Hantavirus: biology, immune responses, and pathogenesis
5 affiliations
- 1The Third Affiliated Hospital of Soochow University, Institutes for Translational Medicine, State Key Laboratory of Radiation Medicine and Protection, Biomedical Basic Research Center (BBRC) of Jiangsu, Suzhou Medical College of Soochow University, Suzhou, Jiangsu China
- 2Department of Experimental Medicine and Biochemical Sciences, University of Rome Tor Vergata, Rome, Italy
- 3Institute of Infection, Immunity and Transplantation, University College London, and University College London Hospitals NHS Foundation Trust, London, UK
- 4CAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China
- 5Unicamillus International Medical University, Rome, Italy
Abstract
The recent Andes virus (ANDV) outbreak on the MV Hondius cruise has raised global public health alarms due to its dangerous ability to person-to-person spread. Hantavirus infections primarily manifest as hemorrhagic fever with Eurasian renal syndrome (HFRS) and Americas hantavirus cardiopulmonary syndrome (HCPS), both characterized by endothelial manifestation. Two principal mechanisms, virus-mediated cytopathy and host-driven immunopathology, have been proposed to account for the pathological progression, while their interplay is yet to be fully explored. In this review, we synthesize the recent research on hantavirus biology, cellular entry mechanisms, and epidemiological characteristics, and particularly highlight that viral immune evasion and subsequent uncontrolled host immune responses act as the core pathogenic drivers. Hantaviruses employ diverse strategies to antagonize type I interferon signaling and autophagy, which delay early innate immune activation and enable extensive viral dissemination. The excessive activation of cytotoxic CD8⁺ T cells, natural killer (NK) cells, combined with functionally impaired regulatory T cells and dysregulated humoral immunity, initiates severe inflammatory cascades, which in turn disrupt endothelial barrier integrity and cause organ vasculopathy. We also outline current therapeutic and preventive strategies, along with key directions for future research. A better understanding of hantavirus immunopathogenesis will help develop improved countermeasures against this zoonotic disease.
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BibTeX
@article{shi2026hantavirus,
title = {{Hantavirus: biology, immune responses, and pathogenesis}},
author = {Yufang Shi and Mauro Piacentini and Alimuddin Zumla and Yu Wang and Qing Li and Ying Wang and Jun Zhou and Gerry Melino and Giuseppe Ippolito},
journal = {Cell Death \& Disease},
year = {2026},
month = sep,
doi = {10.1038/s41419-026-09235-6},
url = {https://doi.org/10.1038/s41419-026-09235-6},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Hantavirus: biology, immune responses, and pathogenesis
AU - Yufang Shi
AU - Mauro Piacentini
AU - Alimuddin Zumla
AU - Yu Wang
AU - Qing Li
AU - Ying Wang
AU - Jun Zhou
AU - Gerry Melino
AU - Giuseppe Ippolito
PY - 2026
DA - 2026/09/14
JO - Cell Death & Disease
DO - 10.1038/s41419-026-09235-6
UR - https://doi.org/10.1038/s41419-026-09235-6
AB - The recent Andes virus (ANDV) outbreak on the MV Hondius cruise has raised global public health alarms due to its dangerous ability to person-to-person spread. Hantavirus infections primarily manifest as hemorrhagic fever with Eurasian renal syndrome (HFRS) and Americas hantavirus cardiopulmonary syndrome (HCPS), both characterized by endothelial manifestation. Two principal mechanisms, virus-mediated cytopathy and host-driven immunopathology, have been proposed to account for the pathological progression, while their interplay is yet to be fully explored. In this review, we synthesize the recent research on hantavirus biology, cellular entry mechanisms, and epidemiological characteristics, and particularly highlight that viral immune evasion and subsequent uncontrolled host immune responses act as the core pathogenic drivers. Hantaviruses employ diverse strategies to antagonize type I interferon signaling and autophagy, which delay early innate immune activation and enable extensive viral dissemination. The excessive activation of cytotoxic CD8⁺ T cells, natural killer (NK) cells, combined with functionally impaired regulatory T cells and dysregulated humoral immunity, initiates severe inflammatory cascades, which in turn disrupt endothelial barrier integrity and cause organ vasculopathy. We also outline current therapeutic and preventive strategies, along with key directions for future research. A better understanding of hantavirus immunopathogenesis will help develop improved countermeasures against this zoonotic disease.
SN - 2041-4889
ER -