The novel coronavirus (COVID-19) pandemic continues to be a global health problem whose impact has been significantly felt in South Africa. With the global spread increasing and infecting millions, containment efforts by countries have largely focused on lockdowns and social distancing to minimise contact between persons. Social distancing has been touted as the best form of response in managing a rapid increase in the number of infected cases. In this paper, we present a deterministic model to describe the impact of social distancing on the transmission dynamics of COVID-19 in South Africa. The model is fitted to data from March 5 to April 13, 2020, on the cumulative number of infected cases, and a scenario analysis on different levels of social distancing is presented. The model shows that with the levels of social distancing under the initial lockdown level between March 26 and April 13, 2020, there would be a projected continued rise in the number of infected cases. The model also looks at the impact of relaxing the social distancing measures after the initial announcement of the lockdown. It is shown that relaxation of social distancing by 2% can result in a 23% rise in the number of cumulative cases whilst an increase in the level of social distancing by 2% would reduce the number of cumulative cases by about 18%. The model results accurately predicted the number of cases after the initial lockdown level was relaxed towards the end of April 2020. These results have implications on the management and policy direction in the early phase of the epidemic.

The spread of Lassa fever infection is increasing in West Africa over the last decade. The impact of this can better be understood when considering the various possible transmission routes. We designed a mathematical model for the epidemiology of Lassa Fever using a system of nonlinear ordinary differential equations to determine the effect of transmission pathways toward the infection progression in humans and rodents including those usually neglected such as the environmental surface and aerosol routes. We analyzed the model and carried out numerical simulations to determine the impact of each transmission routes. Our results showed that the burden of Lassa fever infection is increased when all the transmission routes are incorporated and most single transmission routes are less harmful, but when in combination with other transmission routes, they increase the Lassa fever burden. It is therefore important to consider multiple transmission routes to better estimate the Lassa fever burden optimally and in turn determine control strategies targeted at the transmission pathways.

Major histocompatibility complex class two (MHC-II) molecules are trans-membrane proteins and key components of the cellular immune system. Upon recognition of foreign peptides expressed on the MHC-II binding groove, CD4⁺ T cells mount an immune response against invading pathogens. Therefore, mechanistic identification and knowledge of physicochemical features that govern interactions between peptides and MHC-II molecules is useful for the design of effective epitope-based vaccines, as well as for understanding of immune responses. In this article, we present a comprehensive trans-allelic prediction model, a generalized version of our previous biophysical model, that can predict peptide interactions for all three human MHC-II loci (HLA-DR, HLA-DP, and HLA-DQ), using both peptide sequence data and structural information of MHC-II molecules. The advantage of this approach over other machine learning models is that it offers a simple and plausible physical explanation for peptide–MHC-II interactions. We train the model using a benchmark experimental dataset and measure its predictive performance using novel data. Despite its relative simplicity, we find that the model has comparable performance to the state-of-the-art method, the NetMHCIIpan method. Focusing on the physical basis of peptide–MHC binding, we find support for previous theoretical predictions about the contributions of certain binding pockets to the binding energy. In addition, we find that binding pocket P5 of HLA-DP, which was not previously considered as a primary anchor, does make strong contribution to the binding energy. Together, the results indicate that our model can serve as a useful complement to alternative approaches to predicting peptide–MHC interactions.