# Zoster Vaccine Recombinant, Adjuvanted AS01B adjuvant innate immune activation

## AS01B induces sustained innate immune activation lasting up to 5 years through TLR4-mediated pathways and generates trained immunity in monocytes and NK cells, but direct measurement of innate responses is severely limited with only one of ten studies directly assessing these mechanisms.

## Abstract

Direct measurement of AS01B adjuvant-induced innate immune activation is remarkably limited despite the vaccine’s well-established clinical efficacy. Of 10 studies reviewed, only one directly assessed innate immune responses, finding sustained activation of monocytes, dendritic cells, and NK cells persisting up to 5 years post-vaccination, along with development of trained immunity characterized by enhanced responses to both homologous and heterologous antigens and epigenetic modifications including decreased TGFβ pathway accessibility. Mechanistically, AS01B stimulates local innate activation through TLR4 signaling (MPL) and cytokine induction (QS-21), synergistically recruiting and activating antigen-presenting cells. However, the remaining nine studies focused exclusively on adaptive immunity endpoints—antibodies and T cells—despite these being downstream consequences of adjuvant-mediated innate activation.

The robust adaptive immune responses (97.8% humoral response rate, 93.3% CD4+ T-cell response rate) and vaccine efficacy (≥90% in immunocompetent adults, 42.5-82.5% in severely immunocompromised HSCT recipients) provide indirect evidence of effective innate immune priming, as does the reactogenicity profile with 74.2% reporting injection site pain. The observation that NHBCL patients achieved high efficacy despite low antibody responses suggests cell-mediated immunity—and the innate priming generating it—drives protection. A critical gap exists between AS01B’s well-characterized clinical outcomes and the sparse direct characterization of the innate immune mechanisms underlying its effectiveness.

## Methods

We analyzed 10 sources from an initial pool of 200, using 7 screening criteria. Each paper was reviewed for 9 key aspects that mattered most to the research question.

### Records from Elicit search

- n = 200
- Papers screened using: Vaccine Type, Innate Immune Parameters, Study Population, Comparison Groups, Quantitative Measures, Study Design, Publication Type
- n = 200 Papers screened out
- n = 190 
- Papers included for extraction
- n = 10

## Data extraction

We asked a large language model to extract each data column below from each paper. We gave the model the extraction instructions shown below for each column.

### Study Population:

Extract characteristics of the study population relevant to immune responses to AS01B adjuvant, including:
- Age range and mean age
- Immune status (immunocompetent, immunocompromised, specific conditions)
- Underlying diseases or conditions affecting immune function
- Concurrent medications or treatments that could affect immune responses
- Sample size for immune response analyses
- Any population subgroups analyzed separately

### Vaccine Formulation:

Extract details about the recombinant zoster vaccine with AS01B adjuvant, including:
- Vaccine name/designation (RZV, HZ/su, etc.)
- Glycoprotein E antigen dose and source
- AS01B adjuvant dose and components
- Total vaccination schedule (number of doses, timing between doses)
- Route of administration
- Any comparator vaccines or adjuvants studied

### Innate Immunity Measurements:

Extract all measurements related to innate immune activation by AS01B adjuvant, including:
- Cytokine/chemokine levels (IL-1β, IL-6, TNF-α, type I interferons, etc.)
- Innate immune cell activation markers or frequencies
- Toll-like receptor signaling markers
- Complement activation measures
- Inflammatory markers (CRP, ESR, etc.)
- Local inflammatory responses at injection site
- Time points measured relative to vaccination
- Methods used for measurement

### Adaptive Immunity:

Extract adaptive immune response data that may reflect AS01B adjuvant effects, including:
- Anti-gE antibody responses (GMCs, seroresponse rates, fold-increases)
- T-cell responses (CD4+, CD8+, activation markers, memory subsets)
- B-cell responses and antibody functionality
- Duration of immune responses
- Time points assessed
- Comparison between adjuvanted vs non-adjuvanted formulations if available

### Safety Profile:

Extract safety data relevant to AS01B adjuvant effects, including:
- Local reactions (pain, redness, swelling) - frequency, severity, duration
- Systemic reactions (fever, fatigue, myalgia) - frequency, severity, duration
- Serious adverse events potentially related to adjuvant
- Immune-mediated diseases or autoimmune reactions
- Laboratory abnormalities
- Any dose-limiting toxicities
- Comparison of safety between different populations

