Different virus infect different tissues of the children's body,arousing the immune system to respond,resulting in tissue damage and different diseases.Virus infections have different types and different mechanisms.Viral diseases need to choose the corresponding treatment of antiviral drugs.Clinicians need to be familiar with the mechanism of antiviral drugs,to avoid improper use of drugs.This paper briefly describes the molecular ecology of virus,including structure,classification,characteristics of virus and their replication.

Objective To study the clinical therapeutic effectiveness and the mechanism of Shouti Oral Liquid on simple obesity children with hyperinsulinism. Methods Fourty - three patients were divided randomly into the treatment group (TG) and the control group (CG). TG took Shouti Oral Liquid and CG took metformin. The course of therapy lasted 6 months. The plasma lipid, body fats, insulin resistance index (IR) and some hormones related to obesity before and after therapy were measured and the changes were analyzed. Results The weight, F% , body mass index (BMI), leptin(LP), tumor necrosing factor (TNF - ?), FINS, IR all declined markedly than pre - therapy in both groups. The significant effect, normal effect and total efficiency were 22.7 % , 59.1 %, 81.8 % respectively in TG and9.5%,52.4%,61.9% in CG. The effect in TG was better than that in CG. A short course with Shouti Oral Liquid therapy did not have obvious side effect Conclusions There are lipid metabolism disorder, insulin resistance and high lever LP and TNF - ? obesity children with hyperinsulinism. The total effect with Shouti Oral Liquid is better than that with medicine in the control group and the mechanism was regulating lipid metabolism, decreasing LP and TNF-? and ameliorating insulin resistance.

Objective To investigate the protective effect of Honokiol on the airway inflammation induced by particulate matter 2.5(PM2.5)in the asthmatic mice and its mechanism.Methods Fifty male specific pathogen free (SPF)Balb/c mice were randomly divided into 5 groups.Group A:normal control group;group B:asthmatic model group;group C:PM2.5 exposure asthmatic group;group D:TAK -242 group;group E:Honokiol group. Asthmatic mouse models were established by ovalbumin(OVA)sensitization and challenge.On days 0 and 7,the mice in B-E groups were injected intraperitoneally with injection 100 mg/L OVA and aluminum hydroxide for sensitization;on days 14 to 21,10 g/L OVA solution was given 30 min per day to challenge.During challenge phrase,the mice in C -E groups received intratracheal injection of PM2.5,every other day,4 times totally.On this basis,the mice in group D re-ceived TAK-242 intraperitoneal injection,and the mice in group E received honokiol intragastric administration.Group A was given saline instead of OVA.Animals were sacrificed 24 h after the final inhalation challenge,and the bronchoal-veolar lavage fluid(BALF)of the left lung was used for differential inflammatory cell counts.The expressions of Toll-like receptors 4(TLR4)and nuclear factor(NF)-κB at mRNA level were detected by real-time quantitative PCR. Flow cytometry analysis was performed to measure the levels of Th17 and Treg cells.Results Compared with group A,mice in group B and group C expressed more serious disorders of bronchial epithelial cells,alveolar wall congestion and edema,increased mucus secretion in the airway and infiltration of inflammatory cells in the lung,and those in group C were more obvious than those of group B and group E significantly reduced respiratory inflammation;compared with group A[(4.15 ± 1.35)×108/L,0.012 0 ± 0.002 3],the total number of inflammatory cell counts[(16.79 ± 5.62)×108/L and(24.58 ± 13.46)×108/L],eosinophils proportions(0.113 8 ± 0.022 3 and 0.197 8 ± 0.084 9)in group B and group C,were significantly higher,and the differences were statistically significant(all P<0.05);The total number of inflammatory cell counts and eosinophils proportion in group E(8.56 ± 3.28)×108/L and 0.041 5 ± 0.013 5)were significantly lower than those in group C,and the differences were statistically significant(all P <0.05);The expressions of TLR4 mRNA and NF-κB mRNA in group B and C(1.85 ± 0.56,1.82 ± 0.28 and 2.97 ± 0.41,2.83 ± 0.32)were significantly higher,and the differences were statistically significant(all P <0.05);The expressions of TLR4 mRNA and NF-κB mRNA in group E(1.60 ± 0.28,1.54 ± 0.25)was significantly lower than those in group C,and the differences were statistically significant(all P<0.05);the expressions of Th17 in group B and C[(2.89 ± 0.61)% and(4.96 ± 0.27)%]were significantly higher than those of group A[(1.03 ± 0.35)%] (all P<0.05);The expression of Th17 in group E[(1.83 ± 0.23)%]was significantly lower than that of group C,and the differences were statistically significant(P<0.05);the expressions of Treg in group B and C[(4.96 ± 0.35)%and(2.27 ± 0.41)%]were significantly lower than those of group A[(7.37 ± 0.56)%],and the differences were sta-tistically significant(all P<0.05);The expression of Treg in group E was significantly increased[(6.45 ± 0.38)%] compared with that in group C,and the difference were statistically significant(P<0.05);and those of group D and E were improved remarkably.Conclusions Honokiol can relieve PM2.5 exposure of asthmatic airway inflammation through down-regulating the expression of TLR4 and NF-κB and Th17 and regulating the balance of Th17 and Treg cells.

Objective To investigate the anti-inflammatory and immunosuppressive effects of honokiol in a mouse model of particulate matter ( PM ) 2.5-induced asthma .Methods Female SPF BALB/c mice were randomly divided into five groups:normal saline group (group A), ovalbumin (OVA)-sensitized group ( group B), PM2.5-exposed+OVA-sensitized group ( group C), dexamethasone-treated group (group D) and honokiol-treated group (group E).All mice except those in group A were sensitized and challenged with OVA, and the mice in groups C, D and E were exposed to PM2.5 every two days since the first challenge.Samples of lung sections were stained with hematoxylin and eosin (HE) to observe in-flammatory infiltration.Bronchoalveolar lavage fluid (BALF) and PBMCs were collected from each mouse . Expression of RORγt and Foxp3 at mRNA level was detected by quantitative real-time PCR.Flow cytometry analysis was performed to measure the percentages of Th 17 and Treg cells.ELISA was performed to measure the levels of IFN-γ, IL-10 and IL-17 in the supernatants of cell culture .Results Compared with group B , group C showed an enhanced expression of RORγt at mRNA level, increased IL-17 level and up-regulated percentage of Th17 cells (all P<0.05), but a suppressed expression of Foxp3 at mRNA level, decreased IL-10 level and down-regulated percentage of Th17 cells (all P<0.05).No significant difference in the per-centage of Th1 cells or in the expression of Th 1-related cytokines was observed .The expression of RORγt at mRNA level, IL-17 level and the percentage of Th 17 cells were decreased in PM2.5-exposed mice upon honokiol intervention (all P<0.05), while the expression of Foxp3 at mRNA level, IL-10 level and the per-centage of Treg cells were increased after honokiol intervention (all P<0.05).Honokiol had similar efficacy to dexamethasone in the treatment of asthma .Conclusion Honokiol can alleviate airway inflammation in mice with PM2.5 exposure-induced asthma through regulating the percentages of Th 17 and Treg cells.