{"doi":"10.21007/etd.cghs.2020.0506","title":"Tobacco/HIV-1-Induced Myeloid Cell-Derived Extracellular Vesicles in HIV-1 Pathogenesis","abstract":"Introduction. Introduction. Smoking, which is highly prevalent in people living with HIV/AIDS, has been shown to exacerbate HIV-1 replication, in part via cytochrome P450 (CYP)-induced oxidative stress. CYP enzymes metabolize cigarette smoke condensate (CSC), causing oxidative stress and cytotoxicity. Our previous studies have demonstrated that CSC and specific CSC constituents, benzo(a)pyrene and nicotine, potentially induce CYPs, resulting in higher oxidative stress and subsequent exacerbation of HIV-1 replication in monocytes and macrophages. However, the exact mechanism behind tobacco-induced, oxidative stress-mediated enhancement of HIV-1 replication is still poorly understood. Extracellular vesicles (EVs) have recently gained attention for their unique nature as intercellular messengers which can package proteins, nucleic acids, lipids etc. EVs are known to alter HIV-1 pathogenesis through intercellular communication. Until now, the role of EVs in smoking-enhanced HIV-1 pathogenesis has been mostly unknown. In this study, we investigated the effect of CSC on the characteristics and differential packaging of monocyte-and macrophage-derived EVs, and their influence on HIV-1 replication. We hypothesized that CSC-and/or HIV-1-exposed monocyte and macrophage-derived EVs and their components, especially pro-oxidant factors, are key mediators of HIV-1 replication. Methods. Methods. Two monocytic cell lines, U937 and HIV-1-infected U1 cells, and macrophages derived from these monocytes, as well as macrophages derived from primary human monocytes were used. Cells were treated with 10 g/ml/day CSC. After treatment, the cells were harvested, and the supernatant was collected for isolating EVs by Total Exosome Isolation kit. The isolated EVs were characterized for their biophysical properties. Next, monocyte-derived macrophages were exposed to EVs, as well as subjected to downstream analysis (p24 ELISA, LDH cytotoxicity assay, DNA damage assay, rtPCR, western blot, cytokine analysis).","journal":null,"year":2020,"id":130177,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":0,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9536,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2020-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":582457,"name":"Sanjana Haque","orcid":"0000-0003-1469-6232","position":0,"is_corresponding":true}],"reference_count":245,"raw_metadata":null,"created_at":"2026-07-18T23:15:53.196774Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}