### Study Methodology:

Extract methodological details relevant to measuring AS01B adjuvant immune activation, including:
- Study design (RCT, observational, etc.)
- Blinding and randomization
- Sampling time points for immune measurements
- Laboratory methods and assays used
- Definition of immune response endpoints
- Statistical methods for immune response analysis
- Control groups or comparators
- Sample collection and processing procedures

### Adjuvant Mechanisms:

Extract any data on mechanisms by which AS01B adjuvant activates immune responses, including:
- Proposed or demonstrated pathways of immune activation
- Cellular targets of the adjuvant
- Receptor interactions (TLR4, other pattern recognition receptors)
- Intracellular signaling pathways activated
- Antigen presentation enhancement
- Any mechanistic studies or analyses
- Discussion of how AS01B differs from other adjuvants

### Moderating Factors:

Extract factors that influence AS01B adjuvant effectiveness or immune activation, including:
- Age effects on adjuvant response
- Impact of immunosuppression on adjuvant function
- Sex/gender differences in adjuvant responses
- Prior vaccination history effects
- Genetic factors affecting adjuvant responses
- Timing relative to other treatments or interventions
- Seasonal or environmental factors
- Baseline immune status effects

### Clinical Outcomes:

Extract clinical outcomes that may relate to AS01B adjuvant immune activation, including:
- Vaccine efficacy against herpes zoster
- Duration of protection
- Breakthrough infections and their characteristics
- Post-herpetic neuralgia prevention
- Any correlates of protection identified
- Relationship between immune responses and clinical outcomes
- Efficacy in different patient populations

## Results

### Characteristics of Included Studies

| Study | Full text retrieved? | Study Design | Population | Sample Size (Immunogenicity) | Primary Focus |
|---|---|---|---|---|---|
| Weinberg et al., 2017 | No | Comparative study | Adults 50-70+ years, immunocompetent | Not specified | Comparison of ZV and gE/AS01B CMI responses |
| Cunningham et al., 2018 | Yes | Phase III RCT, observer-blind | Adults ≥50 years | 3,293 humoral, 466 CMI | Immunogenicity of HZ/su in ZOE-50/70 trials |
| Stadtmauer et al., 2021 | Yes | Phase III RCT, observer-blind | Autologous HSCT recipients ≥18 years | 114-1,721 participants | Immunogenicity and efficacy post-HSCT |
| Dagnew et al., 2018 | No | Phase III RCT, observer-blind | Adults ≥18 years with hematologic malignancies | 415 humoral, 132 CMI | End-of-study immunogenicity and efficacy |
| Johnson et al., 2024 | No | Observational | RZV recipients (age not specified) | 10-14 vaccinees | Trained immunity generation |
| Bastidas et al., 2019 | No | Phase IIIB open-label extension | Adults ≥60 years at initial vaccination | 70 participants | 10-year persistence and modeling |
| Pauksens et al., 2017 | No | Phase IIIB open extension | Adults ≥60 years (mean 72.3) | 70 participants | 9-year immune persistence |
| Hastie et al., 2020 | Yes | Phase IIIB open-label extension | Adults vaccinated at ≥60 years (mean 82.6 at additional dosing) | 70 enrolled, 68 in ATP cohort | 10-year persistence and anamnestic response |
| Boutry et al., 2020 | Yes | Extension study (ZOSTER-049) | Adults ≥50 years from ZOE-50/70 | 7,277 for efficacy analysis | Long-term efficacy and immunogenicity |
| Oostvogels, 2017 | No | Phase III RCT, observer-blind | Adults ≥18 years with hematologic malignancies | 415 humoral, 132 CMI | Immunogenicity and safety in HM patients |

All studies evaluated the recombinant zoster vaccine containing varicella-zoster virus glycoprotein E antigen with AS01B adjuvant system. The vaccine was administered as a two-dose schedule, with doses given 1-2 months apart in most studies or 2 months apart specifically. The Cunningham et al. study specified the vaccine formulation as 50 μg recombinant glycoprotein E with 50 μg MPL and 50 μg QS-21, administered intramuscularly.

### Direct Innate Immune Activation Measurements

Only one study directly measured innate immune responses to RZV. Johnson et al. (2024) assessed innate immune cell activation in 10-14 vaccinees, measuring B cell, monocyte, and dendritic cell (DC) responses by PDL1 expression, and NK cell responses by CD25 and CD137 co-expression. These innate responses demonstrated two-phase kinetics: a transient increase post-dose 1 and a persistent increase post-dose 2 lasting up to 1 year. In a verification cohort of 14 vaccinees, DC, NK, and monocyte responses to recombinant gE remained elevated above pre-vaccination levels for up to 5 years.

The study also demonstrated the development of trained immunity, with purified monocytes and NK cells from vaccinees showing increased responses to both homologous (rgE) and heterologous (CMV lysate) stimulation from pre- to post-vaccination. Monocyte ATAC-seq analysis revealed significant chromatin changes in 16 genes, including decreased chromatin accessibility of the TGFβ pathway post-vaccination, potentially representing a mechanism underlying trained immunity development.

### Mechanistic Basis of AS01B Adjuvant Activity

While most studies did not directly measure innate immune activation, Cunningham et al. (2018) described the mechanistic basis of AS01B function. The AS01B adjuvant system stimulates local and transient activation of the innate response, recruiting and activating antigen-presenting dendritic cells and macrophages. QS-21 induces transient local cytokine responses and activates these cells, while MPL acts as a TLR4 agonist that synergizes with QS-21 to enhance immune responses through IFN-γ production. This synergistic effect involves macrophage stimulation and early IFN-γ production, ultimately enhancing gE-antigen presentation by increasing the number of activated antigen-presenting cells.

### Adaptive Immune Responses as Markers of Adjuvant Function

#### Humoral Immune Responses

Across studies in immunocompetent adults, RZV induced robust anti-gE antibody responses. In the ZOE-50 and ZOE-70 trials, 97.8% of HZ/su recipients showed a humoral response compared to 2.0% of placebo recipients. Geometric mean concentrations (GMCs) increased 39.1-fold over baseline at 1 month post-dose 2 and remained 8.3-fold above baseline at 36 months.

Long-term persistence studies demonstrated sustained antibody responses. Pauksens et al. (2017) found anti-gE antibody GMCs plateaued from year 4 onwards, remaining above the pre-vaccination value of 1,213.1 mIU/mL through year 9. Bastidas et al. (2019) reported antibody concentrations plateaued around year 3, remaining 5.9-fold higher than pre-vaccination levels at year 10. Hastie et al. (2020) observed GMCs of 9,123 mIU/mL and 7,384 mIU/mL at months 108 and 120, respectively, compared to a peak of 43,100 mIU/mL at 1 month after initial dose 2. Boutry et al. (2020) found anti-gE antibody concentrations persisted approximately 6 times above pre-vaccination levels up to year 8.

In immunocompromised populations, antibody responses varied. In autologous HSCT recipients, anti-gE antibody GMCs were similar between 18-49 and ≥50-year-olds at 1 month post-dose 2. However, non-Hodgkin B-cell lymphoma (NHBCL) patients showed lower anti-gE antibody GMCs compared to other underlying diseases, likely due to immunotherapeutic agents targeting B cells.

#### Cell-Mediated Immune Responses

RZV induced strong CD4+ T-cell responses across studies. In the ZOE trials, 93.3% of HZ/su recipients showed a gE-specific CD4[2+] T-cell response (expressing ≥2 activation markers) compared to 0% of placebo recipients. Median CD4[2+] T-cell frequencies increased 24.6-fold at 1 month and 7.9-fold at 36 months over baseline, remaining ≥5.6-fold above baseline in all age groups at 36 months. The proportion of CD4 T cells expressing all 4 activation markers increased over time in all age groups.

The Weinberg et al. (2017) comparison of gE/AS01B and ZV found higher CMI responses distinguishing gE/AS01B from ZV recipients after adjusting for age, gender, prior ZV administration, and baseline CMI. Specifically, gE/AS01B recipients showed higher VZV-specific IL2 and gE-specific IL2 and IFNγ spot-forming cells at peak response (p≤0.004), higher VZV-specific CD8+ and gE-specific CD4+ and CD8+ responses measured by proliferation at peak (p<0.05), and higher CD4+ central memory (Tcm%) and effector memory (Tem%) with lower effector T cells (Teff%) at peak response (p≤0.005).

