Mathematical model of multivalent virus-antibody complex formation in humans following acute and chronic HIV infections
A mathematical model of multivalent antibody binding that accounts for the formation of anti-gp41 IgG-virion immune complexes with different numbers of bound antibodies is developed to investigate the mechanisms leading to immune complex formation during acute and chronic HIV infection. The predictions are compared with published temporal virus and anti-gp41 IgG-virion immune complexes data from six acutely infected HIV patients. The model is also used to predict conditions under which the pre-existing or HIV-induced antibodies contribute to viral protection. Under the assumption that the number of binding sites is constant among all virions and that all trimers are bound with the same affinity by monolocal antibodies, the dynamics between the plasma virus population and the plasma anti-gp41 antibody population is determined. Furthermore, the amount and quality of pre-existing antibodies needed for blocking infection is quantified in three cases when multivalent binding (i) has no antiviral effect, (ii) reduces virus infectivity, or (iii) increases virus clearance. The results reported in the paper provide insight into the virus-antibody interactions that can be useful for the design of an antibody-mediated vaccine against HIV.
scientific article; zbMATH DE number 6480833
scientific article