HIV preferentially infects activated CD4+T cells.Current antiretroviral therapy cannot eradicate the virus. Viral infection of other cells such as macrophages may contribute to viral persistence during antiretroviral therapy. In addition to cell-free virus infection, macrophages can also get infected when engulfing infected CD4+ T cells as innate immune sentinels. How macrophages affect the dynamics of HIV infection remains unclear. In this paper, we develop an HIV model that includes the infection of CD4+ T cells and macrophages via cell-free virus infection and cell-to-cell viral transmission. We derive the basic reproduction number and obtain the local and global stability of the steady states. Sensitivity and viral dynamics simulations show that even when the infection of CD4+ T cells is completely blocked by therapy, virus can still persist and the steady-state viral load is not sensitive to the change of treatment efficacy. Analysis of the relative contributions to viral replication shows that cell-free virus infection leads to themajority of macrophage infection.Viral transmission from infectedCD4+Tcells to macrophages during engulfment accounts for a small fraction of the macrophage infection and has a negligible effect on the total viral production. These results suggest that macrophage infection can be a source contributing to HIV persistence during suppressive therapy. Improving drug efficacies in heterogeneous target cells is crucial for achieving HIV eradication in infected individuals. This is a joint work with Ting Guo and Libin Rong.

邱志鹏，南京理工大学江阴校区基础前沿交叉中心主任、教授、博士生导师。主要从事常微分方程、动力系统与生物数学的研究工作，正在或完成主持国家自然科学基金4项，国家自然科学基金国际合作基金1项，教育部留学回国基金1项，参加国家自然科学基金面上项目2项和江苏省自然科学基金青年项目1项，目前已在Bull. Math. Biol., Math. Biosci., J. Diff. Equs., SIAM J. Appl. Math., J. Math. Biol., J. Theor. Biol.等期刊上发表论文50余篇，曾先后访问过美国Purdue大学、Florida大学，意大利Trento大学、加拿大York大学和Alberta大学。