Objective:To investigate the status of viral reservoirs in prostate tissue of patients with human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS), and to investigate the effect of highly active anti-retroviral therapy (HAART) on HIV-1 DNA in prostate tissue of HIV/AIDS patients.Methods:Twelve patients with HIV infection and hyperplasia of prostate who required surgical treatment and admitted to Guangzhou Eighth People′s Hospital from July 2017 to October 2019 were included. Blood and prostate specimens of these patients were collected, and HIV-1 RNA in plasma, CD4 + T lymphocyte count in peripheral blood and HIV-1 DNA level in prostate tissue were tested respectively. The independent sample t test or Mann-Whitney U test was used for statistical analysis. Results:Among the 12 patients, the CD4 + T lymphocytes was (519.8±121.5)/μL and HIV-1 DNA in the prostate tissue was 2 602 (365, 10 700) copies/10 6cells in six patients who had not started HAART. The CD4 + T lymphocytes was (182.8±69.7)/μL and the HIV-1 DNA in the prostate tissue was 144 (36, 563) copies/10 6cells in the six patients who underwent HAART for over six months. There were statistically significant differences in CD4 + T lymphocytes and HIV-1 DNA in the prostate tissue between the two groups ( t=-5.889 and Z=-2.082, respectively, both P<0.05). Conclusion:Prostate tissue can be used as an HIV-1 virus repository with or without HAART, and the size of the prostate tissue virus repository can be reduced by HAART after immune reconstitution.

Purpose: We aimed to investigate the mechanism of phenotypic transformation of corporal cavernosum smooth muscle cells (CCSMCs) under hypoxic conditions in vitro. Materials and Methods: In this study, a hypoxia model was established using cobalt chloride (CoCl2). CCSMCs were treated with different concentrations of CoCl2 for varying time periods, and cell viability was assessed. Hypoxia-inducible factor-1α (HIF-1α), myocardin (Myocd) and phenotypic markers were detected in the CCSMCs. We also transfected the CCSMCs with si-HIF-1α and Ad-Myocd and evaluated the effects on phenotypic modulation of CCSMCs and the relationship between HIF-1α and Myocd was evaluated. Results: CoCl2 inhibited the viability of CCSMCs in a dose- and time-dependent manner, and treatment with 300 µM CoCl2 for 48 hours were the optimal conditions for establishing the hypoxia model. The results showed increased expression levels of HIF-1α and osteopontin and decreased Myocd, alpha-smooth muscle actin, and calponin levels in CCSMCs under hypoxia. HIF-1α knockdown reversed hypoxia-induced phenotypic transformation with elevated Myocd expression. Overexpression of Myocd also reversed the effect of hypoxia on the phenotypic switch, but did not affect HIF-1α expression. Conclusions Our findings showed that HIF-1α was involved in the effect of hypoxia induced by CoCl2 on CCSMC phenotypic modulation, and Myocd overexpression could inhibit this process. Thus, Myocd might be a potential therapeutic target for erectile dysfunction under hypoxia or HIF-1α activation.