Chinese human immunodeficiency virus-1 patients with different routes of transmission exhibit altered expression levels of blood dendritic cell subpopulations.

Viral Immunol

Immunology and Reproductive Biology Laboratory of Medical School and State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, China.

Published: February 2011

Dendritic cells (DCs) play a pivotal role in the pathogenesis of human immunodeficiency virus-1 (HIV-1). Reduced numbers of blood DCs have been observed in individuals with chronic HIV-1 infection. In the present study, we analyzed the expression levels of monocytes, myeloid dendritic cell (mDC) precursors, mDCs, and plasmacytoid dendritic cells (pDCs), in HIV-1-infected patients in China who were infected via different routes of transmission, including heterosexual and homosexual sexual contact, and blood transmission through importation of blood or blood products, to further elucidate their role in HIV. Compared with HIV-negative individuals (n = 40), relative levels of CD11c+CD14⁻mDCs, CD11c++CD123(low) mDCs, and CD11c⁻CD123+ pDCs in total peripheral blood mononuclear cells (PBMCs) were significantly lower in all HIV patients (n = 93), and in those with blood transmission (n = 26) and heterosexual transmission (n = 43), while relative levels of CD11c+CD14⁻mDCs were significantly lower in HIV patients infected via homosexual transmission (n = 24). The results of correlation analysis demonstrated a significant negative correlation between CD4+ T-cell counts and the relative levels of CD11c++CD123(low) mDCs in HIV-I patients infected via blood transmission. There was no significant correlation between CD4+ T-cell counts and the expression level of other DC subpopulations in PBMCs from HIV patients. The results of this study suggest that HIV-1 patients with different routes of transmission exhibit altered expression levels of blood DC subpopulations, which contributes to dysregulated immune responses and pathogenesis of HIV-1.

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http://dx.doi.org/10.1089/vim.2010.0038DOI Listing

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