You're using an outdated browser. Please upgrade to a modern browser for the best experience.
Submitted Successfully!
Thank you for your contribution! You can also upload a video entry or images related to this topic. For video creation, please contact our Academic Video Service.
Version Summary Created by Modification Content Size Created at Operation
1 Yonas Bekele + 2760 word(s) 2760 2021-12-21 08:55:51 |
2 The format is correct Lindsay Dong Meta information modification 2760 2021-12-31 02:48:52 |

Video Upload Options

We provide professional Academic Video Service to translate complex research into visually appealing presentations. Would you like to try it?
No, upload directly Yes

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Bekele, Y. HBV Infection in HIV-1 Infected Individuals. Encyclopedia. Available online: https://encyclopedia.pub/entry/17670 (accessed on 06 December 2025).
Bekele Y. HBV Infection in HIV-1 Infected Individuals. Encyclopedia. Available at: https://encyclopedia.pub/entry/17670. Accessed December 06, 2025.
Bekele, Yonas. "HBV Infection in HIV-1 Infected Individuals" Encyclopedia, https://encyclopedia.pub/entry/17670 (accessed December 06, 2025).
Bekele, Y. (2021, December 30). HBV Infection in HIV-1 Infected Individuals. In Encyclopedia. https://encyclopedia.pub/entry/17670
Bekele, Yonas. "HBV Infection in HIV-1 Infected Individuals." Encyclopedia. Web. 30 December, 2021.
HBV Infection in HIV-1 Infected Individuals
Edit
This entry is adapted from the peer-reviewed paper 10.3390/vaccines9121484

Disease progression and liver-related complications are more common in HIV-1/HBV co-infected than HBV mono-infected individuals. Response to HBV vaccine is suboptimal in HIV-1-infected individuals. Several factors affect HBV vaccine response during HIV-1 infection including CD4+ T cell counts, B cell response, vaccine formulation, schedules, and timing of antiretroviral therapy (ART). Thus, regular follow-up for antibody titer and a booster dose is warranted to prevent HBV transmission in HIV-1 infected people.

HBV HBV vaccine anti-HBs antibodies HIV-1 booster dose B cells

1. Introduction

Vaccines are among the most powerful health interventions and have significantly contributed to prolonging life expectancy worldwide. In this regard, hepatitis B virus (HBV) vaccination is the ideal example for the prevention of chronic infection and related complications including liver cirrhosis and hepatocellular carcinoma (HCC). An HBV vaccine became commercially available in 1982, initially as HBsAg (HBV surface antigen) isolated from patients, and later as a recombinant protein [1], and has proven a 95% efficacy in preventing HBV infection and associated symptoms [2]. Globally, the incidence of HBV infection and death due to chronic HBV infection-related complications declined over the years due to effective nationwide early childhood vaccination [3]. Still, in 2019 alone, 1.5 million and 820,000 people were newly infected and died of HBV-related complications, respectively, according to a WHO report [4]. Some of the challenges of HBV vaccination are that a proportion, corresponding to approximately 10% of vaccinated individuals, do not respond to the vaccine and that a decline of vaccine-specific antibodies to HBV surface (HBs) protein takes place in vaccinated individuals [5].
In a comprehensive study gathering data from individuals born in Israel after the introduction of the HBV vaccine and subsequently tested for anti-HBs Abs, a decline over time in levels of anti-HBs Abs was observed with 66.7% of adolescents scoring negative for HBV antibodies 15 years after vaccination [6]. The mechanism(s) leading to waning humoral responses to the HBV vaccine are not fully understood; it has been proposed that the initial lack of response to the vaccine may be caused by specific HLA alleles or lack of cytokine production (reviewed in [7]) and overlapping mechanisms may likely account for the waning of immune responses. Interestingly, Klinger and colleagues [6] also showed that a booster dose of HBV vaccine provided to HBV seronegative subjects, previously receiving HBV vaccine, led to seroconversion in 93.8% of individuals; this study clearly showed that an anamnestic response to HBV vaccine is present in immunocompetent individuals despite a seronegative status.
The waning of HBV vaccine responses is a major health problem connected to HIV-1 infection. A poor serological response to primary HBV vaccination and a rapid decline of anti-HBs antibody levels, already within the first year from vaccination, has been reported in HIV-1 infected individuals [8][9][10][11][12]; the gradual decline of protective immunity to the HBV vaccine becomes more noticeable over time in HIV-1 infected individuals. As extensively reviewed, the burden of HIV-1 is higher in Sub-Saharan Africa, though a significant decrease in mortality and new cases in 2019 compared to 1990 was reported [13]. Sub-Saharan Africa and East Asia are considered to be high chronic HBV endemic regions and around 10% of HIV-positive individuals are co-infected with HBV [14].
This is an important medical concern considering that people with co-morbidity and/or immunocompromised individuals especially with HIV have a higher chance of developing chronic HBV infection and may also die with liver-related complications. The present review aims at summarizing current knowledge on responses to HBV vaccination and the need for a booster dose in HIV-1-infected individuals. 

2. HBV Infection in HIV-1 Infected Individuals

HBV infection is generally self-limiting in immunocompetent adults; the likelihood of clearing HBV infection is, however, lower in HIV-1-infected compared to healthy individuals. Acute HBV infection can cause acute liver failure and death in both HIV-1-infected and uninfected individuals [13]. The pathogenic effects of HBV and HIV-1 infections are considerably worsened in co-infected patients [14][15]. Elevated levels of HBV DNA, reduced ability to clear circulating hepatitis B envelope antigen (HBeAg), and a higher risk of developing chronic HBV infection were reported in co-infected, compared to HIV-1-negative individuals [14][16]. In addition, the progression rate to cirrhosis and/or HCC is much faster, and liver-related mortality is more common in co-infected individuals [14][16].
Besides, break-through HBV infections were also identified in fully vaccinated HIV-1-infected children [17], in HIV-1 infected adolescents [18], and even in HIV-1 uninfected individuals [19][20][21]. In some of these acutely infected individuals, the infection resolved with negative results upon subsequent testing for HBV DNA and HBeAg [18][21]. In some previous reports, the source of HBV infection in vaccinated HIV-1-infected children was not regularly identified, but the virus could be transmitted from HBsAg positive mothers [17][20], occult HBV infection [21], or exposure to vaccine-escape mutant HBV strains; in the latter context, vaccine-induced protective antibodies are ineffective to neutralize some HBV S gene mutants [22].
Anti-retroviral therapy (ART) effectively slows down disease progression and reduces the death rate in the HIV-1/HBV co-infected individuals [23]. However, liver toxicity is a common side effect of ART in HIV-1/HBV-infected individuals [23]. Besides, drug resistance to lamivudine, which is the most effective drug for the treatment of HBV infection, and cross-drug resistance to other anti-HBV drugs, hampered the global effort to slow down disease progression in co-infected people [23]. Other compounds including interferon-α, pegylated interferon-α, adefovir, entecavir, telbivudine, and tenofovir are used to reduce liver damage and to prevent long-term complications of HBV infection in mono-infected or HBV-HIV-1 co-infected patients [24]. Thus, patients with HIV/HBV still need the best, effective, affordable, and accessible treatment to prevent liver-related complications and death.

3. The Impact of Immunological and Virological Parameters on Response to HBV Vaccine in HIV-1 Infected Individuals

The most common schedule for HBV vaccination is three doses of the vaccine at 0–1–6 months; however, an accelerated vaccination schedule at 0–4–8 weeks is also recommended for high-risk individuals to increase vaccine compliance and elicit higher antibody responses. In the latter schedule, a fourth dose was recommended to slow down the decline of anti-HBs antibodies and for long-term protection. Several studies in different settings showed a decline in the anti-HBs antibodies a few or several years after vaccination, depending on the vaccination strategies and other factors. Lower response to HBV vaccine and short duration of protection were reported in HIV-1-infected individuals. 

In support of the role of CD4+ T cell count, a study conducted in Rwanda reported an association between HBV vaccine response in HIV-1-infected children and adolescents with CD4+ T cell counts higher than 350 cells/μL and a viral load below 40 RNA copies/mL [25]. An association between CD4+ T cell counts and response to HBV vaccine was also observed in adults with AIDS receiving an efavirenz-based ART regiment [26].

Regarding a gender effect, the likelihood of responding to the HBV vaccine was higher in adult HIV-1-infected women, compared to men, when these patients presented with CD4+ T cell counts >350 cells/μL [27].

Initial response to the vaccine was also predictive of sustained vaccine responses. Lopes and colleagues [28] reported that in HIV-1 infected individuals the persistence of protective anti-HBs antibody titers relates to the response levels at primary vaccination; in addition, in patients with a pronounced (>1000 IU/I) vaccine response at primary vaccination, the meantime loss of effective anti-HBs titer was 4.4 years [28]. Similarly, we have also found a direct correlation between anti-HBs antibody titer at 1 month and 6 months from the last dose of HBV vaccination in Ethiopian children (Figure 1). The immunological correlates presented by Lopes et al., (2013) remain somehow unclear, as a high CD4+ T cell count paradoxically was inversely correlated to strong response at primary vaccination.

Vaccines 09 01484 g001 550
Figure 1. Correlation of anti-HBs titer at 1 and 6 months from completed HBV vaccination. Three doses of HBV vaccine were administered to children who were negative for HBsAg and previously unvaccinated, and periphery blood was collected at 1 month and 6 months after the last vaccination. Direct correlation of anti-HBs titers at 1 month and 6 months from the last vaccination dose in both healthy controls (A) and ART-treated HIV-1 infected (B) children. Anti-HBs: Hepatitis B surface antibody; IU/L: international units per liter (Modified from [8][29]).
Regarding the role of ART initiation, the response rate to HBV vaccination in a study conducted in Tanzania was significantly lower in ART-naïve compared to ART-treated HIV-1 infected children with CD4+ T cell counts strongly predicting the levels of anti-HBs antibodies [30]. This latter result also supports a role for CD4+ T cells. The potential role of a CCR5 agonist-based ART regimen in improving immune responses to a double dose intramuscular (IM) HBV vaccination in HIV-1 infected adult patients was investigated [31]. At 1 month from the last vaccination, approximately 90% of the patients had responded to the vaccine and 81% maintained protective antibody levels at 1 year from vaccination [31]. Moreover, the CCR5 agonist-based ART regimen was associated with a wider vaccine response in patients younger than 50 years [31].
The read-out of a successful HBV vaccination is a vaccine-specific antibody response against HBsAg. Severe damage takes place in B cells, which are the cells devoted to antibody production, in HIV-1-infected individuals, both in children and adults [8][32]. This aspect of HIV-1 immunopathology may compromise the response to the HBV vaccine and also the maintenance of protective antibody titers to the HBV vaccine (Figure 2). The major abnormalities found in blood B cells during HIV-1 infection comprise a depletion of the general pool of memory B cells and an expansion of anergic non-typical B cell populations [33].
Vaccines 09 01484 g002 550
Figure 2. Immune responses to HBV vaccine. Antigen captured and processed by antigen-presenting cells (APCs); the processed antigen activates B cells and T cells. B-Tfh cells interact at the border of the GC for the generation of short-lived plasma cells and antibodies, and in the GC for the generation of long-lived plasma cells and development of memory B cells. In HIV-1 infection, inefficient interaction between B-Tfh cells was reported due to exhaustion of cells by direct and indirect effects of HIV-1. NB: naïve B cells, MB: memory B cells; AM: Activated memory B cells; TLB: Tissue-like memory B cells; Tfh: T follicular helper; IL: interleukin; GC: germinal center (Created with BioRender.com).
It is of interest that an expansion of an atypical memory CD19+CD10-CD27-CD21- subset of B cells, expressing high levels of the inhibitor FcRL5 receptor, can be found in HBV-infected patients [34]. HBV appears to have a direct role in compromising B cell function and induction of an atypical B cell phenotype. PD-1 blockade of atypical B cells isolated from chronically HBV-infected individuals could partially restore the biological properties of B cells including homing, cytokine, and antibody production [35]. In a study recently conducted in our laboratory, we showed that primary response to HBV vaccine, measured by antibody titers to HBs antigen, correlated with the frequency of resting and switched memory B cells in HIV-1 infected children [29]. Restoration of B cell function in HIV-1 infected individuals initiating ART during the chronic phase of infection may not be possible [36] and will likely require an early control of HIV-1 viremia resulting from early and prolonged adherence to ART, a strategy not always possible to implement in poor economic settings.

4. Booster or the Additional Dose of HBV Vaccine for HIV-1 Infected Individuals

Long-term protection and anamnestic response were reported after childhood HBV vaccination in immunocompetent individuals (Table 1). Protective anti-HBs titers were measured in only 37% of healthy participants (n = 300) attending the health center of Rafsanjan (Kerman province, southeast of Iran) 20 years from primary vaccination [37]; a single booster was administered to participants who had less than 10 IU/L of anti-HBs and the majority (>97%) responded to re-vaccination, suggesting the presence of an anamnestic response in previously vaccinated immunocompetent individuals [37]. The study shows that in immunocompetent individuals, loss of protective antibody does not necessarily imply the absence of immunity against HBV and contributes to the discussion on whether a booster dose of HBV vaccine should be administered to immunocompetent individuals [38]. Other studies also confirm that administration of booster dose(s) may not be necessary for these individuals and that childhood HB vaccination is sufficient to prevent HBV infection [20][39][40][41][42]. However, further studies should be conducted to prevent breakthrough infection of vaccine escape mutants in immunocompetent individuals living in the hyperendemic regions.

Table 1. Hepatitis B vaccine response in healthy individuals.
No Schedule at Birth Duration of Follow-Ups (Years) Anamnestic Response and Timing Response Rate for Non-Responder upon the 2nd Dose Country References
1 2, 4 & 6 months age 9 months to 16 years Single-dose 10 μg.
At 1 month: 95% for pre-booster detectable anti-HBs.
85% for undetectable pre-booster level.		 3 doses; 92.3% Egypt [39]
2 0, 1, and 6 months 5–15 years 0–1–6 months, 10 μg.
For < 10 mIU/mL *: 95.65% at 1 month.
For > 10 mIU/mL *: 100% at 1 month.		 NA China [43]
3 3 doses, at birth or 12 years 17.2 and 19.3 years after the last vaccination Single-dose; at 1 month 88.8%. Another dose, 100% Italy [44]
4 3 or more doses, at birth or young age   Single-dose; at 1 month 89.9%. 2 more doses; 96.2% Italy [45]
5 4 doses; First 2 years of life Aged 14–15 years Single-dose 10 µg. At 1 month.
For < 6.2 mIU/mL *: 82.9%.
For > 6.2–<10 mIU/mL *: 100%.
For > 10 mIU/mL *: 98.6%.		 NA Germany [46]
6 3 doses, at birth or during adolescence 18–20 years Single-dose 10 μg.
At 1 month: 97.7% for pre-booster detectable anti-HBs.
88.8% for undetectable pre-booster level.		 2 more doses; 100% Italy [47]
7 3 doses; first year of life (2 days of birth, 1.5 and 9 months) 20 years Single-dose 20 μg; 97.1% after 4 weeks. NA Iran [37]
8 3–4 doses; all vaccinated during adulthood 20–30 years Single-dose 20 μg.
For < 10 mIU/mL *: 70% at day 7 and 100% at 1 month.
For > 10 mIU/mL *: 100% at both day 7 and 1 month.		 NA Canada and Belgium [40]
* Levels of anti-HBs antibody before booster dose/s.
Post-vaccination screening for HBV vaccine-specific antibody levels in HIV-1 infected individuals followed by administration of a booster dose may be a sustainable strategy to prevent HBV transmission [48][49].The major challenge of accelerated vaccination, the common schedule in resource-limited settings, is the shorter longevity of induced antibodies compared to standard vaccination; this observation suggested that an accelerated vaccine schedule should be supplemented with an additional dose at 12 months from the last vaccination [50][51]. In this context, it should be taken into consideration that the waning of HBV antibodies is faster in HIV-1-infected compared to healthy individuals [8]; it is, therefore, likely that longevity of vaccine efficacy in this group can be preserved only by providing an additional dose at 1 year from the last vaccination point and possibly again at later time points.
Seven to 25 years from initial HBV vaccination at birth, HIV-1-infected adolescents and young adults who did not present with protective anti-HBs were provided a single IM dose of HBV vaccine; 50% responded, and the response rate was associated with CD4+ T cell counts [52]. An anamnestic response was measured in 82% of HIV-1 infected children who originally had anti-HBs antibodies below protective levels 3 years after revaccination [53] and in half of the HIV-1-infected children experiencing a gradual decline of anti-HBs at 8 weeks after vaccination [54]. These results show that a single HBV vaccine dose may reactivate a serological response in individuals presenting with insufficient levels of protective anti-HBs antibodies. In chronic kidney disease patients, non-responsiveness to recommended HBV vaccination, lower anti-HBs antibody titer, and rapid loss of protective antibodies were documented [55]. These patients who were in pre-dialysis and dialysis benefited from a booster dose to prevent HBV transmission since there is a higher potential to acquire the virus through contaminated dialysis equipment and surfaces [55][56][57]. Similarly, HIV-1 infected individuals had a suboptimal HB vaccine response and a higher chance of acquiring HBV with a serious outcome. Thus, a regular follow-up assessing maintenance of HBV vaccine responses should be implemented for HIV-1-infected individuals, and a booster dose should be given when titers fall below a protective threshold, to prevent HBV infection in this group of immunocompromised individuals.

5. Conclusions

In summary, a rapid waning of specific HBV vaccine antibodies is a major obstacle for HBV vaccination of HIV-1-infected individuals. Although the immunological mechanisms for loss of HBV vaccine antibodies during HIV-1 infection remain poorly characterized, emphasis should be given to impaired B cell immunology found in HIV-1-infected individuals, and chronic HBV infected patients. Searching for biomarkers of HBV vaccine response in HIV-1-infected individuals and the biological and immunological properties of B and T follicular helper (Tfh) cells, important immunological players in vaccine responses should be further evaluated. These future studies should include molecular signatures of B cell signaling and responses which were recently identified [58].
ART administration and adherence remain crucial to control viremia, maintain CD4+ T cell count, and restore immunological functions in HIV-1 infected individuals, including responses to vaccines. In addition to effective ART, vaccination schedules and vaccine doses should be revised to increase the response rate and longevity of HBV vaccine responses in HIV-1 infected individuals. Maintenance of HBV vaccine responses in HIV-1-infected individuals can be achieved only through regular serological monitoring and eventually provision of HBV vaccine booster doses. Priority should be given to these strategies even in less economically privileged settings to ensure the protection of HIV-1-infected children and adults against HBV.

References

  1. McAleer, W.J.; Buynak, E.B.; Maigetter, R.Z.; Wampler, D.E.; Miller, W.J.; Hilleman, M.R. Human hepatitis B vaccine from recombinant yeast. Nature 1984, 307, 178–180.
  2. WHO. Hepatitis B; World Health Organization: Geneva, Switzerland, 2002.
  3. Polaris Observatory, C. Global prevalence, treatment, and prevention of hepatitis B virus infection in 2016: A modelling study. Lancet Gastroenterol. Hepatol. 2018, 3, 383–403.
  4. WHO. Global Progress Report on HIV, Viral Hepatitis and Sexually Transmitted Infections, 2021: Accountability for the Global Health Sector Strategies 2016–2021: Actions for Impact; World Health Organization: Geneva, Switzerland, 2021.
  5. Van Damme, P.; Ward, J.; Shouval, D.; Wiersma, S.; Zanetti, A. Hepatitis B Vaccines. In Vaccines; Plotkin, S.A., Orenstein, W.A., Offit, P.A., Edwards, K.M., Eds.; Elsevier: Philadelphia, PA, USA, 2013; Volume 205, p. 234.
  6. Klinger, G.; Chodick, G.; Levy, I. Long-term immunity to hepatitis B following vaccination in infancy: Real-world data analysis. Vaccine 2018, 36, 2288–2292.
  7. Tajiri, K.; Shimizu, Y. Unsolved problems and future perspectives of hepatitis B virus vaccination. World J. Gastroenterol. 2015, 21, 7074–7083.
  8. Bekele, Y.; Yibeltal, D.; Bobosha, K.; Andargie, T.E.; Lemma, M.; Gebre, M.; Mekonnen, E.; Habtewold, A.; Nilsson, A.; Aseffa, A.; et al. T follicular helper cells and antibody response to Hepatitis B virus vaccine in HIV-1 infected children receiving ART. Sci. Rep. 2017, 7, 8956.
  9. Kerneis, S.; Launay, O.; Turbelin, C.; Batteux, F.; Hanslik, T.; Boelle, P.Y. Long-term immune responses to vaccination in HIV-infected patients: A systematic review and meta-analysis. Clin. Infect. Dis 2014, 58, 1130–1139.
  10. Kim, H.N.; Harrington, R.D.; Crane, H.M.; Dhanireddy, S.; Dellit, T.H.; Spach, D.H. Hepatitis B vaccination in HIV-infected adults: Current evidence, recommendations and practical considerations. Int. J. STD AIDS 2009, 20, 595–600.
  11. Mizusawa, M.; Perlman, D.C.; Lucido, D.; Salomon, N. Rapid loss of vaccine-acquired hepatitis B surface antibody after three doses of hepatitis B vaccination in HIV-infected persons. Int. J. STD AIDS 2014, 25, 201–206.
  12. Whitaker, J.A.; Rouphael, N.G.; Edupuganti, S.; Lai, L.; Mulligan, M.J. Strategies to increase responsiveness to hepatitis B vaccination in adults with HIV-1. Lancet Infect. Dis. 2012, 12, 966–976.
  13. Collaborators, G.H. Global, regional, and national sex-specific burden and control of the HIV epidemic, 1990-2019, for 204 countries and territories: The Global Burden of Diseases Study 2019. Lancet HIV 2021, 8, e633–e651.
  14. Cheng, Z.; Lin, P.; Cheng, N. HBV/HIV Coinfection: Impact on the Development and Clinical Treatment of Liver Diseases. Front. Med. 2021, 8, 713981.
  15. Bianco, E.; Stroffolini, T.; Spada, E.; Szklo, A.; Marzolini, F.; Ragni, P.; Gallo, G.; Balocchini, E.; Parlato, A.; Sangalli, M.; et al. Case fatality rate of acute viral hepatitis in Italy: 1995-2000. An update. Dig. Liver Dis. 2003, 35, 404–408.
  16. Kourtis, A.P.; Bulterys, M.; Hu, D.J.; Jamieson, D.J. HIV-HBV coinfection—a global challenge. N. Engl. J. Med. 2012, 366, 1749–1752.
  17. Levy, V.; Grant, R.M. Antiretroviral therapy for hepatitis B virus-HIV-coinfected patients: Promises and pitfalls. Clin. Infect. Dis. 2006, 43, 904–910.
  18. Parvez, M.K. HBV and HIV co-infection: Impact on liver pathobiology and therapeutic approaches. World J. Hepatol. 2015, 7, 121–126.
  19. Mancinelli, S.; Pirillo, M.F.; Liotta, G.; Andreotti, M.; Mphwere, R.; Amici, R.; Marazzi, M.C.; Vella, S.; Palombi, L.; Giuliano, M. Antibody response to hepatitis B vaccine in HIV-exposed infants in Malawi and correlation with HBV infection acquisition. J. Med. Virol. 2018, 90, 1172–1176.
  20. Lapphra, K.; Angkhananukit, P.; Saihongthong, S.; Phongsamart, W.; Wittawatmongkol, O.; Rungmaitree, S.; Chokephaibulkit, K. Persistence of Hepatitis B Immunity Following 3-dose Infant Primary Series in HIV-infected Thai Adolescents and Immunologic Response to Revaccination. Pediatr. Infect. Dis. J. 2017, 36, 863–868.
  21. Abushady, E.A.; Gameel, M.M.; Klena, J.D.; Ahmed, S.F.; Abdel-Wahab, K.S.; Fahmy, S.M. HBV vaccine efficacy and detection and genotyping of vaccinee asymptomatic breakthrough HBV infection in Egypt. World J. Hepatol. 2011, 3, 147–156.
  22. Mendy, M.; Peterson, I.; Hossin, S.; Peto, T.; Jobarteh, M.L.; Jeng-Barry, A.; Sidibeh, M.; Jatta, A.; Moore, S.E.; Hall, A.J.; et al. Observational study of vaccine efficacy 24 years after the start of hepatitis B vaccination in two Gambian villages: No need for a booster dose. PLoS ONE 2013, 8, e58029.
  23. Powell, E.A.; Razeghi, S.; Zucker, S.; Blackard, J.T. Occult Hepatitis B Virus Infection in a Previously Vaccinated Injection Drug User. Hepat. Mon. 2016, 16, e34758.
  24. Gerlich, W.H. Breakthrough of hepatitis B virus escape mutants after vaccination and virus reactivation. J. Clin. Virol. 2006, 36, S18–S22.
  25. Singh, K.P.; Crane, M.; Audsley, J.; Avihingsanon, A.; Sasadeusz, J.; Lewin, S.R. HIV-hepatitis B virus coinfection: Epidemiology, pathogenesis, and treatment. AIDS 2017, 31, 2035–2052.
  26. De Clercq, E.; Ferir, G.; Kaptein, S.; Neyts, J. Antiviral treatment of chronic hepatitis B virus (HBV) infections. Viruses 2010, 2, 1279–1305.
  27. Mutwa, P.R.; Boer, K.R.; Rusine, J.B.; Muganga, N.; Tuyishimire, D.; Reiss, P.; Lange, J.M.; Geelen, S.P. Hepatitis B virus prevalence and vaccine response in HIV-infected children and adolescents on combination antiretroviral therapy in Kigali, Rwanda. Pediatr. Infect. Dis. J. 2013, 32, 246–251.
  28. Paitoonpong, L.; Suankratay, C. Immunological response to hepatitis B vaccination in patients with AIDS and virological response to highly active antiretroviral therapy. Scand. J. Infect. Dis. 2008, 40, 54–58.
  29. Irungu, E.; Mugo, N.; Ngure, K.; Njuguna, R.; Celum, C.; Farquhar, C.; Dhanireddy, S.; Baeten, J.M. Immune response to hepatitis B virus vaccination among HIV-1 infected and uninfected adults in Kenya. J. Infect. Dis. 2013, 207, 402–410.
  30. Lopes, V.B.; Hassing, R.J.; de Vries-Sluijs, T.E.; El Barzouhi, A.; Hansen, B.E.; Schutten, M.; de Man, R.A.; van der Ende, M.E. Long-term response rates of successful hepatitis B vaccination in HIV-infected patients. Vaccine 2013, 31, 1040–1044.
  31. Bekele, Y.; Lemma, M.; Bobosha, K.; Yibeltal, D.; Nasi, A.; Gebre, M.; Nilsson, A.; Aseffa, A.; Howe, R.; Chiodi, F. Homing defects of B cells in HIV-1 infected children impair vaccination responses. Vaccine 2019, 37, 2348–2355.
  32. Pippi, F.; Bracciale, L.; Stolzuoli, L.; Giaccherini, R.; Montomoli, E.; Gentile, C.; Filetti, S.; De Luca, A.; Cellesi, C. Serological response to hepatitis B virus vaccine in HIV-infected children in Tanzania. HIV Med. 2008, 9, 519–525.
  33. Herrero-Fernandez, I.; Pacheco, Y.M.; Genebat, M.; Rodriguez-Mendez, M.D.M.; Lozano, M.D.C.; Polaino, M.J.; Rosado-Sanchez, I.; Tarancon-Diez, L.; Munoz-Fernandez, M.A.; Ruiz-Mateos, E.; et al. Association between a Suppressive Combined Antiretroviral Therapy Containing Maraviroc and the Hepatitis B Virus Vaccine Response. Antimicrob. Agents Chemother. 2018, 62, AAC.02050-17.
  34. Cagigi, A.; Nilsson, A.; Pensieroso, S.; Chiodi, F. Dysfunctional B-cell responses during HIV-1 infection: Implication for influenza vaccination and highly active antiretroviral therapy. Lancet Infect. Dis. 2010, 10, 499–503.
  35. Amu, S.; Ruffin, N.; Rethi, B.; Chiodi, F. Impairment of B-cell functions during HIV-1 infection. AIDS 2013, 27, 2323–2334.
  36. Poonia, B.; Ayithan, N.; Nandi, M.; Masur, H.; Kottilil, S. HBV induces inhibitory FcRL receptor on B cells and dysregulates B cell-T follicular helper cell axis. Sci. Rep. 2018, 8, 15296.
  37. Burton, A.R.; Pallett, L.J.; McCoy, L.E.; Suveizdyte, K.; Amin, O.E.; Swadling, L.; Alberts, E.; Davidson, B.R.; Kennedy, P.T.; Gill, U.S.; et al. Circulating and intrahepatic antiviral B cells are defective in hepatitis B. J. Clin. Investig. 2018, 128, 4588–4603.
  38. Pensieroso, S.; Galli, L.; Nozza, S.; Ruffin, N.; Castagna, A.; Tambussi, G.; Hejdeman, B.; Misciagna, D.; Riva, A.; Malnati, M.; et al. B-cell subset alterations and correlated factors in HIV-1 infection. AIDS 2013, 27, 1209–1217.
  39. Bagheri-Jamebozorgi, M.; Keshavarz, J.; Nemati, M.; Mohammadi-Hossainabad, S.; Rezayati, M.T.; Nejad-Ghaderi, M.; Jamalizadeh, A.; Shokri, F.; Jafarzadeh, A. The persistence of anti-HBs antibody and anamnestic response 20 years after primary vaccination with recombinant hepatitis B vaccine at infancy. Hum. Vaccines Immunother. 2014, 10, 3731–3736.
  40. Poorolajal, J.; Mahmoodi, M.; Majdzadeh, R.; Nasseri-Moghaddam, S.; Haghdoost, A.; Fotouhi, A. Long-term protection provided by hepatitis B vaccine and need for booster dose: A meta-analysis. Vaccine 2010, 28, 623–631.
  41. Salama, I.I.; Sami, S.M.; Said, Z.N.; Salama, S.I.; Rabah, T.M.; Abdel-Latif, G.A.; Elmosalami, D.M.; Saleh, R.M.; Abdel Mohsin, A.M.; Metwally, A.M.; et al. Early and long term anamnestic response to HBV booster dose among fully vaccinated Egyptian children during infancy. Vaccine 2018, 36, 2005–2011.
  42. Van Damme, P.; Dionne, M.; Leroux-Roels, G.; Van Der Meeren, O.; Di Paolo, E.; Salaun, B.; Surya Kiran, P.; Folschweiller, N. Persistence of HBsAg-specific antibodies and immune memory two to three decades after hepatitis B vaccination in adults. J. Viral Hepat. 2019, 26, 1066–1075.
  43. Cocchio, S.; Baldo, V.; Volpin, A.; Fonzo, M.; Floreani, A.; Furlan, P.; Mason, P.; Trevisan, A.; Scapellato, M.L. Persistence of Anti-Hbs after up to 30 Years in Health Care Workers Vaccinated against Hepatitis B Virus. Vaccines 2021, 9, 323.
  44. Zhao, Y.L.; Han, B.H.; Zhang, X.J.; Pan, L.L.; Zhou, H.S.; Gao, Z.; Hao, Z.Y.; Wu, Z.W.; Ma, T.L.; Wang, F.; et al. Immune persistence 17 to 20 years after primary vaccination with recombination hepatitis B vaccine (CHO) and the effect of booster dose vaccination. BMC Infect. Dis. 2019, 19, 482.
  45. Wu, Z.; Yao, J.; Bao, H.; Chen, Y.; Lu, S.; Li, J.; Yang, L.; Jiang, Z.; Ren, J.; Xu, K.J.; et al. The effects of booster vaccination of hepatitis B vaccine on children 5-15 years after primary immunization: A 5-year follow-up study. Hum. Vaccines Immunother. 2018, 14, 1251–1256.
  46. Bini, C.; Grazzini, M.; Chellini, M.; Mucci, N.; Arcangeli, G.; Tiscione, E.; Bonanni, P. Is hepatitis B vaccination performed at infant and adolescent age able to provide long-term immunological memory? An observational study on healthcare students and workers in Florence, Italy. Hum. Vaccines Immunother. 2018, 14, 450–455.
  47. Bianchi, F.P.; Gallone, M.S.; Gallone, M.F.; Larocca, A.M.V.; Vimercati, L.; Quarto, M.; Tafuri, S. HBV seroprevalence after 25 years of universal mass vaccination and management of non-responders to the anti-Hepatitis B vaccine: An Italian study among medical students. J. Viral Hepat. 2019, 26, 136–144.
  48. Schwarz, T.F.; Behre, U.; Adelt, T.; Donner, M.; Suryakiran, P.V.; Janssens, W.; Mesaros, N.; Panzer, F. Long-term antibody persistence against hepatitis B in adolescents 14–15-years of age vaccinated with 4 doses of hexavalent DTPa-HBV-IPV/Hib vaccine in infancy. Hum. Vaccines Immunother. 2019, 15, 235–241.
  49. Papadopoli, R.; De Sarro, C.; Torti, C.; Pileggi, C.; Pavia, M. Is There Any Opportunity to Provide an HBV Vaccine Booster Dose Before Anti-Hbs Titer Vanishes? Vaccines 2020, 8, 227.
  50. European Consensus Group on Hepatitis B Immunity. Are booster immunisations needed for lifelong hepatitis B immunity? Lancet 2000, 355, 561–565.
  51. Leuridan, E.; Van Damme, P. Hepatitis B and the need for a booster dose. Clin. Infect. Dis. 2011, 53, 68–75.
  52. Jin, H.; Tan, Z.; Zhang, X.; Wang, B.; Zhao, Y.; Liu, P. Comparison of Accelerated and Standard Hepatitis B Vaccination Schedules in High-Risk Healthy Adults: A Meta-Analysis of Randomized Controlled Trials. PLoS ONE 2015, 10, e0133464.
  53. Van Herck, K.; Leuridan, E.; Van Damme, P. Schedules for hepatitis B vaccination of risk groups: Balancing immunogenicity and compliance. Sex. Transm. Infect. 2007, 83, 426–432.
  54. Giacomet, V.; Masetti, M.; Nannini, P.; Forlanini, F.; Clerici, M.; Zuccotti, G.V.; Trabattoni, D. Humoral and cell-mediated immune responses after a booster dose of HBV vaccine in HIV-infected children, adolescents and young adults. PLoS ONE 2018, 13, e0192638.
  55. Lao-Araya, M.; Puthanakit, T.; Aurpibul, L.; Taecharoenkul, S.; Sirisanthana, T.; Sirisanthana, V. Prevalence of protective level of hepatitis B antibody 3 years after revaccination in HIV-infected children on antiretroviral therapy. Vaccine 2011, 29, 3977–3981.
  56. Abzug, M.J.; Warshaw, M.; Rosenblatt, H.M.; Levin, M.J.; Nachman, S.A.; Pelton, S.I.; Borkowsky, W.; Fenton, T.; International Maternal Pediatric Adolescent AIDS Clinical Trials Group P1024 and P1061s Protocol Teams. Immunogenicity and immunologic memory after hepatitis B virus booster vaccination in HIV-infected children receiving highly active antiretroviral therapy. J. Infect. Dis. 2009, 200, 935–946.
  57. Sit, D.; Esen, B.; Atay, A.E.; Kayabasi, H. Is hemodialysis a reason for unresponsiveness to hepatitis B vaccine? Hepatitis B virus and dialysis therapy. World J. Hepatol. 2015, 7, 761–768.
  58. Gilbert, C.L.; Stek, J.E.; Villa, G.; Klopfer, S.O.; Martin, J.C.; Schodel, F.P.; Bhuyan, P.K. Safety and immunogenicity of a recombinant hepatitis B vaccine manufactured by a modified process in renal pre-dialysis and dialysis patients. Vaccine 2014, 32, 6521–6526.
  59. Chaves, S.S.; Daniels, D.; Cooper, B.W.; Malo-Schlegel, S.; Macarthur, S.; Robbins, K.C.; Kobetitsch, J.F.; McDaniel, A.; D’Avella, J.F.; Alter, M.J. Immunogenicity of hepatitis B vaccine among hemodialysis patients: Effect of revaccination of non-responders and duration of protection. Vaccine 2011, 29, 9618–9623.
  60. Fourati, S.; Cristescu, R.; Loboda, A.; Talla, A.; Filali, A.; Railkar, R.; Schaeffer, A.K.; Favre, D.; Gagnon, D.; Peretz, Y.; et al. Pre-vaccination inflammation and B-cell signalling predict age-related hyporesponse to hepatitis B vaccination. Nat. Commun. 2016, 7, 10369.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Infectious Diseases
Contributor MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : Yonas Bekele
View Times: 761
Revisions: 2 times (View History)
Update Date: 31 Dec 2021
Table of Contents
    1000/1000
    Hot Most Recent
    Notice
    You are not a member of the advisory board for this topic. If you want to update advisory board member profile, please contact office@encyclopedia.pub.
    OK
    Confirm
    Only members of the Encyclopedia advisory board for this topic are allowed to note entries. Would you like to become an advisory board member of the Encyclopedia?
    Yes
    No
    Academic Video Service
    Feedback