There are two types of chronic hepatitis B virus carriers: chronic asymptomatic carriers and chronic inactive carriers, which are very different in nature. The former is stable and 75% of them will be cured automatically as long as general checkups are conducted; the latter is more unstable and the disease may recur. We would like to introduce a rare patient with multiple relapses in the hope of attracting extra attention from patients with similar disease. 43 years old. 93 years military physical examination surface antigen positive, 94 years “big three suns” hepatitis, ALT 180 U/L; 95 years ALT 900 U/L more than the second half of the year down to normal, turned into “small three suns”, PCR-HBV DNA negative ( Blogger’s note: it is not stated that there has been treatment, may be due to a strong immune response to the extremely high aminotransferase spontaneous improvement, chronic inactive hepatitis B virus carrier); 96 years, “two pair of half” to one, five positive. After the annual examination, in 2012, there was a normal liver function and HBVDNA positive (blogger’s note: the carrier status is not very stable), the rest of the year liver function and HBV DNA are normal. 2010 onset of disease, ALT 500 U/L more than five times, HBV DNA five times, ultrasound showed mild enlargement of the spleen (the second time the “small triple” hepatitis), ultrasound showed mild enlargement of the spleen (the second time “small triple” hepatitis). “After 3 months of treatment with pelargonid, liver function turned normal, HBV DNA turned negative, continued treatment with pelargonid until one and a half years (June 2011), stopped, and then annual examination of liver function, HBV DNA, ultrasound, for three consecutive years, were normal (chronic inactive hepatitis B virus carrier). DNA five times, ultrasound is basically normal (the third “small triple” hepatitis), the treatment with Pyroxin has been three months, liver function down to normal, HBV DNA turn negative, and now continue to use Pyroxin in the treatment. My uncle died of liver cancer, and both my parents have esophageal cancer. Is interferon effective for me? Should I continue treatment with Paroxetine? What are the characteristics of chronic inactive hepatitis B virus? Patients with chronic hepatitis B who are “triple positive” will become chronic inactive hepatitis B carriers after antiviral treatment or a strong immune response, normalization of liver function, and conversion of viral and E antigen to negative. This status is not very stable, if the original “triple positive” hepatitis through interferon treatment to inactive carriers, in 100 inactive carriers in 1 year, about 15% will recur, and later recurrence will be rare. If hepatitis “triple III” is treated with nucleoside analogs, it will take several years for the E antigen to turn negative and become inactive carrier, but the treatment still needs to be prolonged, and most of those who stop taking the drugs too soon will have recurrence. If the original is “small triple positive” hepatitis, is a mutated virus. After interferon treatment to inactive carrier, there will still be a lot of relapses, and fewer of them can be stabilized in the end. After the nucleoside analogs treatment to inactive carrier, still can not stop the drug, a long time still need to continue to maintain the drug treatment. Why do chronic inactive carriers who have been converted from “small triple positive” have more relapses? The fundamental difference between chronic asymptomatic carrier and chronic inactive carrier: asymptomatic carriers, with the gradual growth of immunity, the virus level gradually decreases during the long decades of carrying process, and only a trace amount of serum virus is found when they turn into “mini-Triple III”, or continue to be negative, and the immunity is able to control the viral replication in the liver cells and end the carrying process (a high level of recovery). The immune system is able to control the replication of the virus in the liver cells and the carrier is terminated (high level of recovery). The vast majority of inactive carriers enter the inactive phase after antiviral treatment. Interferon enhances immunity, but not necessarily sufficiently, and nucleoside analogs remove replicating viruses mainly by the strength of the drug, but basically do not enhance immunity, and do not have a direct effect on the virus in the liver cells. Virus turn negative before “big triple positive” to “small triple positive”, but the reduction of virus in the liver cells is limited; if the treatment is “small triple positive”, the potential mutated virus in the liver’s greatest ability is to evade immune clearance, repeated activity. The greatest ability of the potential mutated virus in the liver is to evade immune clearance, and repeated activity (relapse) is certainly its characteristic. A small number of patients, after long-term treatment with first-line nucleoside analogs, can end up with surface antigen/antibody conversion and end up carrying the virus (low level of healing), and lack of sufficient immunity, and after stopping the drug, there can still be antigenic reversal, or even hepatitis flare-ups. How to choose the antiviral treatment for “small triple positive” hepatitis? If it is only general hepatitis, long-term treatment with first-line nucleoside analogs (entecavir or tenofovir) will only make the disease inactive under drug control. If there is obvious liver fibrosis or even cirrhosis, long-acting interferon therapy (Paroxetine 135μg per week for 72 weeks) is the best for cancer prevention if it has a sustained effect, but the problem is that the recurrence rate of “mini-three-positive” patients is very high, so it is difficult to have a sustained effect. If the surface antigen quantification of the ultrasensitive test is only a few hundred units, it is expected that the surface antigen/antibody conversion can be tried. Otherwise, long-term administration of tenofovir, which is highly potent and has a reliable reversal of hepatic fibrosis, resulting in a very substantial reduction in the incidence of tumors, is also an option. Close relatives with malignant tumors, especially liver cancer, are considered on their own terms.