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. 2025 Mar 13;21(1):2474772. doi: 10.1080/21645515.2025.2474772

Factors affecting the impact of COVID-19 vaccination on post COVID-19 conditions among adults: A systematic literature review

Abby E Rudolph a,✉, Nadine Al Akoury b, Natalija Bogdanenko c, Kristen Markus d, Isabelle Whittle d, Olivia Wright d, Hammam Haridy e, Julia R Spinardi f, John M McLaughlin a, Moe H Kyaw a
PMCID: PMC11913386  PMID: 40079963

ABSTRACT

This systematic literature review summarizes the evidence across 56 publications and pre-prints (January 2020–July 2023) with low-risk of bias based on JBI critical appraisal, that report adjusted estimates for the relationship between COVID-19 vaccination and Post-COVID-19 Condition (PCC) by timing of vaccination relative to infection or PCC-onset. Comparisons of adjusted vaccine effectiveness (aVE) against ≥1 PCC (vs. unvaccinated) across study characteristics known to impact PCC burden or VE against other COVID-19 endpoints were possible for 31 studies where vaccination preceded infection. Seventy-seven percent of pre-infection aVE estimates were statistically significant (range: 7%–95%). Statistically significant pre-infection aVE estimates were slightly higher for mRNA (range: 14%–84%) than non-mRNA vaccines (range: 16%–38%) and aVE ranges before and during Omicron overlapped. Our findings suggest that COVID-19 vaccination before SARS-CoV-2 infection reduces the risk of PCC regardless of vaccine type, number of doses received, PCC definition, predominant variant, and severity of acute infections included.

KEYWORDS: Post-COVID conditions, COVID-19 vaccine, SARS-CoV-2, long COVID, vaccine effectiveness, post-acute sequelae of SARS-CoV-2 infection

Introduction

By July 21, 2024, there were ~776 million confirmed COVID-19 cases globally.1 Due to under-reporting of cases post-pandemic and under-detection of cases globally, this is likely an underestimate. Following the acute phase of a SARS-CoV-2 infection, an estimated 10%–30% experience new-onset or persisting signs, symptoms, or conditions (with no other explanation).2 Although the definition varies by country and across the literature, this is commonly referred to as long COVID, post-COVID-19 conditions (PCC), or post-acute sequelae of COVID-19 (PASC).3,4 Al-Aly and colleagues estimated that by the end of 2023, ~400 million people had experienced PCC at 3 months post-infection, corresponding with an economic impact of $1 trillion each year.5 The risk of PCC is considerably higher following severe COVID-192,6–10; however, due to the vast number of SARS-CoV-2 infections and re-infections (most of which are not severe), over 90% of PCC cases follow a mild SARS-CoV-2 infection.11 The cumulative PCC burden, economic impact, and disability-adjusted-life-years lost due to PCC12–14 will continue to rise as new infections occur each day.

Because COVID-19 vaccines prevent both symptomatic infection and the development of severe COVID-19‑related outcomes,15–17 pre-infection vaccination may reduce the risk of PCC, as many systematic literature reviews (SLRs) have suggested.18–26 Vaccination after PCC-onset could resolve or ameliorate PCC stemming from persisting viral load,27 but prior SLRs report inconclusive findings.21,26,28,29 Existing SLRs are limited, as they have not synthesized findings across key study characteristics known to impact PCC burden or vaccine effectiveness (VE) (i.e., PCC data source and follow-up period; vaccine type and manufacturer, number of doses received, and time since vaccination; severity of the acute infection; inclusion of reinfections; predominant variant).

This SLR summarizes the evidence across studies on predominately adults that report adjusted measures of association for the relationship between COVID-19 vaccination and PCC, by timing of vaccination relative to infection or PCC-onset and across different study design features.

Methods

This SLR was conducted in accordance with the Cochrane group30 and Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines for SLRs.31 Two reviewers (IW and OW) assessed each study’s risk of bias using JBI Critical Appraisal Checklists.32 The study protocol was registered in PROSPERO (CRD42023446417). As this study did not involve human research participants, it was not necessary to seek approval from an ethics committee or Institutional Review Board.

A comprehensive search strategy was developed within the OVID platform across EMBASE, MEDLINE® and Evidence-Based Medicine reviews, and supplemented with WHO COVID library and Google Scholar® searches to collate evidence relating to COVID-19 vaccination and PCC published or posted on pre-print servers between January 1, 2020 and July 18, 2023 (English language only) (eTable S1).

