Yeah, here is an early paper of a math model talking about just that. I've read the switch happens more if when HIV is not controlled with high VL runs.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1346847/
Naïve and Memory Cell Turnover as Drivers of CCR5-to-CXCR4 Tropism Switch in Human Immunodeficiency Virus Type 1: Implications for Therapy
Early human immunodeficiency virus infection is characterized by the predominance of CCR5-tropic (R5) virus. However, in many individuals CXCR4-tropic (X4) virus appears in late infection. The reasons for this phenotypic switch are unclear. The patterns of chemokine receptor expression suggest that X4 and R5 viruses have a preferential tropism for naïve and memory T cells, respectively. Since memory cells divide approximately 10 times as often as naïve cells in uninfected individuals, a tropism for memory cells in early infection may provide an advantage. However, with disease progression both naïve and memory cell division frequencies increase, and at low CD4 counts, the naïve cell division frequency approaches that of memory cells. This may provide a basis for the phenotypic switch from R5 to X4 virus observed in late infection. We show that a model of infection using observed values for cell turnover supports this mechanism. The phenotypic switch from R5 to X4 virus occurs at low CD4 counts and is accompanied by a rapid rise in viral load and drop in CD4 count . Thus, low CD4 counts are both a cause and an effect of X4 virus dominance. We also investigate the effects of different antiviral strategies. Surprisingly, these results suggest that both conventional antiretroviral regimens and CCR5 receptor-blocking drugs will promote R5 virus over X4 virus.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1346847/
Naïve and Memory Cell Turnover as Drivers of CCR5-to-CXCR4 Tropism Switch in Human Immunodeficiency Virus Type 1: Implications for Therapy
Early human immunodeficiency virus infection is characterized by the predominance of CCR5-tropic (R5) virus. However, in many individuals CXCR4-tropic (X4) virus appears in late infection. The reasons for this phenotypic switch are unclear. The patterns of chemokine receptor expression suggest that X4 and R5 viruses have a preferential tropism for naïve and memory T cells, respectively. Since memory cells divide approximately 10 times as often as naïve cells in uninfected individuals, a tropism for memory cells in early infection may provide an advantage. However, with disease progression both naïve and memory cell division frequencies increase, and at low CD4 counts, the naïve cell division frequency approaches that of memory cells. This may provide a basis for the phenotypic switch from R5 to X4 virus observed in late infection. We show that a model of infection using observed values for cell turnover supports this mechanism. The phenotypic switch from R5 to X4 virus occurs at low CD4 counts and is accompanied by a rapid rise in viral load and drop in CD4 count . Thus, low CD4 counts are both a cause and an effect of X4 virus dominance. We also investigate the effects of different antiviral strategies. Surprisingly, these results suggest that both conventional antiretroviral regimens and CCR5 receptor-blocking drugs will promote R5 virus over X4 virus.
Quote:In this paper we develop a mathematical model to explore the relationship between cell turnover and the evolution of viral phenotype. We demonstrate that either an association of cell division with increased viral production or with increased infectivity is consistent with the observed phenotypic changes. We also examine the effects of conventional antiretroviral therapy using this model. Our results suggest that successful treatment, which leads to a reduction in viral load and T-cell turnover (23), should result in a reversion from the CXCR4 phenotype to the CCR5 phenotype. This reversion has been observed in treated patients, especially those with a strong treatment-induced suppression in viral load (48). Finally, we use the model to predict the effects of drugs that block the interaction of the virus with cellular chemokine receptors (CCR5-blocking drugs) on viral phenotype and disease progression. The model suggests that CCR5-blocking drugs will not promote a conversion to X4 virus, and when given early in disease may even delay the emergence of X4 virus. When given after the emergence of X4 virus, CCR5-blocking drugs may still inhibit X4 virus. If R5 virus levels remain significant, then by reducing the level of R5 virus, they may allow some CD4 cell recovery, thereby reducing naïve cell turnover and X4 virus production.
2
