Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Sep;34(5):e2577.
doi: 10.1002/rmv.2577.

Role of Gut Microbiota in Dengue

Adriana Pedreañez  1 , Yenddy Carrero  2 , Renata Vargas  2 , Juan P Hernandez-Fonseca  2   3 , Hugo Hernandez-Fonseca  4   5 , Jesús A Mosquera  2
Affiliations
Review

Role of Gut Microbiota in Dengue

Adriana Pedreañez et al. Rev Med Virol. 2024 Sep.

Abstract

Dengue is a disease caused by a flavivirus (DENV) and transmitted by the bite of a mosquito, primarily the Aedes aegypti and Aedes albopictus species. Previous studies have demonstrated a relationship between the host gut microbiota and the evolution of dengue. It seems to be a bidirectional relationship, in which the DENV can affect the microbiota by inducing alterations related to intestinal permeability, leading to the release of molecules from microbiota dysbiosis that can influence the evolution of dengue. The role of angiotensin II (Ang II) in the microbiota/dengue relationship is not well understood, but it is known that the renin-angiotensin system (RAS) is present in the intestinal tract and interacts with the gut microbiota. The possible effect of Ang II on the microbiota/Ang II/dengue relationship can be summarised as follows: the presence of Ang II induced hypertension, the increase in angiotensinogen, chymase, and microRNAs during the disease, the induction of vascular dysfunction, the production of trimethylamine N-oxide and the brain/microbiota relationship, all of which are elements present in dengue that could be part of the microbiota/Ang II/dengue interactions. These findings suggest the potential use of Ang II synthesis blockers and the use of AT1 receptor antagonists as therapeutic drugs in dengue.

Keywords: RAS; angiotensin II; dengue; flavivirus; gut microbiota; inflammation.

PubMed Disclaimer

References

    1. B. E. Martina, P. Koraka, and A. D. Osterhaus, “Dengue Virus Pathogenesis: An Integrated View,” Clinical Microbiology Reviews 22, no. 4 (2009): 564–581, https://doi.org/10.11128/CMR.00035‐09.
    1. D. Guha‐Sapir and B. Schimmer, “Dengue Fever: New Paradigms for a Changing Epidemiology,” Emerging Themes in Epidemiology 2, no. 1 (2005): 1, https://doi.org/10.1186/1742‐7622‐2‐1.
    1. E. Harris, E. Videa, L. Perez, et al., “Clinical, Epidemiologic, and Virologic Features of Dengue in the 1998 Epidemic in Nicaragua,” American Journal of Tropical Medicine and Hygiene 63, no. 1–2 (2000): 5–11, https://doi.org/10.4269/ajtmh.2000.63.5.
    1. C. C. Carlos, K. Oishi, M. T. Cinco, et al., “Comparison of Clinical Features and Hematologic Abnormalities Between Dengue Fever and Dengue Hemorrhagic Fever Among Children in the Philippines,” American Journal of Tropical Medicine and Hygiene 73, no. 2 (2005): 435–440.
    1. L. M. Proctor, H. H. Creasy, J. M. Fettweis, et al., “The Integrative Human Microbiome Project,” Nature 569, no. 7758 (2019): 641–648, https://doi.org/10.1038/s41586‐019‐1238‐8.