Abstracts of retrieved citations were screened according to study PICOS criteria (eTable S2) by two independent reviewers (IW and OW); a third reviewer (KM) resolved discrepancies. Data from studies meeting the PICOS criteria were extracted by one reviewer and verified by a second. The following study attributes were extracted for each eligible study: author and year; countries; study population; data collection period; PCC follow-up period; data sources for SARS-CoV-2, vaccination, and PCC; predominant variant circulating; vaccination timing relative to infection or PCC-onset; and vaccination definition (eTable S3).

The primary outcome was presence of ≥1 PCC. Adjusted vaccine effectiveness (aVE) against ≥1 PCC was calculated from adjusted estimates of relative risk (aRR) (e.g., risk ratios, odds ratios, or hazard ratios) using the equation aVE=(1-aRR)×100.

Results

Summary of included articles

This review included 97 studies (Figure 1), which were categorized according to timing of vaccination relative to infection or PCC-onset, vaccine type and manufacturer, number of doses received, time since vaccination, PCC data source and follow-up period, proportion of sample hospitalized during the acute infection, predominant variant circulating when diagnosed with COVID-19 or testing positive for SARS-CoV-2, and whether or not reinfections were included. The predominant variant during infection was reported in 30 of the 97 studies; when not reported (n = 67 studies), it was determined using CoVariants, an online tracking database for predominating variant sequences by country.33 Variant of infection could not be determined for only one (1.8%) study. Of the 97 included studies, 80 were rated as having low risk of bias (eTables S4–6). Of these 80 studies, 24 studies presented only unadjusted estimates and were not included in analyses. Thus, findings from the 56 studies reporting adjusted estimates for the relationship between vaccination and PCC are summarized below (Figure 1).

Figure 1.

Figure 1.

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PRISMA flow diagram of included studies.

*Underwent bibliography cross-check, see search strategy detailed in supplementary material.

†Pre-prints that were not published within 6 months of posting to pre-print server were excluded. EBM: Evidence-Based Medicine; NA: not applicable; NMA: Network meta-analysis; SLR: systematic literature review.

Across these 56 studies, estimates for the relationship between vaccination and PCC were calculated when vaccination occurred before infection (n = 39 studies), after infection (n = 4 studies), after PCC-onset (n = 3 studies), and either before or after infection (i.e., ‘mixed timing,’ n = 7 studies). Three studies reported estimates for more than one vaccination timepoint and six studies did not report the timing of vaccination relative to infection or PCC-onset. The most common study design was a retrospective cohort (35.7%, n = 20), followed by cross-sectional (32.1%, n = 18), prospective cohort (25.0%, n = 14), case–control (5.4%, n = 3), and ambidirectional cohort (1.8%, n = 1). Most studies were conducted in Europe (39.3%), followed by the Americas (37.5%), South-East Asia (7.1%), the Western Pacific (5.4%), in more than one WHO region (5.4%), the Eastern Mediterranean (3.6%), and Africa (1.8%). Twenty-six studies (46.4%) were conducted before Omicron predominance, 8 (14.3%) during Omicron predominance, and 21 (37.5%) both before and during Omicron predominance. Most studies (n = 37; 66.1%) measured patient-reported PCC, 18 (32.1%) relied on diagnostic and procedural codes from electronic health records or health insurance claims data, and one (1.8%) used both (eTable S7).

In the 56 studies with low risk of bias, adjusted estimates for the relationship between vaccination and PCC were used to compute aVE against ≥1 PCC (vs. unvaccinated; n = 39 studies), comparative aVEs against ≥1 PCC (n = 11 studies; Figure S1; eTable S8), and aVE against ≥1 specific PCC symptom/condition across 4 organ systems (n = 9 studies; Figure S2; eTable S9). Ten studies estimated associations that could not be converted to aVE (eTable S10). Thirteen studies reported adjusted estimates for at least two of the above relationship types (eTable S11).

