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Rabies among dogs remains a considerable risk to humans and constitutes a serious public health concern in many parts of the world. Conventional mathematical models for rabies typically assume homogeneous environments, with a standard diffusion term for the population of rabid animals. It has recently been recognized, however, that spatial heterogeneity plays an important role in determining spatial patterns of rabies and the cost-effectiveness of vaccinations. In this paper, we develop a spatially heterogeneous dog rabies model by using the θ -diffusion equation, where θ reflects the way individual dogs make movement decisions in the underlying random walk. We numerically investigate the dynamics of the model in three diffusion cases: homogeneous, city-wild, and Gaussian-type. We find that the initial conditions affect whether traveling waves or epizootic waves can be observed. However, different initial conditions have little impact on steady-state solutions. An “active” interface is observed between city and wild regions, with a “ridge” on the city side and a “valley” on the wild side for the infectious dog population. In addition, the progressing speed of epizootic waves changes in heterogeneous environments. It is impossible to eliminate rabies in the entire spatial domain if vaccination is focused only in the city region or only in the wild region. When a seasonal transmission is incorporated, the dog population size approaches a positive time-periodic spatially heterogeneous state eventually. [ABSTRACT FROM AUTHOR]

Stable periodic oscillations have been shown to exist in mathematical models for the CTL response to HTLV-I infection. These periodic oscillations can be the result of mitosis of infected target CD4 cells, of a general form of response function, or of time delays in the CTL response. In this study, we show through a simple mathematical model that time delays in the CTL response process to HTLV-I infection can lead to the coexistence of multiple stable periodic solutions, which differ in amplitude and period, with their own basins of attraction. Our results imply that the dynamic interactions between the CTL immune response and HTLV-I infection are very complex, and that multi-stability in CTL response dynamics can exist in the form of coexisting stable oscillations instead of stable equilibria. Biologically, our findings imply that different routes or initial dosages of the viral infection may lead to quantitatively and qualitatively different outcomes. [ABSTRACT FROM AUTHOR]

Abstract: Human T-cell Lymphotropic Virus Type I (HTLV-I) primarily infects CD4+ helper T cells. HTLV-I infection is clinically linked to the development of Adult T-cell Leukemia/Lymphoma and of HTLV-I Associated Myelopathy/Tropical Spastic Paraparesis, among other illnesses. HTLV-I transmission can be either horizontal through cell-to-cell contact, or vertical through mitotic division of infected CD4+ T cells. It has been observed that HTLV-I infection has a high proviral load but a low rate of proviral genetic variation. This suggests that vertical transmission through mitotic division of infected cells may play an important role. We consider and analyze a mathematical model for HTLV-I infection of CD4+ T cells that incorporates both horizontal and vertical transmission. Among interesting dynamical behaviors of the model is a backward bifurcation which raises many new challenges to effective infection control. [Copyright &y& Elsevier]

Rabies among dogs remains a considerable risk to humans and constitutes a serious public health concern in many parts of the world. Conventional mathematical models for rabies typically assume homogeneous environments, with a standard diffusion term for the population of rabid animals. It has recently been recognized, however, that spatial heterogeneity plays an important role in determining spatial patterns of rabies and the cost-effectiveness of vaccinations. In this paper, we develop a spatially heterogeneous dog rabies model by using the [Formula: see text]-diffusion equation, where [Formula: see text] reflects the way individual dogs make movement decisions in the underlying random walk. We numerically investigate the dynamics of the model in three diffusion cases: homogeneous, city-wild, and Gaussian-type. We find that the initial conditions affect whether traveling waves or epizootic waves can be observed. However, different initial conditions have little impact on steady-state solutions. An "active" interface is observed between city and wild regions, with a "ridge" on the city side and a "valley" on the wild side for the infectious dog population. In addition, the progressing speed of epizootic waves changes in heterogeneous environments. It is impossible to eliminate rabies in the entire spatial domain if vaccination is focused only in the city region or only in the wild region. When a seasonal transmission is incorporated, the dog population size approaches a positive time-periodic spatially heterogeneous state eventually.

Human T-cell leukaemia/lymphoma virus type I (HTLV-I) is a retrovirus that has been identified as the causative agent of HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and other illnesses. HTLV-I infects primarily CD4(+) T cells and the transmission occurs through direct cell-to-cell contact. HAM/TSP patients harbor higher proviral loads in peripheral blood lymphocytes than asymptomatic carriers. Also, HAM/TSP patients exhibit a remarkably high number of circulating HTLV-I-specific CD8(+) cytotoxic T lymphocytes (CTLs) in the peripheral blood. While CTLs have a protective role by killing the infected cells and lowering the proviral load, a high level of CTLs and their cytotoxicity are believed to be a main cause of the development of HAM/TSP. A mathematical model for HTLV-I infection of CD4(+) T cells that incorporates the CD8(+) cytotoxic T-cell (CTL) response is investigated. Our mathematical analysis reveals that the system can stabilize at a carrier steady-state with persistent viral infection but no CTL response, or at a HAM/TSP steady-state at which both the viral infection and CTL response are persistent. We also establish two threshold parameters R(0) and R(1), the basic reproduction numbers for viral persistence and for CTL response, respectively. We show that the parameter R(1) can be used to distinguish asymptomatic carriers from HAM/TSP patients, and as an important control parameter for preventing the development of HAM/TSP.