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Clinical manifestations of SARS-CoV-2 Omicron infection is associated with the stage of liver cirrhosis

BMC Infectious Diseases volume 25, Article number: 630 (2025) Cite this article

Abstract

Background & aim

The impact of Omicron variants on cirrhosis was largely unknown. Herein, we aimed to evaluate the impact of SARS-CoV-2 omicron variants infection on the clinical course and mortality of patients with liver cirrhosis.

Methods

Between 26 December 2022, and 27 January 2023, eighty-two hospitalized patients with cirrhosis and confirmed SARS-CoV-2 infection were enrolled. The clinical and pulmonary CT imaging features were retrospectively collected. A gender and age-matched cohort of 51 non-cirrhotic patients with COVID-19 were also included.

Results

Our results indicated the symptom heterogeneity in patients with cirrhosis infected with omicron variants. Patients with more severe liver disease tended to have less severe respiratory symptoms and less pulmonary lesions. SARS-CoV-2 omicron did not cause obvious perturbation of liver function or cirrhosis decompensation. In comparison with hospitalized COVID-19 patients without liver cirrhosis, cirrhotic patients showed more severe pulmonary lesions and higher levels of inflammatory cytokine IL-6, but no significant increase in mortality. Multivariate analysis identified lung lesions proportion, MELD ≥ 15 score, and APTT as independent predictors for 28-day-mortality in these patients.

Conclusion

SARS-CoV-2 omicron variants caused a more severe inflammatory response in cirrhotic patients than in non-cirrhotic patients, but no further deterioration of liver function. Instead, patients with advanced stage of liver cirrhosis showed milder respiratory symptoms and pulmonary lesions. These results underscore the intricate relationship between Omicron infection and cirrhosis, highlighting the necessity for personalized clinical approaches in managing this specific patient group.

Peer Review reports

Introduction

Since its initial emergence in December 2019, SARS-CoV-2 has exerted profound global health impacts while posing unprecedented challenges to clinical management [1,2,3,4]. Demonstrating accelerated evolutionary progression, the virus reached a critical inflection point with the Omicron variant establishing global predominance by September 2022 [5,6,7,8]. Although Omicron demonstrates attenuated pathogenicity compared to ancestral strains, its heightened transmissibility and immune evasion capacity continue to endanger individuals with chronic comorbidities [9,10,11,12,13,14,15]. Patients with chronic liver disease (CLD), particularly cirrhosis, represent a vulnerable population in this context. China bears the world’s highest CLD burden, with cirrhosis predominantly caused by viral hepatitis, alcoholic liver disease, and metabolic dysfunction-associated steatotic liver disease [16]. Early-phase studies delineates a distinct risk profile in COVID-19 patients with chronic liver disease, demonstrating robust correlations between hepatic functional reserve and clinical outcomes. A meta-analysis integrating 74 studies revealed that CLD significantly elevates COVID-19 mortality risk [17]. Marjot et al. demonstrated significantly elevated COVID-19 mortality in cirrhotic patients compared to non-cirrhotic controls, with further stratification revealing mortality increments of 20.0% for Child-Pugh B and 38.1%for Child-Pugh C cirrhosis relative to non-CLD patients [18]. Notably, 20% of compensated cirrhosis patients progress to acute-on-chronic liver failure (ACLF) post-infection, while nearly half of decompensated cases develop severe hepatic complications [19, 20].

However, whether Omicron maintains this risk profile remains controversial, as recent studies report comparable mortality between cirrhotic and non-cirrhotic cohorts but lack longitudinal hepatic function assessment and quantitative pulmonary imaging characterization [21]. Previous retrospective studies on cirrhotic patients with COVID-19 predominantly relied on conventional severity stratification, lacking phenotype-driven subgroup characterization [18, 22]. To address critical evidence gaps, this study conducted comparative analyses of cirrhotic patients hospitalized for COVID-19-related respiratory symptoms versus those admitted for cirrhosis, all with confirmed Omicron variant infection. Through Artificial intelligence (AI)-assisted quantification of CT imaging coupled with longitudinal hepatic function evaluation, we systematically delineated symptom heterogeneity and characterized pre-/post-infection liver injury patterns in this vulnerable population. Furthermore, we conducted a comparative analysis of COVID-19 clinical manifestations between cirrhotic patients and non-cirrhotic controls infected with the Omicron variant. This study illuminates novel pathways for addressing critical clinical decision-making challenges in balancing COVID-19 containment and cirrhosis-related complications during the Omicron-dominant phase.