Adjusted VE against ≥1 PCC, by timing of vaccination relative to infection or PCC-onset

Thirty-nine studies reported 134 adjusted estimates where aVE against ≥1 PCC (vs. unvaccinated) could be computed. Overall, 93 estimates (n = 31 publications) evaluated pre-infection vaccination (Figures 2 and 3 and corresponding eTables S12 and S13), 7 estimates (n = 4 publications) evaluated post-infection vaccination, 5 estimates (n = 1 publication) evaluated vaccination after PCC-onset, 5 estimates (n = 2 publications) reflect a mix of those vaccinated before and after infection, and 24 estimates (n = 4 publications) did not report vaccination timing (Figure S3 and corresponding eTable S14; eTable S11; eTable S15). Of note, three studies reported estimates for two different vaccination timepoints (two reported both pre- and post-infection estimates;41,43 one reported pre-infection and post-PCC-onset estimates).48

Figure 2.

Figure 2.

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Adjusted pre-infection VE against ≥1 PCC (vs. Unvaccinated) for any or unspecified vaccine type or manufacturer, by vaccine type and number of doses (n = 16 estimates from 19 publications).

Of 62 pre-infection aVE estimates against ≥1 PCC when the vaccine type is mixed or not specified, 52 (83.9%) reported statistically significant estimates (based on the 95% CI); all protective (range: 7%–95%).

CI: confidence interval; NR: not reported; PCC: post-COVID-19 condition; VE: vaccine effectiveness.

References: Abu Hamdh;34 Al-Aly;35 Antonelli;36 Antonelli;37 Ayoubkhani38; Cortellini;39 de Arriba Fernández;40 Durstenfeld;41 Elmanzy;42 Luo;43 Marra;44 Parodi;45 Patel;46 Ranucci;47 Richard;48 Senjam49 Smits;50 Tannous;51 Tosi.52

Figure 3.

Figure 3.

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Adjusted pre-infection VE against ≥1 PCC (vs. Unvaccinated) for mRNA and non-mRNA vaccines, by vaccine type, manufacturer and dose (n = 31 estimates from 12 publications).

Of 8 pre-infection aVE estimates against ≥1 PCC for non-mRNA vaccines, 6 (75%) reported statistically significant estimates (based on the 95% CI); all protective (range: 16%–38%).

Of 23 pre-infection aVE estimates against ≥1 PCC for mRNA vaccines, 14 (61%) reported statistically significant estimates (based on the 95% CI); all protective (range: 14%–84%).

Of 11 pre-infection aVE estimates against ≥1 PCC for BNT162b2 vaccines, 8 (73%) reported statistically significant estimates (based on the 95% CI); all protective (range: 14%–84%).

CI: confidence interval; mRNA: messenger ribonucleic acid; PCC: post-COVID-19 condition; VE: vaccine effectiveness.

References: Ayoubkhani;38 Azzolini;53 Català;54 Di Fusco;55 Ertesvag;56 Gallant;57 Herman;58 Ioannou;59 Kahlert;60 Mohr;61 Perlis;62 Xue.63

Overall, 77% (72/93) of pre-infection aVE estimates (vs. unvaccinated) were statistically significant (aVE range: 7%–95%; Figures 2 and 3). Similarly, of the 21 aVE estimates that were not statistically significant, 12 (57%) suggested a protective effect of pre-infection vaccination. At vaccination timepoints other than before infection, four of five estimates (80%) reflecting a mix of those vaccinated before and after infection were statistically significant (aVE range: 62%–73%), three of seven estimates (43%) reflecting post-infection vaccination were statistically significant (two were protective [aVE range: 28%–40%] and one was not aVE = −47%]), and one of the five estimates (20%) assessing vaccination after PCC-onset was statistically significant (aVE = 41%) (eTable S15). Of the 24 estimates not specifying vaccination timing, 11 (46%) were statistically significant (10 estimates were protective [aVE range: 29%–75%] and one was not aVE = −132%]) (Figure S3, eTable S14, and eTable S15).

Due to the number of studies focusing on vaccination before infection relative to other timeframes, aVE comparisons across subgroups were only possible for studies where vaccination occurred before infection.

Adjusted VE against ≥1 PCC when vaccinated prior to an infection

By number of doses

Statistically significant aVE estimates (vs. unvaccinated) varied by the number of vaccine doses received before infection. For example, 72% (18/25) of estimates for one dose were statistically significant (aVE range: 12%–82%), 64% (9/14) of estimates for ≥1 dose were statistically significant (aVE range: 46%–86%), 88% (36/41) of estimates for 2 doses or primary series completion were statistically significant (aVE range: 7%–90%), 80% (8/10) of estimates for receipt of 3 doses or a booster were statistically significant (aVE range: 13%–84%), and the only estimate for 4 doses was statistically significant (aVE = 95%) (Figures 2 and 3). There was only one estimate for >3 doses (Figure 2) and one estimate for >2 doses (Figure 3), neither of which were statistically significant. Additionally, all three studies that compared complete vs. incomplete vaccination against ≥1 PCC reported greater protection with complete vaccination40,63,64 and all three studies comparing the protection offered by a booster dose (relative to the primary series or fewer than 3 doses) reported no statistically significant difference (Figure S1; eTable S8).40,50,55

By vaccine manufacturer/platform and number of doses

Statistically significant estimates were slightly higher for mRNA vaccines (range: 14%–84%; n = 14/23 estimates from 10 different studies were statistically significant) than non-mRNA vaccines (range: 16%–38%; n = 6/8 estimates from 4 unique studies were statistically significant). For mRNA-specific estimates, aVE appeared to increase with additional doses. For example, 4 of 7 mRNA-specific estimates (including 4 of 5 BNT162b2-specific estimates from 3 unique studies) for 1 dose were statistically significant (aVE range: 14%–51%), 7 of 9 mRNA-specific estimates for 2 doses were statistically significant (aVE range: 22%–75%) and 1 of 3 BNT162b2-specific estimates for 2 doses was statistically significant (aVE = 75%), and all 3 estimates for 3 doses were statistically significant (aVE range: 64%–84%; all BNT162b2) (Figure 3; eTables S13 and S16). Although data are more limited (4 estimates from 2 studies), estimates that directly compare the effectiveness of mRNA and non-mRNA vaccines against ≥1 PCC suggest significantly greater protection for 1 mRNA dose vs. 1 non-mRNA dose54 and for 2 mRNA doses vs. 2 non-mRNA doses (Figure S1; eTable S8).35

By variant

For infections pre-Omicron, 72% of estimates (n = 18/25) from 10 studies were statistically significant and all were protective (aVE range: 7%–50%). For infections during Omicron, 80% of estimates (n = 12/15) from 4 studies were statistically significant and all were protective (aVE range: 10%–70%). The range of statistically significant estimates reflecting infections before and during Omicron overlapped. For estimates reflecting infections during both Omicron and pre-Omicron periods, 79% of estimates (n = 41/52) from 16 studies were statistically significant (aVE range: 12–95%) (Figure 4; eTable S17).

Figure 4.

Figure 4.

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Adjusted pre-infection VE against ≥1 PCC (vs. Unvaccinated), by predominant variant circulating during acute infection.

18 of 25 (72%) pre-infection aVE estimates against ≥1 PCC before Omicron (from 10 studies) were statistically significant (based on the 95% CI); all protective (aVE range: 7%–50%).

12 of 15 (80%) pre-infection aVE estimates against ≥1 PCC during Omicron predominance (from 4 studies) were statistically significant (based on the 95% CI); all protective (aVE range: 10%–70%).

41 of 52 (79%) pre-infection aVE estimates against ≥1 PCC for infections during and before Omicron predominance (from 16 studies) were statistically significant (based on the 95% CI); all protective (aVE range: 12%–95%).

The only pre-infection aVE estimates against ≥1 PCC with variant period not reported (from 1 study) was statistically significant (based on the 95% CI); aVE = 86%). CI: confidence interval; mRNA: messenger ribonucleic acid; PCC: post-COVID-19 condition; VE: vaccine effectiveness.

References: Abu Hamdh;34 Al-Aly;35 Antonelli;36 Antonelli;37 Ayoubkhani;38 Azzolini;53 Brannock;65 Català;54 Cortellini;39 de Arriba Fernández;40 Di Fusco;55 Durstenfeld;41 Elmanzy;42 Ertesvag;56 Gallant;57 Herman;58 Ioannou;59 Kahlert;60 Luo;43 Marra;44 Mohr;61 Parodi;45 Patel;46 Perlis;62 Ranucci;47 Richard;48 Senjam;49 Smits;50 Tannous;51 Tosi;52 Xue.63

