the intracellular infection delay and the other is the immune delay to account for a series of immunological events leading to the CTL response. We show that the global dynamics of the model system are determined by two threshold values R0, the corresponding reproductive number of a viral infection, and R1, the corresponding reproductive number of a CTL response, respectively. If R0 < 1, the infection-free equilibrium is globally asymptotically stable, and the HTLV-I viruses are cleared. If R1<1