Method

Study design and population

After reviewing overall non-elective in-patients from the First Affiliated Hospital of Zhejiang University School of Medicine between 26 December 2022, and 27 January 2023, we conducted an observational cohort study on 82 consecutive patients. Inclusion criteria for patients diagnosed with SARS-CoV-2 infection via reverse-transcriptase polymerase chain reaction (RT-PCR) of nasopharyngeal swab specimens were included in the study, while those with active malignancies, or prior solid-organ transplantation history were systematically excluded to minimize confounding clinical variables. Patients were divided into two groups: Group CR (47 patients hospitalized for respiratory symptoms related to SARS-CoV-2 infection) and Group CC (35 patients hospitalized for complications of cirrhosis). To assess the impact of pre-exited cirrhosis on in-patients with COVID-19, the control patients were selected from non-cirrhosis patients infected with COVID-19 to match at CR cohort for age and gender, hypertension and diabetes mellitus. For those cases involved in the control group, we excluded those who had hepatic dysfunction, other respiratory diseases, malignant tumors, organ transplants and other systemic diseases except hypertension and diabetes mellitus.

Data recorded were clinical, biochemical, radiologic findings, reasons for hospitalization, and survival outcome till day 28. Laboratory testing included a serum C-reactive protein, liver function test, coagulation testing and cytokine. We also assessed the Child-Pugh, model for end-stage liver disease (MELD) scores for cirrhosis patients. To simplify the analysis, COVID-19 positive cases were briefly categorized into two levels of severity based on the oxygen supplementation: severe COVID-19 was identified as need of mask oxygen therapy or higher flow oxygen therapy, the other needed lower oxygen supplementation or not needed oxygen supplementation were milder cases. The liver function perturbations of cirrhotic patients before and after COVID-19 were evaluated by biochemical data and the 2 compared to the last outpatient visit or the end of the last hospitalization before this infection. Due to the retrospective nature of this study, pre-infection medical records could be located for only 40 patients.

Artificial Intelligence (AI)-aided analysis of chest CT

AI-assisted detection system has been increasingly utilized in research settings [23,24,25,26]. Our AI analytical model performs quantitative analysis of thoracic CT scans, identifying inflammatory lesions through multi-region anatomical assessment. The hallmark radiological features of COVID-19 pneumonia– ground-glass opacities (GGO), consolidations, and ​reticular patterns– are reliably identifiable through AI-assisted analysis. However, differentiating mixed patterns remains technically challenging, particularly given the system’ ​limited accuracy in distinguishing between GGO and consolidation areas. We therefore pragmatically merged GGO and consolidation metrics into a unified “lesion” classification ​quantified by lesion proportion, while maintaining separate quantification of ​reticular patterns. Additionally, ​parenchymal bands data were provided and, similar to reticular patterns, were quantified based on the number of discrete lesions.

Statistical analysis

Statistics were performed using SPSS Statistics program (version 25.0) and Graphpad Prism (version 9.0.0). Continuous variables are reported as mean ± standard deviation for normally distributed data or median and interquartile range (IQR) for non-normally distributed data. Categorical variables are presented as percentages (%). The Chi-square test (or Fisher’s exact test) was utilized for categorical variables, while continuous variables were compared using the Student’s t-test, the Mann-Whitney U test, or the Kruskall-Wallis test, as appropriate. Univariate and multivariate Cox regression analyses were employed to identify factors associated with mortality. Kaplan-Meier survival analysis and the Log-Rank test were conducted to assess survival. No imputation was performed on the missing data. For all comparisons, results were considered statistically significant at P < 0.05.

Result

Baseline clinical characteristics of patients with cirrhosis and SARS-CoV-2 infection

From December 26, 2022, to January 27, 2023, 82 hospitalized cirrhosis patients with documented SARS-CoV-2 infection were enrolled. These patients were stratified into two cohorts: 47 patients (57.32%) admitted primarily for SARS-CoV-2-related respiratory symptoms (e.g., fever, chest tightness, dyspnea), and 35 patients (42.68%) hospitalized for cirrhosis complications with minimal or no SARS-CoV-2-related symptoms (Fig. 1). Subsequent analyses compared clinical, biochemical, and pulmonary CT imaging features between groups.

As delineated in Table 1, the respiratory symptom cohort (Group CR) demonstrated higher rates of fever (74.47% vs. 40.00%, p = 0.002), elevated peak body temperatures (38.60 ± 1.18 °C vs. 37.77 ± 0.86 °C, p = 0.001), and greater incidence of severe COVID-19 (36.17% vs. 14.29%, p = 0.027) compared to the cirrhosis complication cohort (Group CC). CT imaging revealed significantly larger total pulmonary inflammatory lesions in the Group CR (16.1 [5.85–43.2]% vs. 3.1 [0.8–13.08]%, p = 0.002), with similar trends across individual lung lobes (p < 0.05). Conversely, the Group CC exhibited elevated markers of hepatic dysfunction (TB, DB, INR, PT, APTT, D-dimer, AST, ALP; p < 0.05), reduced ALB and PLT levels (p < 0.05), higher Child-Pugh score variability (p = 0.01), increased MELD ≥ 15 prevalence (42.86% vs. 17.02%, p = 0.01), and higher rates of decompensation (96.29% vs. 31.43%) and liver failure (31.43% vs. not reported) compared to the Group CR (p < 0.05). These findings indicate distinct clinical profiles: the Group CR manifested more severe respiratory involvement, while the Group CC demonstrated exacerbated hepatic impairment.

Fig. 1
figure 1

Patient Recruitment and Matching Flowchart. This study enrolled 82 cirrhotic patients who were stratified into groups based on their primary admission diagnoses: Group CC (patients hospitalized for complications of cirrhosis) and Group CR (patients hospitalized for respiratory symptoms related to SARS-CoV-2 infection) groups. Concurrently, the Group CR was matched with a control Group(NC) according to the same inclusion and exclusion criteria

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Table 1 Baseline clinical characteristics of patients with cirrhosis and SARS-Cov-2 infection
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Limited hepatic impact of SARS-CoV-2 Omicron variant in cirrhosis

Longitudinal analysis of 40 patients (23 CR, 17 CC) comparing pre- and post-infection parameters revealed minimal hepatic functional changes post-Omicron infection (Table 2). Only ALB levels significantly declined (33.1 [31.1–35.1] g/L vs. 28.6 [26.8–34.9] g/L, p = 0.001), with no significant alterations in other biochemical markers or ascites prevalence. These results suggest Omicron infection does not substantially exacerbate pre-existing liver dysfunction in cirrhotic patients.

Table 2 Comparison of biochemical and clinical characteristics of cirrhotic patients before SARS-Cov2 infection and at SARS-CoV-2 diagnosis
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Exacerbated inflammatory responses in cirrhotic COVID-19 patients

Comparative analysis with non-cirrhotic COVID-19 patients revealed heightened inflammatory burden in cirrhotic individuals (Table 3). The Group CR demonstrated more extensive pulmonary lesions (16.1 [5.58–43.2]% vs. 5.7 [2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17]%, p = 0.02), elevated proinflammatory cytokines (IL-6: 11.96 [4.16–52.31] vs. 5.13 [3.18–7.7] pg/mL, p = 0.026; IL-8: 12.47 [5.58–43] vs. 5.11 [1.88–9.68] pg/mL, p < 0.001), and marked hepatic parameter abnormalities (AST, ALP, GGT, TB, DB, INR, PT, D-dimer; p < 0.05) compared to non-cirrhotic controls. This underscores the dual burden of enhanced systemic inflammation and baseline hepatic compromise in cirrhotic COVID-19 patients.