By PCC definition

Overall, more studies used patient-reported PCC (n = 19) than PCC based on medical codes/claims (n = 11); one study used both PCC based on patient-report and claims/codes. Estimates based on claims/codes were more likely to be statistically significant (89%, n = 41/46 estimates, vs. 67%, n = 31/46 estimates), but the range of statistically significant aVE estimates overlapped for PCC based on medical/claims codes (range: 7%–95%) and patient-report (range: 28%–90%). Estimates based on patient-reported PCC (and particularly those reported closer to the infection date – at 28 days, ≥4 weeks, and 6 weeks post-infection) tended to be higher but were often less precise due to smaller sample sizes (Figure 5; eTables S18 and S19). Slightly lower aVEs were observed for time-to-event analyses (codes/claims-based PCC with longer follow-up periods, for example those specifying PCC follow-up intervals such as 28–365 days, 90–365 days, 8–23 months, ≥30 days), which typically have larger sample sizes and more precise estimates (Figure 5).

Figure 5.

Figure 5.

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Adjusted pre-infection VE against ≥1 PCC (vs. Unvaccinated), by PCC data source.

Forty-one of 46 (89%) pre-infection aVE estimates against ≥1 PCC based on diagnostic and procedural codes from electronic health records or health insurance claims data (from 11 unique studies) were statistically significant (based on the 95% CI); all protective (aVE range: 7%–95%).

Thirty-one of 46 (67%) pre-infection aVE estimates against ≥1 patient-reported PCC (from 19 unique studies) were statistically significant (based on the 95% CI); all protective (aVE range: 28%–90%).

CI: confidence interval; PCC: post-COVID-19 condition; VE: vaccine effectiveness. References: Abu Hamdh;34 Al-Aly;35 Antonelli;36 Antonelli;37 Ayoubkhani;38 Azzolini;53 Brannock;65 Català;54 Cortellini;39 de Arriba Fernández;40 Di Fusco;55 Durstenfeld;41 Elmanzy;42 Ertesvag;56 Gallant;57 Herman;58 Ioannou;59 Kahlert;60 Luo;43 Marra;44 Mohr;61 Parodi;45 Patel;46 Perlis;62 Ranucci;47 Richard;48 Senjam;49 Smits;50 Tannous;51 Tosi;52 Xue.63

By proportion of sample hospitalized during acute infection

Pre-infection vaccination was protective against PCC in studies among those hospitalized during the acute phase (aVE range: 12%–80%; n = 5/5 estimates statistically significant), including a mix of patients who were and were not hospitalized during the acute phase (aVE range: 15%–90%; n = 17/24 estimates statistically significant), and among those not hospitalized during the acute phase (aVE range: 7%–84%; n = 3/6 estimates statistically significant) (Figure S4; eTables S20 and S21).

By other sub-groups and other outcomes

Due to the limited number of studies reporting time since vaccination (eTable S22) and inclusion vs. exclusion of reinfections (Figure S5; eTable S23), no trends were detected. The range of aVE against specific endocrine, neurological, musculoskeletal, or cardiovascular symptoms/conditions (Figure S2; eTable S9) were consistent with the aVE range reported against ≥1 PCC. Other outcomes where VE could not be computed are summarized in eTable S10. For example, Strain and colleagues reported that those vaccinated post-PCC-onset with mRNA vs. non-mRNA vaccines experienced greater symptom improvement.66 Tran and colleagues reported that those vaccinated after infection (vs. unvaccinated) were less likely to report an unacceptable symptom state, more likely to achieve full remission, and experienced less severe long COVID (lower impact on patient quality of life).67 Nehme and colleagues reported a higher PCC symptom prevalence among those who received ≥1 dose before infection (vs. unvaccinated).68 Taquet and colleagues reported significant differences in the risk of some specific PCC as composite endpoints with death for those vaccinated with 1 dose vs. unvaccinated and 2 doses vs. unvaccinated.69

