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Quantification of total HIV‐1 DNA in seminal and blood samples in men under cART
Author(s) -
TorresStrubbe Rafael J.,
GodoyMuñoz Lenin J.,
Figueroa Lysmarie J.,
Hill Martin J.
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.674.4
Subject(s) - semen , viremia , peripheral blood mononuclear cell , biology , viral load , andrology , immunology , real time polymerase chain reaction , human immunodeficiency virus (hiv) , virology , physiology , medicine , genetics , in vitro , gene
Although antiretroviral therapy (ART) exists there are some anatomical sites that serve as drug‐sanctuaries for HIV‐1 treatment. Semen is the principal vector for HIV‐1 transmissions worldwide. Infectious HIV‐1 is found in seminal plasma and in seminal leukocytes. Previous studies have shown that copies of total HIV‐1 DNA are higher in blood than in semen; however, these studies only focus in men with less than two years living with the disease. Studies suggest that semen can be a reservoir promoting the transcription of the virus when it reaches non‐detectable levels. Therefore, we hypothesize that patients undergoing antiretroviral therapy and with non‐detectable viremia should present higher HIV‐1 DNA copies in semen than in blood. Patients with paired semen and blood samples were selected from a previous longitudinal study based on the inclusion criteria. Patient selection criteria included non‐detectable viremia and more than two years under ART. Peripheral blood mononuclear cells and seminal cells were isolated from blood and semen samples from each patient to extract genomic DNA. rtPCR was used to assess total HIV‐1 DNA on each compartment. Our results show higher number of HIV‐1 copies in blood that in seminal cells. Despite the theory of semen being a drug sanctuary and a reservoir for HIV‐1, there may be other factors involve in the ongoing viral replication in blood. Support or Funding Information This work was supported by NIGMS‐NIH grants: 5SC3GM088032‐08 (MH), UPR‐Ponce Research Initiative for Scientific Enhancement (R25GM096955) The authors also acknowledge the support from the Molecular and Genomics Core (MAGIC) at Ponce Health Sciences University (NIMHD Grant MD007579). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .