万赛维好吗？

It is suitable for the treatment of patients with acquired immunodeficiency syndrome (AIDS) combined with cytomegalovirus (CMV) retinitis and the prevention of CMV infection in high-risk solid organ transplant patients. Human viruses to which Vancevir is sensitive include human cytomegalovirus (HCMV), Vancevir is sensitive to herpes simplex virus-1 and herpes simplex virus-2 (HSV-1, HSV-2), human herpesvirus-6, 7, 8 (HHV-6, 7, 8), Epstein-Barr virus, varicella-zoster virus (VZV) and hepatitis B virus.

Vancevir can inhibit viral activity mainly by inhibiting the synthesis of viral DNA: Vancevir competitively inhibits viral DNA polymerase, preventing deoxyguanosine triphosphate from binding to DNA. Vancevir's ganciclovir triphosphate binds to viral DNA, terminating or limiting the elongation of the viral DNA chain. The IC50 of the antiviral effect of ganciclovir on CMV in vitro ranges from 0.08μM (0.02ug/ml) to 14μM (3.5ug/ml).

Is Vancevi effective?

A randomized, open-label study compared the effectiveness of valganciclovir and ganciclovir induction in the treatment of newly infected AIDS-associated CMV retinitis. 160 patients were randomly treated with oral valganciclovir 900 mg or intravenous ganciclovir 5 mg·kg-1, bid, and then changed to qd after 3 weeks, and then treated for 1 week. After 4 weeks, all patients received oral valganciclovir (900 mg, qd) for maintenance treatment. The CD+4 cell count and highly active antiretroviral therapy (HAART) status of patients in each group before treatment were similar.

The first endpoint of induction therapy is the progression of CMV retinitis at 4 weeks of treatment, and the second endpoint is the progression time of CMV retinitis and the achievement of satisfactory efficacy. The number of patients with progression of CMV retinitis was similar in the oral valganciclovir group and the intravenous ganciclovir group, at 10%. The median time to disease progression in the oral valganciclovir group was longer than that in the intravenous ganciclovir group, 160 d and 125 d respectively, while the mean time to disease progression was similar, 226 d and 219 d respectively. Oral valganciclovir and intravenous ganciclovir induction therapy achieved similar rates of satisfactory efficacy at 4 weeks, 72% and 77% respectively. Analysis of subgroup data including CD+4 cell count, CD+4 cell count increase and HAART at the start of treatment and 4 weeks after treatment showed that the efficacy of valganciclovir and ganciclovir was similar.