Discussion

This SLR summarizes the evidence across studies that report an adjusted estimate for the relationship between COVID-19 vaccination and PCC, by timing of vaccination relative to infection or PCC-onset and across study characteristics known to impact PCC burden or VE against other COVID-19 endpoints. Despite heterogeneity across studies included in this SLR with respect to study design, population, PCC definition, follow-up period and data source, definition of ‘vaccinated,’ and predominant variant circulating, there is consistent evidence suggesting that pre-infection COVID-19 vaccination reduces the risk of ≥1 PCC. Regardless of the number of doses or vaccine type received, 77% of adjusted pre-infection VE estimates against ≥1 PCC (vs. unvaccinated) were statistically significant and all statistically significant findings were protective (range: 7%–95%). Evidence was limited for vaccination at other timepoints relative to infection or PCC-onset. Collectively, these findings are consistent with guidance provided by the Centers for Disease Control and Prevention,70 International Coalition of Medicines Regulatory Authorities,71 World Health Organization,72 European Medicines Agency73 and United Kingdom Health Security Agency.74

Among studies where vaccination occurred before the index infection, aVE estimates varied by vaccine type and the number of doses received. For example, the range of protection offered by vaccination (based on comparisons across strata or direct comparisons) was slightly higher for mRNA vaccines than other vaccine types. This is consistent with other studies that reported higher VEs for mRNA than non-mRNA vaccines based on direct comparisons75,76 or differences across strata based on vaccine type or manufacturer.40,77–81 We also observed a dose response for mRNA-specific aVEs, whereby additional doses offered greater protection (i.e., VE range for 1 dose: 14%–51%; 2 doses: 22%–75%; and 3 doses: 64%–84%); however, this trend is based on only 10 studies that reported mRNA-specific estimates. Other studies (including those published after this SLR’s search period) have reported higher VEs for additional doses, regardless of vaccine type.21,75,76,82–91 Further, two studies specifically showed the benefit of additional doses during Omicron predominance (4 vs. 3 doses,92 and 3 vs. 2 doses).93 Additionally, more recently published mRNA-specific and BNT162b2-specific VEs reported by dose fall within the range of those summarized in this SLR (2 mRNA doses vs. unvaccinated [VE = 57%],94 ≥2 BNT162b2 doses vs. unvaccinated [VE = 78%],78 2 doses BNT162b2 vs. unvaccinated [VE = 51%],89 2 doses mRNA-1273 vs. unvaccinated (VE = 52%),89 and vaccinated with BNT162b2 bivalent vs. unvaccinated or not up-to-date [VE range = 41%–43%].95 Taken together, the trend is that the mRNA vaccines offer greater protection.

Other studies have reported a lower PCC burden during Omicron predominance,37,90,96,97 however, directly comparing VE estimates across different variant periods is challenging due to other time-varying factors98 which may impact the likelihood of experiencing PCC (i.e., changes in SARS-CoV-2 pathogenicity and disease severity which may be impacted by changes in baseline immunity due to a combination of prior vaccination and SARS-CoV-2 infections [and among those vaccinated, time since most recent dose], and improved medical care including the use of antivirals). We present the range of pre-infection aVE against ≥1 PCC for those infected (1) during Omicron predominance and (2) when other variants predominated. The aVE range was slightly higher during periods of Omicron predominance and a greater proportion of estimates were statistically significant; however, there were fewer studies conducted during Omicron than during periods when other variants predominated. Our findings suggest that pre-infection vaccination offers protection against PCC regardless of the variant causing infection and is consistent with findings reported by other studies.75,91,99–101 Our findings are also consistent with those demonstrating that 70%–76% of the reduced PCC burden from pre-Omicron to Omicron variant periods was attributed to COVID-19 vaccinations.90

Woodrow and colleagues previously reported higher estimates for PCC based on self-report vs. health records.102 Consistent with this finding, we observed the highest aVE estimates for PCC at 1 month post-infection (all patient-reported PCC). Although there is the potential for PCC to be misclassified in both data sources, the consistent trends observed across studies with different PCC data sources suggest that pre-infection COVID-19 vaccination likely reduces the risk of PCC.

Although the PCC burden has been reported to be higher among those hospitalized during the acute phase,2,8,34,48,59,83,90,103–108 we did not observe differences in the range of pre-infection aVE against ≥1 PCC based on the proportion of the sample hospitalized during the acute phase. This may reflect (1) heterogeneity in other study design characteristics (e.g., predominant variant, number of vaccine doses, PCC definition, PCC data source), (2) survival bias (those experiencing PCC must have survived to experience PCC), and (3) heterogeneity in disease severity among those hospitalized i.e. admitted to the intensive care unit, requiring supplemental oxygen or mechanical ventilation, etc.).

