ltered dynamics and differential infection profiles of lymphoid and myeloid cell subsets during acute and chronic HIV-1 infection.
Centlivre M., Legrand N., Legrand N., Steingrover R., van der Sluis R., Grijsen ML., Bakker M., Jurriaans S., Berkhout B., Paxton WA., Prins JM., Pollakis G.
The dynamics of immune cell populations during acute HIV-1 infection are not fully deciphered, especially for non-T cells. In this study, we tested whether specific cellular subsets of the innate arm of the immune response are affected early after HIV-1 infection. Using a cohort of HIV-1-infected individuals, we have monitored the relative frequency of blood T lymphocytes, monocytes, and DCs at various infection stages and measured their respective intracellular HIV-1 DNA loads. The HIV-1 DNA load in naive CD4(+) T lymphocytes, which are lost very early during acute infection, was ten- to 100-fold lower than in CD57(-) and CD57(+) memory CD4(+) T lymphocytes. We observed that despite rapid, persistent loss after HIV-1 infection, pDCs represented a non-negligible HIV-1 DNA reservoir. CD16(+) proinflammatory cDCs and monocytes accumulated gradually, and HIV-infected CD16(+) monocytes contained higher HIV-1 DNA loads than their CD16(-) counterpart during acute infection. During chronic infection, CD16(+) cDCs exhibited higher HIV-1 DNA loads than the CD16(-) population. Overall, our results demonstrate that non-T cell compartments are a major HIV-1 DNA reservoir, and CD16(+) monocytes and CD16(+) cDCs potentially play an important role in HIV-1 dissemination.