Table 3 Comparison of clinical and biochemical characteristics of cirrhotic patients and no-cirrhosis patients
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Predictors of 28-Day mortality in cirrhotic COVID-19 patients

The overall 28-day mortality rate was 18.29% (n = 15), with median survival of 7 (4–12) days. Mortality rates differed non-significantly between CR (12.8%, 95% CI 2.9–22.7) and CC groups (25.7%, 95% CI 10.5–40.9; p = 0.134) (Figs. 2A-B). Multivariate analysis identified MELD ≥ 15 (HR 42.406; 95% CI 1.320–1362.248), prolonged APTT (HR 1.282; 95% CI 1.060–1.550), and pulmonary lesion extent (HR 1.072; 95% CI 0.014–1.134) as independent mortality predictors (Table 4). Survival curves (Figs. 3A-C) confirmed significantly higher mortality with MELD ≥ 15, elevated APTT (> median), and extensive lung involvement (> median). Etiology of cirrhosis, comorbidities, and other biochemical markers showed no mortality association in univariate analysis.

Fig. 2
figure 2

28-day probability of overall mortality and mortality related to causes of hospitalization (A): The 28-day probability of overall mortality. (B): The 28-day probability of overall mortality according to the causes of hospitalization

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Fig. 3
figure 3

28-day probability of overall mortality according to APTT, MELD and lesions proportion. (A): The 28-day probability of overall mortality according to APTT ≥ 38.9. (B): The 28-day probability of overall mortality according to lesions proportion ≥ 29.7%. (C): The 28-day probability of overall mortality according to MELD ≥ 15. CR: patients hospitalized for respiratory symptoms related to SARS-CoV-2 infection; CC, patients hospitalized for complications of cirrhosis

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Table 4 Risk factors of 28-day mortality in cirrhotic patients at COVID-19 diagnosis
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Discussion

This study characterizes the clinical, biochemical, and pulmonary CT imaging features of cirrhotic patients infected with the SARS-CoV-2 Omicron variant. Our findings reveal heterogeneity in COVID-19 manifestations among cirrhotic patients: those hospitalized for respiratory symptoms related to SARS-CoV-2 infection exhibited more extensive pulmonary lesions and higher inflammatory markers but no significant increase in 28-day mortality compared to non-cirrhotic controls. Conversely, patients admitted primarily for hepatic decompensation demonstrated milder respiratory symptoms and less severe pulmonary involvement. Notably, our findings indicate that Omicron infection in cirrhotic patients did not induce significant perturbations in liver function parameters, with the exception of a marked reduction in serum albumin levels.

