摘要
To explore the antiviral effect and mechanism of polysaccharide from Spirulina platensis （PSP） on herpes simplex virus type 2 （HSV-2）, a standard strain of HSV-2 （333 strain） was used to investigate the antiviral effect of PSP in vitro. PSP in various concentrations was applied to different stages of HSV-2 replication cycle. Finally, the virus infectivity （TCID50）, cytopathic effect （CPE）, and MTT staining method for viable cells （MTT assay） were used as markers to evaluate the effect of PSP on HSV-2. The quantity of HSV-DNA was detected by real-time fluorescence quantitative PCR （FQ-PCR）. The HSV-2 infected Vero cell tdtrastructures were observed by transmission electron microscopy （TEM）. The results showed that PSP had little cytotoxic effect on Vero cells, it could not directly inactivate HSV-2 infectivity. PSP not only interfered in adsorption of HSV-2 to Vero cells but also inhibited HSV-2 biosynthesis in the ceils. FQ-PCR results showed that the inhibitory rate on HSV- DNA also increased in a dose-dependent and time-dependent manner. TEM also confirmed that PSP exhibited pronounced inhibitory effect on HSV-2. In conclusion, the antiviral effect of PSP on HSV-2 may be attributed to the inhibition of virus adsorption, virus replication and synthesis in cells.
To explore the antiviral effect and mechanism of polysaccharide from Spirulina platensis (PSP) on herpes simplex vims type 2 (HSV-2), a standard strain of HSV-2 (333 strain) was used to investigate the antiviral effect of PSP in vitro . PSP in various concentrations was applied to different stages of HSV-2 replication cycle. Finally, the virus infectivity (TCID50),cytopathic effect (CPE), and MTT staining method for viable cells (MTT assay) were used as markers to evaluate the effect of PSP on HSV-2. The quantity of HSV-DNA was detected by real-time fluorescence quantitative PCR (FQ-PCR). The HSV-2 infected Vero cell ultrastructures were observed by transmission electron microscopy (TEM). The results showed that PSP had little cytotoxic effect on Vero cells, it could not directly inactivate HSV-2 infectivity. PSP not only interfered in adsorption of HSV-2 to Vero cells but also inllibited HSV-2 biosynthesis in the cells. FQ-PCR results showed that the inhibitory rate on HSV-DNA also increased in a dose-dependent and time-dependent manner. TEM also confirmed that PSP exhibited pronounced inhibitory effect on HSV-2. In conclusion, the antiviral effect of PSP on HSV-2 may be attributed to the inhibition of vims adsorption, vims replication and synthesis in cells.
