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Updated: May 5, 2026

Sequencing of Bacterial Microflora in Peripheral Blood: our Experience with HIV-infected Patients
Published on: June 11, 2011
Human immunodeficiency virus-related microbial translocation and progression of hepatitis C
Ashwin Balagopal1, Frances H Philp, Jacquie Astemborski
1Division of Infectious Diseases, Viral Hepatitis Center, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
Background & Aims:
Human immunodeficiency virus (HIV)-1 infection has been associated with enhanced microbial translocation, and microbial translocation is a mechanism through which alcohol and some enteric conditions cause liver disease. We hypothesized that HIV promotes liver disease by enhancing microbial translocation.
Methods:
We studied human cohorts in which hepatitis C virus (HCV) and HIV outcomes were carefully characterized.
Results:
HIV-related CD4(+) lymphocyte depletion was strongly associated with microbial translocation as indicated by elevated levels of circulating lipopolysaccharide (LPS), LPS-binding protein, soluble CD14, and fucose-binding lectin (AAL) reactive to immunoglobulin G specific for the alpha-galactose epitope and suppressed levels of endotoxin core antibodies (EndoCAb IgM) in HIV-infected subjects compared with the same persons before they had HIV infection and compared with HIV-uninfected subjects. The same measures of microbial translocation were strongly associated with HCV-related liver disease progression (cirrhosis), eg, LPS, odds ratio, 19.0 (P = .002); AAL, odds ratio, 27.8 (P < .0001); in addition, levels of LPS were elevated prior to recognition of cirrhosis.
Conclusions:
Microbial translocation may be a fundamental mechanism through which HIV accelerates progression of chronic liver disease.
Insights
Human immunodeficiency virus (HIV) infection enhances microbial translocation, a key factor in liver disease progression. This study links HIV-related immune changes to increased microbial translocation, accelerating liver damage, particularly in hepatitis C virus (HCV) coinfection.
Area of Science:
- Immunology
- Hepatology
- Infectious Diseases
Background:
- Human immunodeficiency virus (HIV)-1 infection is linked to increased microbial translocation.
- Microbial translocation is a known mechanism contributing to alcohol- and enteric-related liver disease.
- HIV may promote liver disease by enhancing microbial translocation.
Purpose of the Study:
- To investigate the hypothesis that HIV infection promotes liver disease by enhancing microbial translocation.
- To assess the association between HIV infection, immune status, and markers of microbial translocation.
- To evaluate the role of microbial translocation in the progression of liver disease, particularly in the context of hepatitis C virus (HCV) coinfection.
Main Methods:
- Study of human cohorts with characterized hepatitis C virus (HCV) and HIV outcomes.
- Measurement of microbial translocation markers including lipopolysaccharide (LPS), LPS-binding protein, soluble CD14, and fucose-binding lectin (AAL).
- Assessment of endotoxin core antibodies (EndoCAb IgM) and correlation with HIV status, CD4(+) lymphocyte counts, and liver disease progression.
Main Results:
- HIV-related CD4(+) lymphocyte depletion strongly correlated with microbial translocation markers (elevated LPS, LPS-binding protein, soluble CD14, AAL; suppressed EndoCAb IgM).
- These microbial translocation markers were significantly associated with HCV-related liver disease progression to cirrhosis.
- Elevated LPS levels were observed prior to the clinical recognition of cirrhosis, suggesting early involvement.
Conclusions:
- Microbial translocation is a potential fundamental mechanism driving accelerated chronic liver disease progression in HIV-infected individuals.
- HIV-associated immune dysregulation contributes to increased microbial translocation.
- Targeting microbial translocation may be a therapeutic strategy to mitigate liver disease progression in HIV patients.
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