Long-term persistence of CMI was observed across studies. Pauksens et al. found the median frequency of gE-specific CD4+ T-cells expressing ≥2 activation markers plateaued at 3.4-fold above pre-vaccination levels from year 4 through year 9. Bastidas et al. reported CD4+ T-cells expressing ≥2 activation markers plateaued at 3.3-fold above pre-vaccination levels from around year 4 to year 10. Hastie et al. observed CD4+ T-cell frequencies of 414 and 402 at months 108 and 120, compared to a peak of 1,809 at 1 month after initial dose 2.

In HSCT recipients, CD4[2+] T-cell frequencies were similar between 18-49 and ≥50-year-olds, and despite lower humoral responses in NHBCL patients, CD4[2+] T-cell frequencies were similar between NHBCL and other underlying diseases. The proportion of polyfunctional CD4 T cells increased over time, accounting for 79.6% of gE-specific CD4 T cells at 24 months post-dose 2.

Stadtmauer et al. (2021) noted that RZV induces a memory T-cell profile linked to IL-2 production, differing from the live attenuated zoster vaccine’s effector response profile dominated by IFN-γ. Increased IL-2 production is linked to long-term persistence of cellular responses and vaccine-induced protection.

#### Anamnestic Responses

Hastie et al. (2020) evaluated the immunogenicity of additional RZV doses administered 10 years after initial vaccination in 62 participants (mean age 82.6 years). A single additional dose elicited strong anamnestic humoral and CMI responses, without further increases after a second additional dose. This demonstrates the vaccine’s capacity to establish robust immune memory that can be recalled even in elderly populations.

## Safety Profile and Reactogenicity

Reactogenicity provides indirect evidence of innate immune activation, as local and systemic reactions reflect inflammatory responses to the adjuvant.

In hematologic malignancy patients, pain was the most frequent local solicited adverse event, reported by 48.2% of participants, while fatigue was reported by 47.8%. RZV was more reactogenic than placebo in this population, though the occurrence of unsolicited adverse events, serious adverse events (SAEs), and potential immune-mediated diseases (pIMDs) was similar between study groups. No safety concerns were identified.

In the long-term follow-up study by Hastie et al., pain was the most frequent solicited local adverse event, reported by 74.2% of participants receiving additional doses, with 3.2% experiencing grade 3 pain. Common systemic adverse events included fatigue and myalgia. No vaccine-related SAEs or potential immune-mediated diseases were reported.

Pauksens et al. reported no vaccine-related serious adverse events or suspected herpes zoster episodes during 9-year follow-up. Bastidas et al. similarly reported no relevant safety events during years 9-10 post-initial vaccination. Across studies, the safety profile was consistently described as clinically acceptable.

## Clinical Efficacy

RZV demonstrated high vaccine efficacy against herpes zoster across diverse populations. In the ZOE trials of immunocompetent adults, efficacy was age-independent with 91% efficacy in individuals aged 80 years or older, remaining high for the 4-year duration of the ZOE-70 trial. Pauksens et al. reported high efficacy with limited waning over 4 years. In the ZOSTER-049 extension study, overall vaccine efficacy was 84.0% (95% CI: 75.9-89.8%) during at least 2 years of follow-up, and 90.9% (95% CI: 88.2-93.2%) from 1 month post-dose 2 until the end of year 2 observation.

In immunocompromised populations, efficacy varied by underlying disease. Dagnew et al. reported 87.2% efficacy in patients with hematologic malignancies who had completed or were undergoing anticancer immunosuppressive therapies. In autologous HSCT recipients, vaccine efficacy against herpes zoster ranged from 42.5% to 82.5% across underlying diseases, with statistically significant efficacy in NHBCL and multiple myeloma patients. Notably, efficacy was high in NHBCL patients despite their lower humoral responses, suggesting that cell-mediated immune responses are the main mechanistic driver for protection against herpes zoster.

The relationship between immune responses and clinical outcomes is supported by the persistence of both humoral and cell-mediated immunity corresponding to sustained protection. Boutry et al. found that anti-gE antibody concentrations persisted approximately 6 times above pre-vaccination levels and gE-specific CD4+ T-cell frequencies remained above baseline through year 8 post-vaccination, with correlates of protection identified as the persistence of these immune responses.

