Journal
BLOOD
Volume 103, Issue 6, Pages 2170-2179Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2003-09-3129
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Funding
- NCI NIH HHS [N01-CO-124000] Funding Source: Medline
- NIAID NIH HHS [AI52048, R21 AI52060, R01 AI40877] Funding Source: Medline
- NICHD NIH HHS [P01 HD41752] Funding Source: Medline
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HIV-1 subverts antigen processing in dendritic cells (DCs) resulting in viral uptake, infection, and transfer to T cells. Although DCs bound monomeric gp120 and HIV-1 similarly, virus rarely colocalized with endolysosomal markers, unlike gp120, suggesting HIV-1 alters endolysosomal trafficking. Virus within DC intracellular compartments rapidly moved to DCCD4(+) lymphocyte synapses when introduced to CD4(+) lymphocyte cultures. Although viral harboring and transfer from nonlysosomal compartments was transient, given DC-associated virus protein, nucleic acids, and infectious HIV-1 transfer to CD4(+), lymphocytes decayed within 24 hours. However a second long-term transfer phase was apparent in immature DCs after 48 hours as a zidovudine-sensitive rise in proviral DNA. Therefore, DCs transfer HIV-1 to CD4(+) lymphocytes in 2 distinct phases. Immature and mature DCs first divert virus from the endolysosomal pathway to the DC-T-cell synapse. Secondly, the later transfer phase from immature DCs is through de novo HIV-1 production. Thus, the controversy of DCs being infected or not infected for the mechanics of viral transfer to CD4(+) lymphocytes can be addressed as a function of time. (C) 2004 by The American Society of Hematology.
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