Current evidence regarding pulmonary CT features in cirrhotic patients following SARS-CoV-2 infection remains limited. This study is the first to employ AI-based CT quantification for assessing pulmonary infiltration extent, integrating multidimensional clinical data to delineate the clinical phenotypic heterogeneity of cirrhotic patients infected with the SARS-CoV-2 Omicron variant. While prior studies reported similar qualitative chest imaging features between cirrhotic and non-cirrhotic individuals [27], our quantitative analysis provides critical insights. This study demonstrated that cirrhotic patients hospitalized with COVID-19-related respiratory syndrome exhibited more severe pulmonary lesions and significantly elevated IL-6/IL-8 levels compared to non-cirrhotic COVID-19 patients. These findings corroborate the established association between pre-existing liver disease and poorer prognostic outcomes in SARS-CoV-2 infection [28, 29]. We propose that compensatory cirrhosis with low-grade systemic inflammation predisposes to immune hyperactivation upon SARS-CoV-2 infection (“second-hit” mechanism) [30]. Paradoxically, patients admitted primarily for hepatic decompensation exhibited higher COVID-19-related fever incidence and more severe pulmonary involvement. These findings may be linked to divergent immune profiles across cirrhosis stages [30]. Previous studies of HIV-infected cases with COVID-19 have indicated that immunosuppression due to HIV infection may be protective against COVID [31,32,33,34]. A recent study observed that HIV-infected individuals have a lower risk of Omicron variant infection than HIV-negative people [35]. It was assumed that lower CD4 count in HIV-infected individuals could reduce the excessive immune response to COVID-19, resulting in milder symptoms in these individuals [36]. Immune dysfunction associated with cirrhosis includes a distinct spectrum of immune alterations, which varied at different stages [37]. Patients with advanced cirrhosis usually showed high-grade systemic inflammatory phenotype with intense immune paralysis, in contrast to the low-grade systemic inflammatory phenotype in compensated cirrhosis [30]. One of the hallmarks in the immunopathology mechanisms of severe cases in COVID-19 is a hyperinflammatory innate immune response along with an inadequate adaptive response may elicit extensive local and systemic tissue injury [38]. The immune paralysis in advanced cirrhosis might partly explain the milder respiratory symptoms of COVID-19 and less pulmonary CT lesions as immunosuppression may tamper the cytokine storm of COVID-19.

Multivariate analysis identified MELD ≥ 15, prolonged APTT, and pulmonary lesion burden as independent predictors of 28-day outcomes. The exceptionally wide confidence interval for MELD ≥ 15 (1.320–1362.248) necessitates validation in expanded cohorts. Previous studies demonstrated that COVID-19 infection significantly increases the proportion of cirrhotic patients progressing to end-stage liver disease (MELD ≥ 15), with MELD scores established as an independent predictor of mortality [39]. Moon et al. further demonstrated a strong correlation between COVID-19 mortality and MELD scores in cirrhotic populations [29]. In our cohort, despite statistical uncertainties, the high event rate (39.1%) in the MELD ≥ 15 subgroup highlights its potential utility for risk stratification. Future prospective studies with larger sample sizes will refine these effect estimates.

Notably, Omicron infection did not significantly elevate liver enzymes in cirrhotic patients, contrasting with earlier variants [40, 41]. This discrepancy may reflect the attenuated virulence of Omicron, as demonstrated by Zhang et al. in their analysis of 1,001 hospitalized patients showing a lower incidence of liver injury compared to Delta-variant infection [42]. Notably, Twohig et al. further observed reduced mortality rates among cirrhotic patients during the Omicron-dominant phase relative to earlier variant waves [43].However, the observed serum albumin decline post-infection aligns with reported risks of ascites exacerbation, suggesting Omicron-dominant may indirect hepatic dysfunction via systemic inflammation rather than direct viral cytopathy [41, 43, 44]. Pulmonary lesion severity remained a key prognostic determinant, consistent with the Moon et al. [27]. Further multicenter studies are needed to elucidate causal relationships between albumin dynamics and delayed hepatic decompensation in this population.

Several limitations of this study should be explicitly acknowledged. Firstly, the inherent constraints of our single-center retrospective design, particularly regarding sample size limitations exacerbated by reduced cirrhotic admissions during the COVID-19 pandemic.Secondly, the current AI-based imaging analysis system exhibits technical constraints in accurately differentiating ground-glass opacities from consolidation areas, necessitating pooled analysis of heterogeneous lesion types when assessing pneumonia severity. This non-specific evaluation approach might hinder precise interpretation of pathophysiological mechanisms. Future multicenter prospective cohort studies incorporating refined AI lesion segmentation algorithms should be conducted to validate these findings and further elucidate the heterogeneous mechanisms underlying Omicron variant infection in cirrhotic populations.

