Post-vaccination exposure - want to understand vaccine mechanism & future reactivation risks

Hello, I’m a new user and have been reading posts for the last week or so. First of all, thank you for being a resource and comfort to everyone looking for more information to better understand their situation, this is a great community.

I’m 38, Female, born and raised in the US, based in the US. I recently received some surprising HepB results and am trying to make sense of what happened, and hoping to find answers here. Some background:

Mid-1990s (when I was around 10 years old): Got the entire 3-shot Hep B vaccine series.

August 2019 routine Hep B screening:
Hep B surface antigen: Negative
Hep B surface antibody: Reactive
Hep B core antibody: Negative
From reading posts in this forum and internet research, my understanding of these August 2019 results is that I was at the time immune thanks to vaccination.

September 2023 routine Hep B screening:
Hep B surface antigen: Negative
Hep B surface antibody: Reactive
Hep B core antibody: Positive
From reading posts in this forum and internet research, my understanding is that at some point after August 2019, I was likely “exposed” to Hep B, hence the Core Antibody test is now positive in Sept 2023.

I have no idea how or when I was exposed to Hep B, but looking back, I think the highest likelihood might’ve been pre-pandemic in Fall 2019, soon after my August 2019 routine screening. I had zero symptoms and I had no idea I was exposed until this routine Hep B test in September 2023. I am quite distressed and scared and searching for answers now, hoping that more knowledge can combat my fear and anxiety.

So, given these facts, these are some questions that are perplexing me:

  1. What is the layman’s definition of “exposure”? In layman’s terms, does exposure mean “the hepatitis b virus entered my body?”

  2. Let’s say that my vaccine was still very effective in Fall 2019 (which is likely the case, given my August 2019 results showing the reactive surface antibody from vaccination). And then let’s say the Hepatitis B definitively entered my body in Fall 2019. In that moment of entry, if my prior vaccine is doing its job correctly, what is happening inside my body? Is the vaccine’s antibodies recognizing that Hepatitis B virus has entered my body, and then fighting the virus on the spot? And then, IF the vaccine is successful and does what it is supposed to do, does it effectively KILL the Hepatitis B virus so that there is no trace of it left? (I read some article about sterilizing immunity, so I guess what I’m asking is whether the Hep B vaccine is sterilizing/killing off the virus entirely once it enters your body). Or…is the reality of what actually happens in this kind of post-vaccine exposure scenario that the vaccine successfully fights off the Hepatitis B virus and prevents CHRONIC infection? And then you have the Core Antibody left as a marker of the fact that the Hepatitis B virus did enter your body? Sorry if this question is confusing…part of what I’m really wondering is…when people say the Hep B vaccine is effective and “prevents infection”, what does that actually mean: (1) does it mean that it offers “sterilizing immunity” and that if the Hep B virus does in fact enter your body after you’re vaccinated, the vaccine will kill off every bit of the virus and leave no trace DNA at all, OR (2) does vaccine efficacy means that in the event that the HBV definitively enters your body after you are vaccinated, the vaccine will ensure that you only get an ACUTE infection rather than a chronic infection? I think I’ve read a lot of articles saying “hepatitis B virus prevents infection” but given what happened to me, I’m just really trying to understand what it really prevents, and how the vaccine works if HBV does enter your body after you’re vaccinated. And part of what I’m also trying to understand here is whether the positive Core Antibody means that the HBV is still hiding somewhere sleeping (and thus suggesting the vaccine prevented CHRONIC infection), or whether the positive Core Antibody could also serve as just simple proof that HBV entered the body but was eliminated in its entirety (and thus the vaccine prevented infection (both acute AND chronic) entirely and essentially sterilized HBV as soon as it came into the body).

  3. I’ve also read a number of posts on here about reactivation of HBV and that that usually happens in the context of strong immunosuppression, which I understand. My follow-up question is…in a person who had acute/resolved infection…let’s say that years down the line, you need chemo for cancer or immunosuppressants for an auto-immune disease, and then you inform your doctor about your prior resolved HBV infection, and then they prescribe you antivirals…generally speaking, how effective are anti-virals in preventing reactivation in someone who had a resolved infection? With this question, what I’m trying to understand is…in the grand scheme of things, how much should I be worried about this “resolved” HBV case when it comes to the future of my health? (And thus why I asked question #2, which is to try to understand if there is indeed HBV sleeping in me or not…I guess we may never know, but trying to arm myself with more knowledge). Is the risk of reactivation basically comparable to the risk of being diagnosed with some random cancer or autoimmune disease?

