There are different views on which of the two forms of viral spread is more efficient in vivo between cell-free and cell-associated virus. In this study, discrete time human immunodeficiency virus models are formulated and analysed with the goal of determining the form of viral spread that is more efficient in vivo. It is shown that on its own, cell-free viral spread cannot sustain an infection owing to the low infectivity of cell-free virus and cell-associated virus can sustain an infection because of the high infectivity of cell-associated virus. When acting concurrently, cell-associated virus is more efficient in spreading the infection upon exposure to the virus. However, in the long term, the two forms of viral spread contribute almost equally. Both forms of viral spread are shown to be able to initiate an infection.
BackgroundThe presence of an asymptomatic phase in an HIV infection indicates that the immune system can partially control the infection. Determining the immune mechanisms that contribute significantly to the partial control of the infection enhance the HIV infection intervention strategies and is important in vaccine development. Towards this goal, a discrete time HIV model, which incorporates the life cycle aspects of the virus, the antibody (humoral) response and the cell-mediated immune response is formulated to determine immune system components that are most efficient in controlling viral levels. Ecological relationships are used to model the interplay between the immune system components and the HIV pathogen. Model simulations and transient elasticity analysis of the viral levels to immune response parameters are used to compare the different immune mechanisms.ResultsIt is shown that cell-mediated immune response is more effective in controlling the viral levels than the antibody response. Killing of infected cells is shown to be crucial in controlling the viral levels. Our results show a negative correlation between the antibody response and the viral levels in the early stages of the infection, but we predicted this immune mechanism to be positively correlated with the viral levels in the late stage of the infection. A result that suggests lack of relevance of antibody response with infection progression. On the contrary, we predicted the cell-mediated immune response to be always negatively correlated with viral levels.ConclusionNeutralizing antibodies can only control the viral levels in the early days of the HIV infection whereas cell-mediated immune response is beneficial during all the stages of the infection. This study predicts that vaccine design efforts should also focus on stimulating killer T cells that target infected cells.Electronic supplementary materialThe online version of this article (doi:10.1186/1756-0500-7-737) contains supplementary material, which is available to authorized users.
The role of antibodies in HIV-1 infection is investigated using a discrete-time mathematical model that considers cell-free and cell-associated transmission of the virus. Model analysis shows that the effect of each type of antibody is dependent on the stage of the infection. Neutralizing antibodies are efficient in controlling the viral levels in the early days after seroconversion and antibodies that coat HIV-1-infected cells and recruit effector cells to either kill the HIV-1-infected cells or inhibit viral replication are efficient when the infection becomes established. Model simulations show that antibodies that inhibit viral replication are more effective in controlling the infection than those that recruit Natural Killer T cells after infection establishment. The model was fitted to subjects of the Tsedimoso study conducted in Botswana and conclusions similar to elasticity analysis results were obtained. Model fitting results predicted that neutralizing antibodies are more efficient in controlling the viral levels than antibodies that coat HIV-1-infected cells and recruit effector cells to either kill the HIV-1-infected cells or inhibit viral replication in the early days after seroconversion.
Unique severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2/COVID-19) prevention measures to distinct age, geographical and community groupings can only be effectively and efficiently implemented with a clear understanding on dynamics of the disease. Dynamics include disease spread, different risk factors and their level of influence and individual attributes that aid the spread. The paper aims at determining the major COVID-19 spread risk factors in Zimbabwe by identifying individual, age and community groupings, their risk levels given the complex heterogeneous population. COVID-19 data for 37 individuals as provided by the Ministry of Health and Child Care (MoHCC) for the period from 20 March-14 May 2020 is used. Generalised Mixture Models were implemented to achieve the objectives. Results show that gender, age, mode of infection and history of travel were the main predictors of COVID-19 spread in Zimbabwe. However, their effects were distributed differently across two clusters. Children (0-14) years, females and those with imported infections were among high level risk spread groups. Whilst low risk groups consist non travelers, males and those infected by local transmission. We thus recommend that the Zimbabwean government need to prioritise children, females, and non-travelers when implementing prevention measures.
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