Conclusion

In conclusion, SARS-CoV-2 Omicron variants elicit a more pronounced inflammatory response in cirrhotic patients compared to non-cirrhotic patients, yet they do not exacerbate liver function or lead to cirrhosis decompensation. Cirrhotic patients with advanced liver disease tend to exhibit milder respiratory symptoms and pulmonary lesions. These findings highlight the complex interplay between Omicron infection and cirrhosis, emphasizing the need for tailored clinical management strategies for this patient population.

Data availability

All data and materials in this article are included in the manuscript.

Abbreviations

COVID-19:

Corona Virus Disease 2019

SARS-CoV-2:

Severe Acute Respiratory Syndrome Coronavirus-2

ACLF:

Acute-on-chronic liver failure

CT:

Computerized tomography

PCR:

Polymerase chain reaction

CR:

Patients hospitalized for respiratory symptoms related to SARS-CoV-2 infection

CC:

Patients hospitalized for complications of cirrhosis

MELD:

Model for end-stage liver disease

AI:

Artificial intelligence

IQR:

Interquartile range

HBV:

Hepatitis B virus

AIH:

Autoimmune hepatitis

ALB:

Albumin

ALT:

Alanine aminotransferase

AST:

Aspartate aminotransferase

ALP:

Alkaline phosphatase

GGT:

γ-glutamyltransferase

TB:

Total bilirubin

DB:

Direct bilirubin

INR:

International normalized ratio

PT:

Prothrombin time

APTT:

Activated partial thromboplastin time

PLT:

Platelets

WBC:

White blood cell

HGB:

Hemoglobin

CRP:

C reactive protein

IL-1β:

Interleukin- 1β

IL-2:

Interleukin- 2

IL-4:

Interleukin- 4

IL-6:

Interleukin- 6

IL-8:

Interleukin- 8

IL-10:

Interleukin- 10

IL-17A:

Interleukin- 17 A

IL-12P70:

Interleukin- 12P70

IFN-α:

Interferonα

IFN-γ:

Interferonγ

TNF-α:

Tumor necrosis factor-α

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Funding

This study was funded by Shandong Provincial Laboratory Project (SYS202202), the Research Project of Jinan Microecological Biomedicine Shandong Laboratory (JNL-2025001 A), Natural Science Foundation of China(32270068), National Key R&D Program of China (2021YFC2301804, 2022YFC3602000).

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Authors and Affiliations

  1. Shandong First Medical University, Jinan City, 250022, China

    Fengjiao Wang

  2. Jinan Microecological Biomedicine Shandong Laboratory, Jinan City, 250022, China

    Fengjiao Wang & Lanjuan Li

  3. State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, National Medical Center for Infectious Diseases, Zhejiang University School of Medicine, 79 Qingchun Rd, Hangzhou City, 310003, China

    Lingxiao Zhu, Yanfei Chen & Lanjuan Li

Authors
  1. Fengjiao Wang
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  2. Lingxiao Zhu
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  3. Yanfei Chen
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  4. Lanjuan Li
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Contributions

Z.L. played a role in the acquisition of clinical data from patients with COVID-19 and liver cirhosis, while W.F. is responsible for the procurement, organization, and analysis of clinical data, as well as the composition of articles. All authors read and approved the final manuscript.

Corresponding authors

Correspondence to Yanfei Chen or Lanjuan Li.

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Ethics approval and consent to participate

Our study received approval from the Institutional Review Boards at the The First Affiliated Hospital, Zhejiang University School of Medicine (IIT20210312B-R1). As a retrospective study using anonymized clinical data, the ethics committee waived the requirement for individual patient consent. We certify that the study was performed in accordance with the 1964 Declaration of Helsinki and later amendments.

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Not applicable.

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The authors declare no competing interests.

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Wang, F., Zhu, L., Chen, Y. et al. Clinical manifestations of SARS-CoV-2 Omicron infection is associated with the stage of liver cirrhosis. BMC Infect Dis 25, 630 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12879-025-11040-z

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  • DOI: https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12879-025-11040-z

Keywords

BMC Infectious Diseases

ISSN: 1471-2334

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