## Factors Influencing Adjuvant Response

### Age Effects

Most studies found minimal age effects on RZV-induced immune responses. Weinberg et al. reported that gE/AS01B efficacy does not vary with age of the vaccinee, unlike the live attenuated zoster vaccine whose efficacy decreases with age. In the ZOE trials, humoral responses were age-independent, though CMI responses declined modestly with age. However, AS01B enhanced antigen presentation in older adults, overcoming immunosenescence. In HSCT recipients, anti-gE antibody GMCs and CD4[2+] T-cell frequencies were similar between 18-49 and ≥50-year-olds.

Long-term persistence studies found cellular and humoral responses at year 9 were similar across age strata (60-69, ≥70 years). Hastie et al. demonstrated that adults aged ≥60 years at initial vaccination (mean age 82.6 at additional dosing) maintained immune responses for up to 10 years and mounted strong anamnestic responses to additional doses even at advanced age.

### Immunosuppression Effects

Immunosuppression affected adjuvant responses differentially depending on the mechanism. In hematologic malignancy patients receiving immunosuppressive cancer therapy, RZV induced robust humoral and cellular immune responses at 1 month post-dose 2. However, the timing relative to treatment influenced responses, with vaccine administration occurring ≥10 days pre- or post-immunosuppressive cancer therapy.

In HSCT recipients vaccinated 50-70 days post-transplant when immune suppression was near maximum, responses varied by underlying disease. NHBCL patients showed lower anti-gE antibody GMCs, likely due to immunotherapeutic agents targeting B cells commonly used in this population. However, CD4[2+] T-cell frequencies were similar between NHBCL and other underlying diseases, and vaccine efficacy remained high in NHBCL patients despite weaker humoral responses.

## Synthesis

This systematic review identified a notable gap between the robust clinical efficacy and adaptive immune responses induced by RZV and the limited direct measurement of innate immune activation by the AS01B adjuvant. Only one study (Johnson et al., 2024) directly assessed innate immune responses, finding sustained activation of monocytes, dendritic cells, and NK cells for up to 5 years, along with evidence of trained immunity development. This trained immunity manifested as enhanced responses to both homologous and heterologous antigens and was associated with epigenetic changes including decreased TGFβ pathway accessibility.

The mechanistic understanding of AS01B comes primarily from one source (Cunningham et al., 2018), which described how MPL and QS-21 synergistically activate innate responses through TLR4 signaling and local cytokine production. Yet the remaining nine studies focused exclusively on adaptive immunity endpoints—antibodies and T cells—despite these adaptive responses being downstream consequences of adjuvant-mediated innate activation.

This disconnect between measurement and mechanism is partially explained by the study designs and objectives. The large phase III trials (ZOE-50, ZOE-70) and their extensions prioritized clinically relevant endpoints (efficacy, long-term protection) and regulatory requirements (antibody titers, T-cell frequencies) over mechanistic investigations of adjuvant function. The inclusion of immunocompromised populations (HSCT recipients, hematologic malignancy patients) further shifted focus toward whether the vaccine could overcome immune deficits rather than how the adjuvant activated immunity.

The indirect evidence for innate activation is threefold. First, the reactogenicity profile—with 74.2% of recipients reporting injection site pain and nearly half reporting fatigue—indicates local and systemic inflammatory responses consistent with innate immune activation. Second, the robust and rapid adaptive responses (97.8% humoral response rate, 93.3% CD4+ T-cell response rate) suggest effective adjuvant priming of antigen-presenting cells. Third, the development of polyfunctional memory T cells and the ability to mount strong anamnestic responses decades later indicate high-quality immune priming consistent with effective innate-adaptive crosstalk.

The persistence of adaptive responses for 10 years with predictions extending to 15-20 years suggests AS01B establishes durable immune memory. The Johnson et al. finding of innate immune activation persisting for 5 years challenges traditional models where adjuvant effects are transient, raising questions about whether AS01B induces a form of “adjuvant imprinting” that durably modifies innate immune cell function.

The clinical outcomes provide the ultimate validation of AS01B’s effectiveness: ≥90% efficacy in immunocompetent adults and 42.5-82.5% efficacy even in severely immunocompromised HSCT recipients. The observation that NHBCL patients showed high efficacy despite low antibody responses suggests CMI responses—and by extension, the innate priming that generates them—are the critical correlates of protection.