Findings from this SLR should be interpreted with caution given the heterogeneous study designs, data sources, and definitions for vaccinated and PCC. Given that many studies in this review did not report the time between vaccination and infection, we were unable to assess the impact of time since vaccination on VE against ≥1 PCC. It was consequently difficult to tease apart the impact of changing variants and time since last dose. For example, of 93 aVE estimates against ≥1 PCC (vs. unvaccinated), the majority (86%) operationalized ‘vaccinated’ as receipt of one dose (n = 25), ≥1 dose (n = 14), or 2 doses or primary series completion (n = 41). If VE against PCC wanes over time, as a few studies reported,89,109,110 the wide range of aVEs observed for receipt of two doses or the primary series (7%–90%) could be explained by varying lengths of time since vaccination. Similarly, there may be heterogeneity in multi-year studies where receipt of the primary series in 2021 conveys a different level of protection than completion of the primary series in 2023. Further, the dose response observed in some studies may reflect more time since primary series completion than a booster dose, for example. Few studies have evaluated the protection offered by adapted vaccines (i.e., bivalent, XBB.1.5, and JN.1) and most lack information on prior SARS-CoV-2 infections (including time since last infection and variant causing last infection) which can create an imbalance in the immune histories of the comparison groups and has been shown to impact VE against SARS-CoV-2 infection111,112 and the likelihood of PCC.92 SLR/meta-analyses113–115 have also shown that those treated with antivirals during the acute phase have a reduced risk of PCC. However, antiviral use during the acute phase was not documented or accounted for in the studies summarized here, further contributing to the heterogeneity across studies.

Conclusion

Our findings provide a comprehensive synthesis of aVE estimates for COVID-19 vaccination against PCC from publications and pre-prints spanning January 2020 through July 2023. Our analyses describe trends in the effectiveness of COVID-19 vaccines for preventing PCC across key factors known to impact the risk of PCC and the effectiveness of vaccines against other COVID-19 endpoints (e.g., acute infection severity, PCC definition and data source, type and number of vaccine doses, and predominant variant). Collectively, our findings suggest that COVID-19 vaccination received prior to SARS-CoV-2 infection reduces the subsequent risk of developing PCC regardless of the predominant variant circulating.

Supplementary Material

Supplementary Materials Clean.docx
KHVI_A_2474772_SM3456.docx (2.8MB, docx)

Biography

Abby E. Rudolph received her MPH in Epidemiology from Columbia University Mailman School of Public Health, a PhD in Infectious Disease Epidemiology at Johns Hopkins University Bloomberg School of Public Health, and a postdoc in Global Public Health at the University of California San Diego. She has worked across different sectors, with positions at non-profit organizations, local health departments, healthcare centers, universities, and in industry. Her independent academic research portfolio focused primarily on the intersection of infectious disease and substance use epidemiology and was funded by several different NIH institutes (NIDA, NIAID, NIMH, NICHD, NIDCR, and NCRR) and the CDC (PI of an $8.7 million contract to study post-COVID-19 conditions). Her independent research has made significant contributions to: (1) the evaluation of recruitment strategies for “hidden” populations, (2) methodological innovations for network analysis and approaches to combine spatial and network analyses, (3) research ethics associated with data collection approaches, and (4) health services research. She joined Pfizer as Director of COVID-19 Epidemiology and Scientific Affairs in October 2022.

Funding Statement

This study was funded by Pfizer Inc.

Disclosure statement

Nadine Al Akoury, Moe H. Kyaw, Abby E. Rudolph, Julia Spinardi, John M. McLaughlin, and Hammam Haridy are employees of Pfizer Inc. and may hold stock or stock options. Kristen Markus, Isabelle Whittle, and Olivia Wright are employees of Adelphi Values PROVE™. Adelphi Values PROVE™ received funding from the study sponsor for the conduct of the review

Author contribution statement

All authors were involved in study conception and design, material preparation, data collection and analysis. The first draft of the manuscript was written by Abby E Rudolph, Isabelle Whittle, Olivia Wright, and Kristen Markus, and all authors provided comments on subsequent drafts. All authors read and approved the final manuscript.

Data availability

All data supporting the findings of this study are available within the paper and its Supplementary Information.

Supplementary material

Supplemental data for this article can be accessed online at https://doi.org/10.1080/21645515.2025.2474772

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Supplementary Materials

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Data Availability Statement

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