Thank you so much for reading my long questions!! I appreciate the support of this community.

Hi @myg,

Welcome to the community. Wow, you have really educated yourself and done a good amount of homework. I am impressed with your intelligent questions and your reasoning abilities. I am sure you are well aware with all the reading you have done, that one of the experts will be with you as soon as they can. I just wanted to let you know that I was so impressed that I couldn’t wipe the smile off my face.


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Dear @myg,

I want to join @PuallyHBV in welcoming you to the forum and thank you for your great questions.

Yes, exactly!

It is likely that if an anti-HBc antibody response is seen, then it is likely (2) in this case because there is not enough HBc in a small amount of input virus to generate the immune response. That said, it is also likely that the anti-HBs response also does confer some measure of sterilising immunity through neutralising the virus your exposed to, but the biggest effect (and the main effect that’s really important from a public health perspective) is that it effectively prevents disease/chronic infection (like pretty much every other vaccine).

It really depends on the type of immunosuppression that is used in this case. I believe the ones that target B-cells in particular can have a reactivation risks of >10%, others are <10%. I also believe the standard of care in such cases is just wait and see if HBV DNA becomes detectable during the immunosuppression before prescribing antivirals because of exactly the reason you are providing (we don’t know whether or not replicative virus is still hiding out in your liver or not).

Hope this helps!


@PuallyHBV Thank you for the very warm welcome and your kind words! I feel happy that my questions put a smile on your face, and thank you for letting me know! I am already feeling the support of this community! I think the internet and Reddit research rabbit hole is very helpful in empowering me with more knowledge but I also need to set my limits, otherwise it’ll increase my health anxiety haha. I also wanted to make sure that I did as much reading and research as possible before posting a question in this forum, in order to be mindful of everyone’s time…I wanted to make sure I wasn’t wasting anyone’s time by asking questions that have already been answered or easily Google-able. It’s clear there are so many kind and generous souls in here who are volunteering their free time to help answer questions, and I definitely wanted to be respectful of that. :slight_smile:

@ThomasTu First of all, thank you so much for your generosity with your knowledge and your time. It means so much to me, and I can see from this forum that you and other experts have provided so much relief and comfort to others too. Thank you, truly.

I had a few follow-up questions to your answers:

  1. Does exposure for a vaccinated individual always lead to, at the very very minimum and in the best case scenario, a self-limited and asymptomatic acute infection? Or, can it be that exposure for a vaccinated individual could also lead to not even an acute infection and simply, in the best case scenario, a 100% elimination of the virus? Both questions are in the context of a vaccinated person.

  2. Does exposure that doesn’t result in acute infection still lead to production of anti-HBc? Or does anti-HBc only appear if the virus took hold and caused an acute infection?

  3. You mentioned that “there is not enough HBc in a small amount of input virus to generate the immune response” - can you clarify this sentence? I wasn’t able to find out what this means through Google. Am I to understand from this that if only a little bit of HBV enters your body, then that’s not enough for the vaccine’s surface antibodies to realize that something sinister has come inside and it won’t fight it off? And that the consequence is that an acute infection occurs?

  4. Regarding your answer re: reactivation, in the event that “HBV DNA becomes detectable during the immunosuppression”, then:

  1. Does “detectable HBV DNA” mean that an infection/reactivation has definitively occurred?
  2. During the course of taking antivirals in the context of reactivation, is the most likely result of taking those antivirals that the HBV infection then becomes just an acute infection and then the surface antigen becomes negative again after a period of taking the meds (aka you “recover” from the reactivation)? How often does reactivation in the context of immunosuppression turn into a chronic infection situation?

Thank you again! I really love to understand the “why” behind things…as knowledge is comforting and a relief. I’ve read so many medical articles lately, but without the help of people like yourself, sometimes it’s hard to parse through all the medical lingo and make sense of everything…so I especially appreciate your time so much!

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Hi @myg,

Thomas’ answers as always are spot-on. I’ll answer your followup questions. FYI…I am a senior member of the HBV research community (PhD, not MD).