Future mechanistic studies should systematically measure innate activation markers (cytokines, cell activation, transcriptional changes) alongside adaptive responses to fully characterize AS01B’s mode of action and identify which components of the innate response drive protective immunity. The trained immunity findings warrant investigation of whether AS01B-induced epigenetic reprogramming contributes to its exceptional durability and whether this mechanism could be leveraged in other vaccine contexts.

## References

1. [A. Weinberg, Michael J. Johnson, Miranda Kroehl, Nancy Lang, D. Reinhold, and 1 more (2017). A comparison of the immunogenicity of a live attenuated herpes zoster vaccine (ZV) and the recombinant gE/AS01B candidate vaccine in older adults. Journal of Immunology](/content/review/5a70c0cb-8f0e-4423-afab-38fc3d834736/source/ss-255646906/index.html)
2. [A. Cunningham, T. Heineman, Himal Lal, O. Godeaux, R. Chlibek, and 18 more (2018). Immune Responses to a Recombinant Glycoprotein E Herpes Zoster Vaccine in Adults Aged 50 Years or Older. Journal of Infectious Diseases](/content/review/5a70c0cb-8f0e-4423-afab-38fc3d834736/source/ss-3854235/index.html)
3. [E. Stadtmauer, K. Sullivan, Mohamed El Idrissi, B. Salaun, A. Alonso Alonso, and 25 more (2021). Adjuvanted recombinant zoster vaccine in adult autologous stem cell transplant recipients: polyfunctional immune responses and lessons for clinical practice. Human Vaccines & Immunotherapeutics](/content/review/5a70c0cb-8f0e-4423-afab-38fc3d834736/source/ss-237214663/index.html)
4. [Alemnew F Dagnew, O. Ilhan, W. Lee, D. Woszczyk, J. Kwak, and 20 more (2018). 149. Immunogenicity, Safety, and Post-hoc Efficacy Assessment of the Adjuvanted Recombinant Zoster Vaccine in Adults with Hematologic Malignancies: A Phase 3, Randomized Clinical Trial. Open Forum Infectious Diseases](/content/review/5a70c0cb-8f0e-4423-afab-38fc3d834736/source/ss-53850506/index.html)
5. [Michael J. Johnson, Megan Crotteau, Debashis Ghosh, Myron J. Levin, Adriana Weinberg (2024). Trained Immunity Generated by The Recombinant Zoster Vaccine (RZV). Journal of Immunology](/content/review/5a70c0cb-8f0e-4423-afab-38fc3d834736/source/ss-273931325/index.html)
6. [A. Bastidas, Grégory Catteau, S. Volpe, T. Mrkvan, Adaora Enemuo, and 8 more (2019). 2905. Long-term Immunological Persistence of the Adjuvanted Recombinant Zoster Vaccine: Clinical Data and Mathematical Modeling. Open Forum Infectious Diseases](/content/review/5a70c0cb-8f0e-4423-afab-38fc3d834736/source/ss-204946418/index.html)
7. [K. Pauksens, S. Volpe, T. Schwarz, J. Smetana, Nicole Toursarkissian, and 5 more (2017). Persistence of Immune Response to an Adjuvanted Varicella‐Zoster Virus Subunit Candidate Vaccine for up to Year 9 in Older Adults. Open Forum Infectious Diseases](/content/review/5a70c0cb-8f0e-4423-afab-38fc3d834736/source/ss-32731443/index.html)
8. [Andrew Hastie, Grégory Catteau, Adaora Enemuo, T. Mrkvan, B. Salaun, and 8 more (2020). Immunogenicity of the Adjuvanted Recombinant Zoster Vaccine: Persistence and Anamnestic Response to Additional Doses Administered 10 Years After Primary Vaccination. Journal of Infectious Diseases](/content/review/5a70c0cb-8f0e-4423-afab-38fc3d834736/source/ss-219399154/index.html)
9. [C. Boutry, Andrew Hastie, Meng-yuan Shi, J. Díez-Domingo, J. Tinoco, and 4 more (2020). 8. The Adjuvanted Recombinant Zoster Vaccine (RZV) Confers Long-term Protection Against Herpes Zoster: Interim Results of an Extension Study (ZOSTER-049) of Two Clinical Trials (ZOE-50 and ZOE-70). Open Forum Infectious Diseases](/content/review/5a70c0cb-8f0e-4423-afab-38fc3d834736/source/ss-230800008/index.html)
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