With the widespread use of antiviral treatment drugs, there are some typical misconceptions after antiviral treatment resistance, and some explanations are given below. Myth 1: If you are drug resistant, all your previous treatment is wasted, so you might as well not treat it in the first place. Hepatitis B virus infection is a risk factor for the development of cirrhosis and liver cancer. From the development pattern of chronic hepatitis B, the direct harm brought by repeated inflammatory necrosis is liver fibrosis and loss of liver function, and the indirect harm is the possibility of genetic mutation due to excessive proliferation of hepatocytes, leading to the occurrence of liver cancer. If chronic hepatitis B patients are not treated, 12% to 25% of them may develop cirrhosis within 5 years. If patients with cirrhosis are not treated, 20% to 23% may develop into liver failure within 5 years and require liver transplantation; 6% to 15% may develop hepatocellular carcinoma. Myth 2: Treatment will still be resistant to drugs at the end, when is the end of eating. It is now clear that after antiviral treatment, hepatitis B virus replication is inhibited, liver function improves, and the progress of the disease can be controlled. In large global studies, the risk of cirrhosis, liver dysfunction and liver cancer was significantly lower in patients treated with antiviral therapy than in those who were not treated with antiviral therapy. Therefore, the patient definitely benefits during this period of treatment, and it also gains time and timing for further treatment of the patient. In fact, drug resistance is not scary, what is scary is losing confidence in the treatment. After drug resistance, as long as you continue treatment by switching to other effective antiviral therapy drugs, the virus is again suppressed and liver function will soon return to normal again. Myth 3: If you change or add other antiviral drugs when you are resistant to them, will there be no cure in the future? The process from viral mutation to clinical drug resistance is a gradual one. In order to accurately reflect this process from viral mutation to clinical resistance, doctors have divided the resistance after viral mutation into three stages: genetic resistance, virological resistance and clinical resistance. The “genetic resistance” refers to the mutation of the hepatitis B virus genome in the process of antiviral treatment, forming a new resistant viral gene sequence, but the amount of this resistant virus strain in the body is very small, has not yet formed a “climate”, only through the virus gene Virological resistance” refers to the continued development of genetic resistance based on the gradual increase in the number of mutant viral strains, due to their replication, so that the level of HBVDNA in the blood rebound, generally between (1 × 103) to (1 × 106) copies/mL, has not yet caused abnormal liver function and obvious Virological resistance continues to develop, HBVDNA level rises to more than 1×106 copies/mL, and eventually liver function abnormalities and liver histological damage occur, that is, the development to the “clinical resistance” stage. For the treatment of lamivudine resistance, there was a very famous study by Italian doctors a few years ago. They divided the patients into two groups, with the first group changing treatment regimens early in the virological resistance phase (to adefovir monotherapy or to a combination of lamivudine and adefovir) and the second group continuing treatment with lamivudine after resistance was detected and not changing regimens until the “clinically resistant” phase developed. The results showed that in the first group of patients, there was little difference between the results of switching to adefovir monotherapy or the combination of lamivudine and adefovir; unlike the second group of patients, only 38% of patients treated with adefovir monotherapy achieved virological response, while 81% of patients treated with the combination of lamivudine + adefovir achieved virological response. This indicates that the earlier the treatment regimen is changed after drug resistance, the better the efficacy and the lesser the medication used. Therefore, treatment should be promptly changed to other effective antiviral drugs after drug resistance is detected. Myth 4: Treatment after drug resistance often requires combination therapy, so the more drugs you take, the more you can use entecavir alone? The choice of drugs for treatment after drug resistance is mainly based on the presence or absence of the same hepatitis B virus resistance sites between drugs. Since the resistance sites of adefovir and entecavir are different, you can choose to switch to entecavir monotherapy after adefovir resistance. Lamivudine, telbivudine and entecavir have the same viral resistance sites. After lamivudine and telbivudine resistance, even though entecavir has a stronger antiviral effect and a lower resistance rate, switching to entecavir monotherapy still results in 40% of patients having resistance again after 5 years, even if the dose is doubled. Therefore, doctors often choose to use adefovir after lamivudine or telbivudine resistance, but because of the weaker antiviral effect of adefovir, the original drug plus adefovir combination therapy is often used. This situation can be changed after tenofovir is marketed in China, because tenofovir has a stronger antiviral effect and does not have the same resistance sites as lamivudine or telbivudine, and can be replaced with tenofovir monotherapy after lamivudine or telbivudine resistance.