Semen-derived enhancer of viral infection(SEVI) is a peptide fragment (PAP248-286) from prostatic acid phosphatase(PAP), which can enhance human immunodeficiency virus infection. The mechanisms of SEVI include: (1) SEVI with several cationic amino acid residues reduced electrostatic repulsion between HIV virus and the target cells; (2) The disorder state of SEVI in the human body fluids was helpful to the interaction between virus and the target cell membranes; (3) SEVI could capture HIV particles directly and speed the velocity of virus on the surface of the target cells and improve adsorption and fusion. Currently, the substances of inhibiting SEVI activity include: EGCG from green tea, small molecule compound of aminoquinoline Surfen, ThT analogs BTA-EG6. Those compounds might block the combination of HIV and SEVI or prevent the formation of amyloid fibers, and then reduce the enhancement of SEVI. The studies on the biological characteristics and mechanisms of SEVI have a big benefit for the prevention and treatment of HIV infection.
HIV Infections ; etiology ; transmission ; Humans ; Male ; Semen ; physiology ; Sexually Transmitted Diseases, Viral ; etiology ; Static Electricity

Objective To investigate the effects of atorvastatin on parathyroid hormone1-34 (PTH1-34) induced neonatal rat cardiomyocytes hypertrophy and on the expression changes of small GTP-binding protein (K-Ras) and extracellular signal regulated protein kinases 1/2 (ERK1/2).Methods Neonatal rat cardiomyocytes hypertrophy was established with 10-7 mol/L rPTH1-34 in the presence or absence of 10-5 mol/L atorvastatin or 10-4 mol/L mevalonic acid (MVA).Cardiomyocyte diameter was measured by Motic Images Advanced 3.0 software,the synthetic rate of protein in cardiomyocytes was determined by 3 H-leucine incorporation and single-cell protein content was measured by BCA.The concentration of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were determined by ELISA.Protein expression of ERK1/2、p-ERK1/2 and K-Ras was detected by Western blot.Results Compared to PTH1-34 group,cellular diameter was decreased 12.07 μm,3 H-leucine incorporation decreased 1622 cpm/well and singlecell protein content decreased 84.34 pg,ANP or BNP concentration reduced 7.13 μg/L or 20.04 μg/L,protein expression of K-Ras,ERK1/2 or p-ERK1/2 downregulated 0.81,0.19 and 1.44 fold,respectively,in PTH1-34 plus atrovastatin co-treated cardiomyocytes (all P ＜ 0.05).Compared to PTH1-34 plus atrovastatin co-treated group,cardiomyocyte diameter increased 4.95 μm,3H-leucine incorporation increased 750 cpm/well and single-cell protein content increased 49.08 pg,ANP or BNP increased 3.12μg/L or 9.35 μg/L aud protein expression of K-Ras,ERK1/2 or p-ERK1/2 upregulated 0.52,0.06 and 1.19 fold (all P ＜ 0.05) in MVA,PTH1-34 and atrovastatin co-treated cardiomyocytes.Conclusions Atrovastatin attenuates PTH1-34 induced neonatal rat cardiomyocytes hypertrophy through downregulating K-Ras and ERK1/2 pathway.