Abstract
Macrophages and CD4(+) T cells are natural target cells for HIV-1, and both cell types contribute to the establishment of the viral reservoir that is responsible for continuous residual virus replication during antiretroviral therapy and viral load rebound upon treatment interruption. Scientific findings that support a critical role for the infected monocyte/macrophage in HIV-1-associated diseases, such as neurological disorders and cardiovascular disease, are accumulating. To prevent or treat these HIV-1-related diseases, we need to halt HIV-1 replication in the macrophage reservoir. This article describes our current knowledge of how monocytes and certain macrophage subsets are able to restrict HIV-1 infection, in addition to what makes macrophages respond less well to current antiretroviral drugs as compared with CD4(+) T cells. These insights will help to find novel approaches that can be used to meet this challenge
| Original language | English |
|---|---|
| Pages (from-to) | 187-208 |
| Journal | Future Virology |
| Volume | 6 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2011 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
-
SDG 3 Good Health and Well-being
Fingerprint
Dive into the research topics of 'HIV-1 and the macrophage'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver