Abstract
Background
Availability of the hepatitis B virus (HBV) vaccine in the United States since 1982 and recommendations for universal/catch-up vaccination of infants and children since the 1990s may be associated with lower HBV prevalence among people with human immunodeficiency virus (HIV; PWH) born after 1980.
Methods
Active HBV infection prevalence, defined as the proportion of patients with a positive hepatitis B surface antigen result, was assessed among PWH at entry into a clinical cohort. Patients were categorized into birth-year cohorts of 1940–1959, 1960–1979, or 1980–1999 and then further dichotomized into pre- and post-1980 birth-year cohorts. Log binomial regression was used to assess the association of birth-year cohort with hepatitis B surface antigen positivity, adjusting for race/ethnicity, HIV infection risk factor, baseline HIV viral load and CD4+ cell count, HBV active therapy, and year of/age at cohort entry.
Results
Among 5598 PWH, most were male (67%) and Black (77%), with a mean age (SD) of 39.7 (9.6) years at cohort entry. Approximately a third of the participants (30%) identified as men who have sex with men, and 39% reported a history of injection drug use. At cohort entry, the majority had a CD4+ cell count <350/µL and a viral load >1000 copies/mL. The HBV prevalence was 6.7% overall but varied by birth-year cohort: 6.2% for 1940–1959, 7.9% for 1960–1979, and 2.6% for 1980–1999. The risk of HBV infection was lower in the post-1980 than in the pre-1980 cohort (adjusted prevalence ratio, 0.19 [95% confidence interval, .09– .42]).
Conclusions
PWH born after 1980 had a lower prevalence of HBV coinfection than those born before 1980, supporting the potential impact of universal childhood HBV vaccination.
Keywords: Hepatitis B, people with HIV, vaccination
Chronic hepatitis B virus (HBV) infections remain a significant source of worldwide disease and death with an estimated 254 million people infected worldwide and 1.1 million HBV-related deaths in 2022 [1]. Progression to liver cirrhosis and hepatocellular carcinoma are major drivers of HBV-associated disease and death [2]. Despite the availability of an effective HBV vaccine in the United States since 1982, there were 14 229 new cases of chronic HBV reported in the United States in 2021, adding to the 1.25–2.49 million Americans living with chronic HBV as of 2019 [3]. In endemic countries, perinatal transmission remains the most common mode of transmission [2]. In low-prevalence countries, such as the United States, most cases are attributable to injection drug use (IDU) or high-risk sexual behavior, including heterosexual contact with multiple sexual partners and sex between men who have sex with men (MSM) [2].
Due to shared modes of transmission, people with human immunodeficiency virus (HIV; PWH) have higher rates of HBV coinfection, with an estimated 5%–11% of PWH coinfected with HBV compared with the 0.3% of the general US population with HBV infection [2, 4–7]. Once acutely infected with HBV, PWH not on HIV antiretroviral therapy are less likely to clear acute infections, resulting in higher rates of progression to chronic infections [8].
An effective HBV vaccine has been available in the United States since 1982, when the Advisory Committee on Immunization Practices (ACIP) made its first recommendation for the vaccination of individuals at high risk of HBV infection, including those with shared risk factors for HIV (history of IDU or MSM) [9]. The ACIP serially expanded its recommendations to include universal vaccination of infants (1991) and routine vaccination of unvaccinated children aged 11–12 years (1995) and ≥19 years (1999) [10]. These vaccination policies have been linked to reduced HBV incidence rates in the general US population since the 1990s [3, 10]. In the United States, MSM and people who inject drugs remain at high risk of HBV infection. Among PWH, an initial decline in the incidence of HBV infections between 1997 to 2000 was followed by an increase in incidence from 2000 to 2008 [11].These data were from PWH with a median age of 27.2 years [11]. Less is known about the differential impact of HBV vaccination policies on HBV prevalence in PWH based on birth year.
To study the impact of US HBV vaccination policy and availability on HIV-HBV coinfection rates, we assessed hepatitis B surface antigen (HBsAg) seroprevalence rates among PWH in birth-year cohorts (1940–1959, 1960–1979, and 1980–1999) differentially affected by the risk-based recommendation of 1982 and the pediatric HBV vaccination recommendations of the 1990s.
METHODS
Study Sample and Setting
This study analyzes data from the Johns Hopkins HIV Clinical Cohort (JHHCC), an observational cohort of PWH enrolled in care at the Johns Hopkins Bartlett Specialty Practice in East Baltimore, Maryland. This is an infectious disease clinic providing comprehensive clinical care (including mental health and low threshold substance use disorder care) to patients with HIV, hepatitis C virus, HBV, and other infectious diseases. A detailed description of the study cohort has been published elsewhere [12]. Briefly, PWH accessing care at the clinic are approached by research staff and invited to enroll in the JHHCC study, with cohort enrollment occurring with first enrollment into HIV care. For those who agree to study participation, written informed consent is obtained for enrollment and sharing of their medical data. These surveys are self-administered on electronic tablets. Clinical and laboratory data are abstracted from patients’ medical records. For this study, we included PWH enrolled in the JHHCC between 1989 and 2023 who were ≥18 years old at cohort entry, had documented HBsAg serologic testing within 12 months of cohort entry, and were born between 1 January 1940 and 31 December 1999. Only data at cohort entry were included in analyses to reduce the impact of HIV care engagement (eg, HBV vaccination as a component of HIV care) on HBV outcomes.
Measures
Our primary exposure was birth-year cohort. Birth-year cohort analyses are accepted as an approach to assess the causal impact of early life exposures on outcomes later in life [13]. As such, birth-year cohort was selected as an approach to assess associations between potential early exposures of birth dose or childhood HBV vaccination and the subsequent outcome of HBV infection.
Participants were categorized into birth-year cohorts of 1940–1959, 1960–1979, or 1980–1999, which were further dichotomized into pre- and post-1980 cohorts. The 1980–1999 cohort represented individuals who would have been universally eligible for HBV vaccination before 2022, per ACIP vaccination recommendations [14]. Participants born between 1980 and 1999 were not further stratified due to insufficient cohort size. PWH born before 1940 were excluded due to their small number and to align with the average life expectancy in the United States (77.5 years), ensuring that we have a sufficiently large and relevant sample to power our analysis [15].
Our primary outcome was documented HBV infection, defined as a positive HBsAg result, within 12 months of clinical cohort entry. For patients with multiple HBsAg serologic tests performed during this period, results from the test closest to their cohort entry date were used.
Sociodemographic variables included in our analyses were age at cohort entry, gender (cisgender male, cisgender female, transgender male or female, or other), and race/ethnicity (Black and non-Black). HIV acquisition risk factors were self-reported at cohort entry, including a history of IDU and identification as MSM. CD4+ cell counts and HIV viral load (VL) measurements were conducted as part of routine clinical care. In this analysis, we included the earliest CD4+ cell count and HIV VL for each person, obtained within 6 months of cohort enrollment. We categorized CD4+ cell counts as <350/µL, 350–499/µL, or >500/µL and VLs as <1000 or ≥1000 copies/mL. A VL threshold of <1000 copies/mL was selected to reflect the limit of detection of VL assays at the earliest points of VL measurement. We categorized participants on either tenofovir, lamivudine or emtricitabine within the first year of cohort entry as being on HBV active therapy. Consistent with HBV testing guidelines for PWH, patients were routinely screened for HBV with HBsAg and antibody to HBsAg (anti-HBs), but data on antibody to hepatitis B core antigen (anti-HBc) were sparse [16].
Statistical Analysis
We conducted a cross-sectional analysis of participant data at the point of entry into the HIV clinical cohort. We used descriptive statistics to assess the sociodemographic and clinical characteristics of PWH included in our study at presumed entry into HIV care. We then recorded the proportions of PWH with HBV infection and with HBV immunity by 20-year birth-year cohorts. Association between birth-year cohort (pre-1980 vs post-1980) and HBsAg positivity was assessed using log binomial regression. Our adjusted model included race/ethnicity, HIV infection risk factors (MSM status and IDU history), HBV-active therapy (tenofovir, lamivudine, or emtricitabine), CD4+ cell count, and VL at cohort entry, and year of and age at cohort entry as covariates. We calculated the prevalence difference between the pre-1980 and post-1980 cohorts in HBsAg positivity, adjusting for covariates in the model by estimating marginal effects, with standard errors computed using the Delta method.
To assess for the presence of effect measure modification by HIV acquisition risk factors (MSM status and IDU history) on the multiplicative scale, we created an interaction term between birth-year cohort and these variables in a subanalysis. We then used a likelihood ratio test to assess whether the addition of HIV acquisition risk factors and the interaction term were required to explain the hypothesized association between birth-year cohorts (before and after 1980) and the prevalence of HBV infection in the extended model. We further examined effect measure modification by MSM status and IDU history in stratified analyses. We compared prevalence ratios and 95% confidence intervals (CIs) for the association between birth-year cohorts (before and after 1980) and the prevalence of HBV infection among participants who did or did not identify as MSM and those who did or did not have a history of IDU. Stata/BE software (version 17.0; StataCorp) was used for all analyses.
RESULTS
Between 1989 and 2023, a total of 8079 PWH were enrolled in the JHHCC. Of these, 5714 (71%) had documented HBsAg tests performed within 1 year of cohort entry and were included in the current study. Patients born before 1940 or after 1999 (n = 106) and those with perinatal transmission (n = 10) were excluded. A total of 5598 patients were included in our study.
Study participants’ baseline demographic and clinical characteristics are presented in Table 1. Most participants were male (67%) and Black (77%), with a mean (SD) age of 39.7 (9.6) years at cohort entry. Approximately a third of the participants (30%) identified as MSM, and 39% reported a history of IDU. The majority (59%) of study participants had a CD4+ cell count of <350/µL at cohort entry. The VL at cohort entry was <1000 copies/mL in 23% of participants, >1000 copies/mL in 49%, and missing in 28%.
Table 1.
Baseline Characteristics of Patients by Birth-Year Cohort
| Sociodemographic and Clinical Characteristics | Patients by Birth-Year Cohort, No. (Column %)a | |||
|---|---|---|---|---|
| Total (N = 5598) |
1940–1959 (n = 2347) |
1960–1979 (n = 2789) |
1980–1999 (n = 462) |
|
| Age at baseline, mean (SD), y | 39.7 (9.6) | 46.0 (7.9) | 36.4 (7.5) | 27.4 (4.9) |
| Gender identity | ||||
| Female | 1811 (32) | 624 (27) | 1084 (39) | 103 (22) |
| Male | 3754 (67) | 1712 (73) | 1694 (61) | 348 (75) |
| Transgender | 31 (1) | 10 (0) | 11 (0) | 10 (2) |
| Other | 2 (0) | 1 (0) | 0 (0) | 1 (0) |
| Race | ||||
| Non-Blackb | 1267 (23) | 455 (19) | 709 (25) | 103 (22) |
| Black | 4331 (77) | 1892 (81) | 2080 (75) | 359 (78) |
| MSM | 1656 (30) | 518 (22) | 831 (30) | 307 (66) |
| IDU | 2186 (39) | 1263 (54) | 890 (32) | 33 (7) |
| CD4+ cell count at entryc | ||||
| <350/µL | 3321 (59) | 1488 (63) | 1645 (59) | 188 (41) |
| 350–499/µL | 957 (17) | 372 (16) | 496 (18) | 89 (19) |
| ≥500/µL | 530 (9) | 191 (8) | 268 (10) | 71 (15) |
| HIV VL at cohort entryd | ||||
| <1000 copies/mL | 1305 (23) | 458 (20) | 673 (24) | 174 (38) |
| ≥1000 copies/mL | 2722 (49) | 954 (41) | 1499 (54) | 269 (58) |
| Any HBV-active regimene | 1176 (21) | 568 (24) | 600 (22) | 8 (2) |
| Tenofovir | 240 (4) | 94 (4) | 144 (5) | 2 (<1) |
| Lamivudine | 1057 (19) | 526 (22) | 523 (19) | 8 (2) |
| Emtricitabine | 44 (1) | 13 (1) | 30 (1) | 1 (<1) |
Abbreviations: HBV, hepatitis B virus; HIV, human immunodeficiency virus; IDU, injection drug use; MSM, men who have sex with men; VL, viral load.
aData represent no. of patients (column %) unless otherwise specified.
bThe non-Black category included White (1091 of 5598 patients [19%]), Hispanic (120 of 5598 [2%]), and other (56 of 5598 [1%]).
cCD4+ cell counts at cohort entry were missing for 791 of 5598 patients (14%).
dHIV RNA VLs at cohort entry were missing for 1571 of 5598 patients (28%).
eThe HBV-active regimens were not mutually exclusive.
The proportion of participants born in each of the birth-year cohorts was 42% (n = 2347) for 1940 −1959, 50% (n = 2789) for 1960–1979, and 8% (n = 462) for 1980–1999. There were more female participants in the 1960–1979 cohort (39%) than in the 1940–1959 (27%) and 1980–1999 (22%) cohorts. The 1980–1999 cohort had a higher proportion of MSM (66%) than the 1940–1959 (22%) and 1960–1979 (30%) cohorts. The proportion of participants with a history of IDU decreased with each subsequent birth-year cohort: 54% for 1940–1959, 32% for 1960–1979, and 7% for 1980–1999.
HBV Prevalence and Immunity by Birth-Year Cohort
The overall prevalence of HBV coinfection was 6.7% (95% CI, 6.0%–7.4%). By birth-year cohort, the prevalence of HBV was 6.2% (95% CI, 5.3%–7.2%) for 1940–1959, 7.9% (6.8%–9.0%) for 1960–1979, and 2.6% (1.4%–4.7%) for 1980–1999 (Table 2).
Table 2.
Hepatitis B Surface Antigen Seroprevalence by Birth-Year Cohort and HIV Acquisition Risk
| Birth-Year Cohort | HBsAg Seroprevalence, No./Total in Cohort or Subgroup (%) | |||||
|---|---|---|---|---|---|---|
| Total (N = 5598) |
MSM (n = 1656) |
Non-MSMa | IDU (n = 2186) |
Non-IDU (n = 3412) |
||
| Female (n = 1811) |
Male (n = 2128) |
|||||
| 1940–1959 | 146/2347 (6.2) | 55/518 (10.6) | 15/624 (2.4) | 76/1204 (6.3) | 69/1263 (5.5) | 77/1084 (7.1) |
| 1960–1979 | 219/2789 (7.9) | 95/831 (11.4) | 41/1084 (3.8) | 82/872 (9.4) | 79/890 (8.9) | 140/1899 (7.4) |
| 1980–1999 | 12/462 (2.6) | 9/307 (2.9) | 3/103 (2.9) | 0/52 (0) | 1/33 (3.0) | 11/429 (2.6) |
| Total | 377/5598 (6.7) | 159/1656 (9.6) | 59/1811 (3.3) | 158/2128 (7.4) | 149/2186 (6.8) | 228/3412 (6.7) |
Abbreviations: HBsAg, hepatitis B surface antigen; IDU, injection drug use; MSM, men who have sex with men.
aOf the 3 patients who were not MSM and reported their gender identity as transgender or other, 1 had a positive HBsAg serologic result.
When further dichotomized to pre- and post-1980 birth-year cohorts, the risk of HBV coinfection was significantly lower in the post-1980 relative to the pre-1980 cohort, with an unadjusted prevalence ratio (PR) of 0.37 (95% CI, .21–.65). When adjusted for age, race/ethnicity, MSM status, history of IDU, CD4+ cell count at cohort entry, HBV-active regimen, and VL at cohort entry, the adjusted PR was 0.19 (95% CI, .09–.42) and the adjusted prevalence difference was −0.06 (−.07 to −.04) (Table 3), consistent with approximately 6 fewer infections per 100 individuals in the post-1980 compared with the pre-1980 cohort.
Table 3.
Prevalence Ratios and Prevalence Differences for Hepatitis B Virus Coinfection by Birth-Year Cohort
| Birth-Year Cohort | Crude | Adjusteda | ||
|---|---|---|---|---|
| PR (95% CI) | PD (95% CI) | PR (95% CI) | PD (95% CI) | |
| 1940–1979 | … | Reference | … | Reference |
| 1980–1999 | 0.37 (.21–.65) | −0.05 (−.06 to −.03) | 0.19 (.09–.42) | −0.06 (−.07 to −.04) |
Abbreviations: CI, confidence interval; PD, prevalence difference; PR, prevalence ratio.
aPRs and PDs adjusted for age, race, ethnicity, status as men who have sex with men, history of injection drug use, enrollment year, hepatitis B virus–active regimen, CD4+ cell count, and viral load at cohort entry.
HBV Prevalence by HIV Acquisition Risk Factors and Birth-Year Cohorts
Among participants identifying as MSM, the prevalence of HBV coinfection was 9.6%, compared with 5.5% in non-MSM participants (Table 2). The HBV prevalence by birth-year cohort was 10.6% for 1940–1959, 11.4% for 1960–1979, and 2.9% for 1980–1999 among MSM and 5.0%, 6.3%, and 1.8%, respectively, among non-MSM (Figure 1). The post-1980 cohort had a significantly lower risk of HBV coinfection than the pre-1980 cohort among participants identifying as MSM (PR, 0.17 [95% CI .07–.43]), while the risk of HBV coinfection among participants who identified as non-MSM was not statistically significant (0.34 [.10–1.13]).
Figure 1.
Timeline of key hepatitis B virus vaccination recommendations by the Advisory Committee of Immunization Practices and the corresponding ages of patients in the pre- and post-1980 birth-year cohorts. Abbreviation: HBsAg+, hepatitis B surface antigen positive.
The prevalence of HBV coinfection was 6.8% in participants with and 6.7% in those without a history of IDU. The prevalence of HBV coinfection by birth-year cohort was 5.5% for 1940–1959, 8.9% for 1960–1979, and 3.0% for 1980–1999 birth cohorts among participants with a history of IDU and 7.1%, 7.4%, and 2.6% among those without a history of IDU. The post-1980 cohort was less likely to have HBV coinfections than the pre-1980 cohort among participants without a history of IDU (PR, 0.19 [95% CI, .09–.44]) (Figure 1). Among those with a history of IDU, the likelihood of HBV coinfection in the post-1980 cohorts compared with the pre-1980 cohort was not statistically significant (PR, 0.41 [95% CI, .06–2.95]).
Overall, stratum-specific estimates demonstrated a consistent significantly lower HBV prevalence among post-1980 compared with pre-1980 birth-year cohorts across MSM and non-IDU populations, while stratum-specific estimates were nonsignificant among non-MSM and IDU populations. There was no evidence of effect measure modification by MSM or IDU status (Supplementary Tables 1 and 2).
DISCUSSION
In our cohort of PWH, the overall prevalence of HBV infection was 6.7%, consistent with the 5%–11% HIV-HBV coinfection rates cited in the current literature [2, 4–6, 17, 18]. Among PWH born after 1980, we found an HBV prevalence of 2.6%, significantly lower than the 7.1% in those born before 1980 and the 5%–11% in the general population of PWH [2]. The 81% lower prevalence in the post-1980 compared with the pre-1980 birth-year cohort in adjusted analyses suggest that HBV prevalence among PWH is significantly lower among a population of PWH that were more likely to have received childhood HBV vaccination.
Despite the ACIP's 1982 recommendation for HBV vaccination of high-risk individuals, including those with shared risk factors for HIV, vaccine uptake was poor and concerns of possible HIV transmission through the HBV vaccine raised in 1982–1983 hindered vaccine acceptance in the United States [19]. In the 2004 National Health Interview Survey, only 45% of adults at high risk for HBV were reported to have received ≥1 dose of the HBV vaccine [20]. Among 18 000 PWH receiving HIV care between 2009 and 2012 in the United States, >30% were not vaccinated for HBV and/or had no documented immunity/infection status [2]. Fewer than 10% of eligible participants received the HBV vaccine during the study period [2].
Conversely, there has been immense progress in vaccinating children since the recommendation for universal HBV vaccination of all infants in 1991 and the catch-up vaccination of previously unvaccinated children aged 11–12 and 0–19 years in 1995 and 1999, respectively [10]. With mandated HBV vaccination prior to middle school entry and the inclusion of HBV vaccine in the routine childhood vaccination schedule, the national HBV vaccination rates in children aged 19–35 months and 13–15 years increased from 16% to 90% and from near 0% to 67%, respectively, between 1993 and 2000 [10, 21]. Participants in our pre-1980 cohort were missed by all 3 recommendations for universal vaccination implemented in 1991, 1995, and 1999 (Figure 2) and subject only to the 1982 recommendation for risk-based vaccination.
Figure 2.
Hepatitis B surface antigen (HBsAg) seroprevalence by birth-year cohort and key human immunodeficiency virus/hepatitis B virus acquisition risk factors. Abbreviations: IDU, injection drug use; MSM, men who have sex with men.
Between 2013 and 2018, the National Health and Nutrition Examination Survey (NHANES) reported an undetectable prevalence of chronic HBV infection among the general public in those born between 1999 and 2012 and <0.5% prevalence in those born between 1969 and 1998 [22]. Although our study's post-1980 birth-year cohort had the lowest HBV prevalence among the 3 cohorts, at 2.6% it is still substantially higher than that of the general US population born after 1980. This discrepancy highlights the potential issue of differential childhood vaccine uptake among those at higher risk of future HIV acquisition. Individuals disproportionately affected by social determinants of health such as poor healthcare access and limited educational opportunities both contributing to poor health literacy, are less likely to have received complete HBV vaccination during childhood and are at a higher risk of future HIV infection. Furthermore, PWH exposed to HBV after acquiring HIV have a weakened immune response, and their anti-HBs titers may have waned depending on the length of time since their childhood HBV vaccination. A weakened immune response decreases the ability to clear an acute HBV infection, leading to higher rates of progression to chronic infection [23].While our study demonstrated an almost 2-fold increase in HBV prevalence among PWH who identify as MSM (vs non-MSM), we did not find any effect modification in the association between birth-year cohorts (pre- and post-1980 cohorts) and the prevalence of HBV coinfection by MSM status.
Research on HBV coinfection prevalence in PWH by birth year is sparse, and there have been no US-based studies in the context of the timeline of the HBV vaccination schedule and vaccine rollout. However, studies from different countries report similar temporal associations between HIV-HBV coinfection rates and HBV vaccination recommendations and/or availability. A South Korean study found decreasing rates of HBV coinfection among PWH born before 1985 (5.8%), between 1985 and 1995 (2.0%), and after 1995 (0%) [17]. The HBV vaccine was first made available in South Korea in 1985, and universal vaccination of infants was first recommended in 1991 prior to becoming mandated in 1995 [17, 24].
In contrast, a study from North Central Nigeria from 2015 found minimal differences in HBV coinfection rates in PWH born between 1976 and 1985 (5.6%) and those born in 1986 and later (5.3%) [25]. Although HBV vaccine had been a part of the pediatric immunization schedule, it only became widely available in Nigeria in 2004, by which time most individuals in both birth-year cohorts were ineligible for vaccination due to the national policy of limiting HBV vaccination to infants [26, 27]. As of 2023, only 17% of newborns in Africa received the birth dose of the HBV vaccine, which has significant implications for the global HIV-HBV coinfection burden, given the high HIV prevalence in Africa [27]. Guideline recommendations for vaccinations need to be supported by vaccine availability, accessibility, and delivery to effectively prevent HBV infection at the individual and population level.
Our study has several limitations, including the use of a convenience sample of PWH with HBsAg results available within 1 year of entry into a clinical cohort as a proxy for entry into HIV care. As such, data on actual hepatitis B vaccination status are not available. Data on HBsAg status were not available for the entire cohort, and there were statistically significant differences in age at baseline study visit, race/ethnicity, CD4+ cell count and VL at cohort entry, and the percentage of patients identifying as heterosexual or MSM between patients with and those without documented HBsAg status (Supplementary Table 3). In addition, resolved HBV infections were not considered, as anti-HBc data were not readily available in the cohort due to clinic-based practice patterns deprioritizing anti-HBc. As such, the scope of our study is limited to current HBV coinfections in PWH. Moreover, we did not account for the immigration status of participants in our study, as those born in the United States or who migrated before age 18 years may have had different access to HBV vaccination and risk of HBV exposure compared with those who migrated to the United States as adults. Participants’ country of birth/immigration status was not available for analysis because it is not captured as a standardized structured variable within the cohort database and is inconsistently documented in clinical notes, limiting our ability to assess this potentially important factor. Finally, the substantially lower number of PWH in the 1980–1999 birth-year cohort relative to other cohorts is a limitation of the data available for this analysis.
In conclusion, prior to 2021, people born before 1980 relied on a risk-based vaccination strategy for HBV vaccination, which has not been vigorously implemented or effective [20, 28, 29]. Conversely, high uptake of the universal HBV vaccination recommendation for children has had a significant impact on lowering HBV incidence rates in the United States [10] and likely contributed to the lower prevalence of HBV seen in PWH born between 1980 and1999 compared with older cohorts in our study, a finding that was consistent across HIV risk acquisition groups most commonly linked to HBV acquisition (MSM and IDU). These findings highlight the importance of HBV vaccination in preventing HBV infection before individuals engage in high-risk activities. Increasing public awareness of the importance of HBV vaccination and clinicians’ enthusiasm for its importance is essential in ensuring that all individuals have the benefit of HBV prevention.
Supplementary Material
Notes
Author contributions. Conceptualization: S. J. L., T. V., and O. F. N. Methodology: S. J. L., T. V., C. R. L., and O. F. N. Data collection: J. K., L. N. S., and R. D. M. Data curation and analysis: T. V. Writing of original draft: S. J. L. and T. V. Interpretation of data and review, editing and final approval of the manuscript: All authors.
Disclaimer. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Data availability statement. The data underlying this article will be shared on reasonable request to the corresponding author.
Financial support. The work was supported by the National Institutes of Health (grants K01AA028193, U01DA036935, K08MH118094, R01MD018539, and P30A1094189).
Contributor Information
So Jeong Lee, Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
Tarfa Verinumbe, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Catherine R Lesko, Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA.
Anthony Fojo, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Joyce Jones, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Jeanne Keruly, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
LaQuita N Snow, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Richard D Moore, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Mark Sulkowski, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Oluwaseun Falade-Nwulia, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Supplementary Data
Supplementary materials are available at Open Forum Infectious Diseases online. Consisting of data provided by the authors to benefit the reader, the posted materials are not copyedited and are the sole responsibility of the authors, so questions or comments should be addressed to the corresponding author.
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