  1. Vaccination usually leads to block of detectable HBV infection in the body, but not always, and the degree of protection may not necessarily stay the same with time. The vaccine works in 93-95% of people (I’m a non-responder). If anti-HBs antibodies are high (>10 mIU/mL is a typical threshold), then they almost always block detectable infection. However, antibody levels tend to decline with time. We don’t know how long HBV vaccination works, but it is clear that around 20 or so years post-vaccination that some people’s levels decline to the point where a very limited infection can occur that is then promptly cleared by the immune system. My guess is that is what happened in your case.

  2. A simple exposure with no productive infection of a cell would almost certainly not yield anti-HBc antibodies as there is vanishingly little of that protein transferred in a typical infection incident. It is likely that if HBc appears, that a limited and infection occurred that was was then cleared.

  3. See my answer #2. The immune system needs to see enough protein to react to it. If there is too little, it cannot see it to act against it. HBV exposures usually involve transfer of very tiny amounts of blood, and the HBc protein in that volume would almost always be too little to trigger an immune response by itself.

4.1) Yes.

4.2) Taking antivirals suppresses production of virus and reduces HBV transmission to other cells. It does not directly affect the immune response. Whether the virus returns to undetectability in the absence of drug depends on the body’s immune system. However, in this scenario, the body had already essentially beaten the virus once, and when immune suppression is relaxed, it would normally do so again. I am not a physician, so I don’t know how often an over chronic infection results from reactivation secondary to immunosuppression. My guess would be not often if the immune suppression drugs are reduced to allow natural immune control of HBV to re-assert itself.

Welcome to the Community, and I wish you the very best.



Hi @john.tavis!

Thank you very much for jumping in and answering my remaining questions! That all makes sense, and it’s super helpful to know what is happening within my body and any future risks. I appreciate the guidance and support and it’s making me feel better already.

I’m Asian American, and from a young age, I’ve known that HBV affects Asian American communities at a higher rate relative to the general US population. I have close family/friends who have been affected by HBV…so I’ve been scared of it for a long time. My test results from this month was triggering in many respects because of this long-standing fear that I’ve held for so long. I hope that through continued education and learnings and reading posts from this treasure trove of a forum and internet research, that I’ll be less scared going forward.

Thank you all so much for the support so far. It means so much. I appreciate you all!


You don’t have hep b. You were exposed to it. Same as me. I had an acute hep b in the past too but I cleared the infection. Although I understand your anxiety. Even after resolution of acute, I’m still traumatized. I pray for strength every morning and night. I’m glad to feel better day by day.


@GodisGood thank you for the empathy and solidarity! And the reassurance that the scary feelings may go away with time! I wish you well too!!


Hello there, I had a follow-up question regarding risks of HBV reactivation related to taking Paxlovid for COVID.

I recently tested positive for COVID and just started taking Paxlovid. I haven’t found any articles or research that directly studies the effect of Paxlovid on the risk of hepatitis B reactivation in someone who had a previous acute resolved infection (surface antigen currently negative, but surface antibody is reactive and core antibody also positive). However, I did find some articles that talked about how direct-acting antivirals taken by patients to treat Hepatitis C could result in Hepatitis B reactivation. See here for an example article: Direct-Acting Antivirals and the Risk of Hepatitis B Reactivation in Hepatitis B and C Co-Infected Patients: A Systematic Review and Meta-Analysis - PMC

And then I noticed that some of the DAAs that were included in the Hepatitis C study include ritonavir, which is one of the drugs that is included in Paxlovid.

I’ve searched far and wide for guidance on the interaction between Paxlovid and HBV reactivation for a person with an acute resolved case of HBV and haven’t found anything that is directly on point.

And now I’m getting a bit scared about potentially increasing my risk of reactivating HBV by using Paxlovid, but then I’m also worried about not taking Paxlovid because my COVID symptoms are quite uncomfortable right now.

Any medical guidance on the interaction between Paxlovid and HBV reactivation in a person who is currently HBsAG negative/HBsAB reactive/HBcAB positive?

Thank you again so much!

Hello @myg
I’m not a doctor, medical expert or health professional .
I have chronic hepatitis B., for 40 years.
I am happy for you that you cleared the virus, you are one of the lucky ones.
Sorry to hear sad you have Covid at the moment. It’s not nice being sick.

Sorry I don’t have an answer for you. Someone else should respond soon.

Dear @myg,

Ritonavir is is a drug originally developed for treating HIV infection. However, this drug also inhibits one of the key enzymes which the liver uses to metabolize many drugs (called cytochrome p450-3A4). For this reason, ritonavir is commonly used as part of many other medicines to increase the stability of other antiviral drugs and improve their efficacy in increases the levels of these drugs in the body.

