Now it seems that there are four main domestic oral nucleoside (acid) analogues: lamivudine, adefovir esters, tipifudine, and entecavir. There are three main drugs in terms of resistance sites, the first being L-nucleoside analogues, mainly lamivudine and telbivudine. Lamivudine should be used as site 204, which is not easily resistant to V-valine and I-isoleucine, and after this resistance lamivudine is resistant. Tebivudine is sometimes different from lamivudine in that it is theoretically resistant only to I-isoleucine. If it is not the I variant, it should be the V variant, and lamivudine resistance should be able to be added to temivudine, but often when there is resistance at site 204, there is also resistance at site 180, and these two resistances are added together, and additive resistance. The original single site resistance, the virus replication is weaker, if only 204 site resistance, the virus replication is weaker, not as strong and fast as the wild strain, so immediately after the resistance stop or change the drug, 204 site lamivudine resistance will be quickly repaired over, the wild strain because of the fast replication is covered. However, it is different if it is added with the 180 locus resistance. 180 locus is equivalent to the compensatory locus, which compensates for the weakness of not strong replication ability, so it will not be worse than the wild strain replication ability, and both of them will be resistant after a long time. In addition, the 180 and 204 sites in the use of tebivudine, if only the 204 site, not I resistance, only V resistance, tebivudine is effective, this time lamivudine has been resistant, but if 180 resistance added, tebivudine is also resistant. Our general drug resistance detection, first of all, means more trouble, secondly, now mainly with sequencing methods, sensitivity is not strong. The strain of drug resistance must be greater than 20% to 40% to be detected, so if the number of drug resistance is not large to a certain extent can not be detected. The first of these is that the company’s products are not only available in the market, but also in the market. The only thing left is Entecavir. The actual fact is that you can’t use this type of drug, but you can only use it if you have a high genetic resistance site, and there are three resistance sites that are resistant to the drug. However, after a period of time, another resistance site can easily appear. So entecavir cannot be used either. So if the patient is heavy and there is no other way, entecavir can be used for a short time to bring down the virus. If the patient is suitable, interferon can also be added. Interferon currently does not appear to cross-resist with nucleoside (acid) analogs, and it rarely develops resistance. With interferon alone, it has a weak antiviral effect and can easily fail to suppress resistant strains. If the patient’s financial situation allows, it is best to have entecavir + interferon, the two drugs together can inhibit both drug-resistant strains and wild strains. If the economic conditions are poor, only one can be chosen. Now there is a foreign drug is tenofovir, and adefovir ester is the same class of drugs, but it is less toxic to the kidneys than adefovir ester. Adefovir is more nephrotoxic, only 10 mg per day, small dose, slow onset and weak effect. Tenofovir has lower nephrotoxicity, the dose can be used up to 300 mg, the dose is 30 times larger than adefovir, because it is an independent resistance site, the same as adefovir, so if adefovir ester is resistant, it should also be resistant, but its dose is larger, so it can be treated. That’s why tenofovir is now used abroad and is cheaper than adefovir ester. Tenofovir now seems to be far more effective than adefovir esters and is effective against many resistant strains because of the high dose. It is effective against lamivudine, entecavir resistance, etc. But at present the domestic are unable to buy, can only be treated in accordance with the method I just mentioned.