I. Pharmacological mechanism Tenofovir is phosphorylated into tenofovir diphosphate by cellular kinase, which competes with 5’triphosphate deoxyadenylate and participates in the synthesis of viral DNA, and enters into the viral DNA due to the lack of 3’hydroxyl group and leads to the obstruction of viral DNA prolongation, which inhibits the replication of the virus. Tenofovir is poorly absorbed orally, and tenofovir disoproxil (TDF), its ester precursor, has significantly increased intestinal absorption and uptake. Tenofovir is mainly excreted through glomerular filtration and active renal tubular secretion, with a clearance half-life of about 17h and a longer intracellular half-life of about 95h, so it can be administered once daily. Compared with adefovir (ADV), HBV DNA <400 copies/mL, and Knodell's inflammatory necrosis score improved by at least 2 orders of magnitude, and no progression of fibrosis as a complete response, a group of 375 HBeAg-negative patients, respectively, 71/49 (TDF group/ADV group), and 266 HBeAg-positive patients, respectively, 66/12 (TDF group/ADV group), and 266 HBeAg-positive patients, respectively, 66/12 (TDF group/ADV group). 66/12 (TDF group/ADV group) of 266 HBeAg-positive patients in the other group, respectively. (ii) Efficacy of TDF in lamivudine (LAM)/ADV-treated patients. In a subgroup analysis of the 2 phase III clinical studies described above, the efficacy of tenofovir monotherapy in LAM-treated patients with poor response or drug-resistant chronic hepatitis B was evaluated, comparing the response to TDF at 96 weeks in LAM-naïve patients (n = 375) with that in LAM-treated patients (n = 51) In the treated group, the mean duration of LAM was 95.9 weeks, and 10% had a LAM-resistant variant. The analysis showed that TDF had durable anti-HBV activity in both groups. 92% and 84% of patients in both groups had undetectable V DNA at 96 weeks. The above study shows that TDF still has good anti-HBV activity in patients with poor response to LAM or ADV treatment or LAM resistance, and can achieve durable inhibition of HBV replication in most patients. However, this result still needs to be verified by long-term, multi-center and large-sample clinical observation. Third, TDF for the treatment of pregnant patients with chronic hepatitis B Currently, TDF is categorized as a class B drug.There is less information on the use of TDF for the treatment of CHB in pregnancy, and HIV-infected pregnant women treated with TDF-containing regimens provide a lot of human safety data. According to data released by the American Pregnancy Registry of Anti-Retroviral Drugs (APR), the incidence of neonatal birth defects (NBD) in pregnant women using TDF alone or in combination in early and mid-late pregnancy was 2.2%, which was not significantly different from the overall population incidence of NBD (2.72%); there was no statistically significant difference in the incidence of NBD in the early versus the mid-late gestation dosing population. Fourth, drug resistance For primary treatment patients treated with TDF monotherapy for 192 weeks, none of the TDF drug resistance-related HBV polymerase or RT region mutations occurred. However, the current data on the treatment response rate to TDF in nucleotide-treated patients, especially in ADV-resistant patients, is of mixed opinion. This may be related to the relatively short observation time or small observation scale of TDF treatment, and it is still necessary to expand the scale and long-term observation, so as to clarify whether there is any occurrence of resistance to long-term TDF treatment and whether NA-treated patients influence the occurrence of TDF resistance variants.