You are correct that a small proportion of patients with HCV / HBV co-infection (where the HBV infection was not known at the time) experience reactivation following treatment for HCV infection. We do not fully understand the basis for this reactivation but many small molecules used in antiviral medications also have effects on immune function so this could be at least part of the explanation. Ritnonavir is not used for any approved drugs for HBV infection so there is no good data available on the potential of ritonavir to cause HBV reactivation.

Paxlovid is a drug product which also uses ritonavir to boost the antiviral effects of nirmatrelvir (the actual medication targeting SARS CoV2 replication. Again you are correct there is also no data on HBV reactivation with nirmatrelvir either.

I am sorry there is not more information to guide you in this. However, Paxlovid is only a 5 day course of treatment so the impact (if any) on HBV reactivation is expected to be much less than in the case of HCV treatment (which is typically 8-12 weeks).

Best regards,


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Thank you for the words of support @Caraline! It is very much appreciated, and I hope to get over covid soon!

Thank you for the detailed response @availlant! Your response definitely makes sense, and I was also thinking that because Paxlovid is such a short course, the effect might be minimal. I didn’t end up finishing the course due to my anxiety of any side effects related to HBV reactivation. And so, now…unfortunately, my additional worry is whether COVID itself might reactivate HBV. Most of the articles that I have found relate to the use of COVID treatment drugs as a potential trigger for reactivation, not the COVID virus in and of itself being the trigger for an HBV reaction. But then I ran into something like this article: Livers | Free Full-Text | Can Hepatitis B Virus (HBV) Reactivation Result from a Mild COVID-19 Infection?

I’m not a scientist, but my layperson logic is basically wondering if my body’s current act of dealing with and fighting off COVID would somehow disrupt the normal immune balance of my body, such that the immunity that normally would keep HBV in check and asleep is no longer strong enough to keep it asleep? To analogize, I’m wondering if the inactive/sleeping HBV is normally “guarded” by guards, and then suddenly there’s some sort of other immediate commotion elsewhere in the building, and then the guards need to run away to fight that other issue for now…so then since nobody is guarding it anymore, the HBV takes this chance to escape and wreck havoc? Is that how things work?

Hi @myg,

Thanks for stimulating such interesting discussion about such a timely subject. I want to note that a lot of things are still being figured out with SARSCoV2. Think about how long we’ve known about Hep B (>50 years) and are still discovering things about it. We’ve only known about this virus for 4 years or so, and so a lot still needs to be done over time.

Regarding reactivation of HBV with Hep C treatment, I was under the impression that there is interaction between the viruses that contributes as well. Hep C infected cells will release interferons and these can suppress Hep B replication. When you treat Hep C and remove it, you also remove this interferon secretion, which can allow the Hep B to bounce back. This is what could be happening in some cases rather than being driven by the meds themselves.

Generally the immune system is pretty specific, people with Hep B don’t seem to do worse when they’re infected by other viruses (e.g., they respond to colds and flus similar to people without HBV infection). So I’m not sure how much this “pulling the guards away” effect would have an impact. I would like to ask any immunologists around (e.g., @nina.le.bert, @Greg, @mat or any other @ScienceExperts) to provide some of their expertise to this question and/or tell me I’m being a silly virologist.


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Hi Thomas,

You are not being a “silly virologist” (although I’ve seen that happen!).

HBV’s immune suppression is specific to itself. It does not pre-dispose people to other infections. The immunologists can chime in with details. Note that our understanding of how HBV suppresses immunity to itself is incomplete. We know some aspects. For example: HBs soaks up anti-HBs antibodies and blocks the antibodies’ ability to stop infection of new cells, and HBs induces anergy (ie, failure to respond) to HBs by T cells (a major class of white blood cells). But we don’t know all the ways that the virus blocks the immune response to itself, in large part because the animal models where such experiments can be done are not all that good.



Thank you @ThomasTu and @john.tavis for the additional information and your scientific takes! It makes a lot of sense that there is a lot we don’t currently know, but I do appreciate you sharing what we do know. I’m someone who is sometimes nervous and anxious when there is uncertainty and I always try to grasp for more information, but I think part of my learnings here is to try to be more comfortable and ok with a bit of uncertainty and not knowing - and to just live. :slight_smile:


Dear @myg,

I think your comment about being " ok with a bit of uncertainty and not knowing - and to just live" is very wise. I wish you the very best.