Persistence of Hepatitis B surface antigen (HBsAg) in the serum is one of the defining features of chronic hepatitis B. Regardless of the exact phase and the eligibility for treatment, many patients with chronic hepatitis B are concerned whether their blood test will clear after treatment. Therefore, can it really clear?
If so, which specific treatment is documented to do that? Even after clearance of the viral marker, does the risk of liver damage decrease?
To understand the presence of HBsAg in chronic hepatitis B carriers (CAH-B), one must understand where the template of HBsAg RNA comes from. Following initial HBV infection where the relaxed circular DNA (rcDNA) enters the hepatocyte nucleus, the rcDNA is converted either to cccDNA or integration of the double-stranded linear DNA (dslDNA) into host DNA. Whereas cccDNA has all of the HBV genetic code to produce all HBV proteins, full length pregenomic RNA and rcDNA to produce infective virions, integrated dslDNA generally is unable to support viral replication, but generally has the genetic code for HBsAg in the integrated dslDNA. Thus, clearance of HBsAg depends on the ability to eliminate the reservoir of cccDNA and integrated dslDNA. Whereas nucleos(t)ide analogs (NAs) are excellent in suppressing generation of the full-length pregenomic RNA and rcDNA generation, they are much less effective at eliminating cccDNA and unable to interfere with integrated dslDNA. This requires antiviral immune clearance, by cytolytic CD8 HBV specific T cells - the spontaneous loss of HBsAg in CAH-B that are HBV DNA negative is low, on the order of 1-2% per year. However, more recently, the rate of HBsAG clearance can be enhanced with the use of interferons. To achieve HBsAg loss, either IFN adding on NAs or NAs switching to IFN at an appropriate time is advised, as these two strategies can improve the rate of HBsAg loss compared to NAs monotherapy. The progression of liver disease to cirrhosis or hepatic decompensation generally stops when patients lose HBsAg unless other causes of liver injury are present
Hepatitis B never really goes away; once you clear HBsAg, your risk of liver damage and liver cancer diminishes tremendously. It's worth a celebration, but you need to continue to be monitored as you age
Yes incase of acute hepatitis B and Some cases of CHB with interferon therapy.
We are usually treating CHB with tenofovir or Entecavir which usually targets the viral particle in blood stream so inspite of attaining below detection level of HBV DNA its vey rare to have clearance of HBsAg from serum
In our experience the the earlier Interferon based treatment was associated with more clearance of HBsAg , but the topic remains controversial
As the HBV DNA gets associated with the Host DNA and form CCC DNA and gets incorporated into the host genome . It has been seen that some patients who are HBeAg negative having very less or below detection DNA can also turn up to have HCC, so HCC monitoring at interval of 6 month is very essential. The Role of BCP and PC mutations are also hot topics
Thank you John Julian Fung , Mohmmed Faris , Abu Saleh Md Sadequl Islam and Manoj Kumar Gupta for your answers. However, I am afraid some of the answers seem contradictory.
To clarify, what I really want to know is
1. Is there a possibility that HbsAg can get negative after successful treatment of chronic hepatitis B? If yes,
2. Which specific treatment regimens can help achieve that?
3. What is the probability of getting the negative results after treatment?
John Julian Fung has addressed most of the questions well. Therefore, should we agree on that HbsAg can clear after successful treatment of chronic hepatitis B especially when interferon is used? (although still knowing the probability would help to know what to expect).
Can clear occasionally as mentioned by others after treatment often after years of initial HBV DNA negativity and e antigen seroconversion. But even then beware of occult infection [HBsAg negative but HBV DNA positive]
The literature is somewhat conflicting with regards to the magnitude of conversion, perhaps due to differences in HBV genotypes, IL28 genotypes. The spontaneous clearance of HBsAg is about 1-2% per year, with the addition of pegylated interferon-alpha 2a, the clearance rates increases to 8-20% with 1-2 years of therapy, depending on the country of study. There are significant side effects that require dose reduction or even discontinuation (5-30% patients).
As long as HBsAg can clear spontaneously in few cases, it would be cleared in few cases after treatment
Hepatitis B surface antigen (HBsAg) seropositivity indicates the presence of hepatitis B viral (HBV) infection (acute or chronic). The disappearance of HBsAg from serum with development of the corresponding antibody, anti-HBs, indicates conventional resolution of infection. The likelihood of spontaneous HBsAg seroconversion during acute HBV infection varies according to patient age and immune competence. Up to 97% of healthy adults with acute HBV will clear the infection. In contrast, HBsAg seroconversion in chronically infected patients is a relatively uncommon event, with an incidence of only 0.8%-2% per annum. Chronically infected whitepatients who typically acquired HBV infection in adulthood have a higher rate of spontaneous HBsAg loss than Asian patients with presumed vertical acquisition of HBV.
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