A group of scientists from Xiamen University have developed a spatial model of HIV based on the Monte Carlo approach that details the virus' random behavioral dynamics. The model suggests that a particular type of T cell could be useful in the development of an AIDS vaccine.
The research is published April 29 in the New Journal of Physics in a paper titled “A stochastic spatial model of HIV dynamics with an asymmetric battle between the virus and the immune system.”
HIV infection is characterized by three phases: a spike in viral load during early acute infection, followed by a relatively steady state lasting many years, and finally a precipitous rise of viral load leading to the onset of AIDS. It is now well known that HIV has two significant capabilities, namely infection of immune system cells and mutation away from any opposing selective force. The mechanisms that promote long-term co-evolution of HIV and the immune system, leading finally to the development of AIDS, however, remain obscure.
The researchers’ goal was to create a more detailed and realistic simulation by incorporating many important features of HIV dynamics, which include infections, replications and mutations of viruses, antigen recognitions, activations and proliferations of lymphocytes, as well as diffusions, encounters, and interactions of virions and lymphocytes.
The interactions between viruses and the immune system in all the three phases were investigated. The researchers assessed the relative importance of various immune system components in the acute phase. The dynamics of how the two important factors, namely the viral diversity and the asymmetric battle between HIV and the immune system, result in AIDS were also investigated.
The model successfully reproduced the three-phase pattern observed in HIV infection, and the simulation results for the time distribution from infection to AIDS onset were also in good agreement with the clinical data, the Xiamen team reports.
They say that the different duration of the asymptomatic phase across patients is due to stochastic effects associated with viral evolution. There is good agreement between the model's predictions and the clinical data concerning the proportion of patients who develop AIDS after a given time following infection.
Additionally, patterns emerging from the new model suggest that CD8+ T cells could be used to stimulate a stronger response against the virus, the researchers report. This particular type of T cell does not appear to be as preferentially targeted by HIV as its counterpart and also appears to be more actively involved in suppressing the virus down during the first acute phase of the infection.