Association of dynamics of anellovirus loads with hospital-acquired pneumonia in brain-injured patients during the intensive care unit stay.

Anelloviridae Hospital-acquired pneumonia Torque Teno Virus critically-ill

Journal

The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675

Informations de publication

Date de publication:
01 Mar 2024
Historique:
received: 05 10 2023
revised: 15 02 2024
accepted: 28 02 2024
medline: 2 3 2024
pubmed: 2 3 2024
entrez: 1 3 2024
Statut: aheadofprint

Résumé

Critical illness induces immune disorders associated with an increased risk of hospital-acquired pneumonia (HAP) and acute respiratory distress syndrome (ARDS). Torque Teno Virus (TTV), from the Anelloviridae family, are proposed as a biomarker to measure the level of immunosuppression. Our objective was to describe the kinetics of TTV DNA loads and their association with critical-illness related complications. We performed a longitudinal study in 115 brain-injured patients from a prospective cohort, collected endotracheal and blood samples at three time points (T1, T2, T3) during the two weeks post-admission in intensive care unit, and measured viral DNA loads using the TTV R-gene® kit (Biomerieux) and a pan-Anelloviridae in house qRT-PCR. TTV DNA was detected in the blood of 69, 71, and 64% of brain-injured patients at T1, T2 and T3 respectively. Time-associated variations of TTV and Anellovirus (AV) DNA loads were observed. Using a linear mixed-effects model, we found that HAP and ARDS were associated with lower blood AV DNA loads. Our results show that HAP or ARDS in critically ill patients are associated to changes in AV DNA loads, and should be evaluated further as a biomarker of immune disorders leading to these complications.

Sections du résumé

BACKGROUND BACKGROUND
Critical illness induces immune disorders associated with an increased risk of hospital-acquired pneumonia (HAP) and acute respiratory distress syndrome (ARDS). Torque Teno Virus (TTV), from the Anelloviridae family, are proposed as a biomarker to measure the level of immunosuppression. Our objective was to describe the kinetics of TTV DNA loads and their association with critical-illness related complications.
METHODS METHODS
We performed a longitudinal study in 115 brain-injured patients from a prospective cohort, collected endotracheal and blood samples at three time points (T1, T2, T3) during the two weeks post-admission in intensive care unit, and measured viral DNA loads using the TTV R-gene® kit (Biomerieux) and a pan-Anelloviridae in house qRT-PCR.
RESULTS RESULTS
TTV DNA was detected in the blood of 69, 71, and 64% of brain-injured patients at T1, T2 and T3 respectively. Time-associated variations of TTV and Anellovirus (AV) DNA loads were observed. Using a linear mixed-effects model, we found that HAP and ARDS were associated with lower blood AV DNA loads.
CONCLUSION CONCLUSIONS
Our results show that HAP or ARDS in critically ill patients are associated to changes in AV DNA loads, and should be evaluated further as a biomarker of immune disorders leading to these complications.

Identifiants

pubmed: 38428995
pii: 7617596
doi: 10.1093/infdis/jiae110
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© The Author(s) 2024. Published by Oxford University Press on behalf of Infectious Diseases Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Auteurs

L Castain (L)

Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN2, F-44000, Nantes, France.
Nantes Université, CHU Nantes, Service de Virologie, F-44000, Nantes, France.

M Petrier (M)

Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN2, F-44000, Nantes, France.

S Bulteau (S)

Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN2, F-44000, Nantes, France.

C Peltier (C)

Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN2, F-44000, Nantes, France.

C Poulain (C)

Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN2, F-44000, Nantes, France.
Nantes Université, CHU Nantes, Service d'Anesthésie Réanimation, F-44000, Nantes, France.

M Bouras (M)

Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN2, F-44000, Nantes, France.
Nantes Université, CHU Nantes, Service d'Anesthésie Réanimation, F-44000, Nantes, France.

B M Imbert-Marcille (BM)

Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN2, F-44000, Nantes, France.
Nantes Université, CHU Nantes, Service de Virologie, F-44000, Nantes, France.

J Poschmann (J)

Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN2, F-44000, Nantes, France.

A Roquilly (A)

Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN2, F-44000, Nantes, France.
Nantes Université, CHU Nantes, Service d'Anesthésie Réanimation, F-44000, Nantes, France.

C Bressollette-Bodin (C)

Nantes Université, CHU Nantes, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN2, F-44000, Nantes, France.
Nantes Université, CHU Nantes, Service de Virologie, F-44000, Nantes, France.

Classifications MeSH