Role of ISGylation during Human Parainfluenza Virus Type 3 Infection 3302

Abstract Description Human parainfluenza virus type 3 (HPIV3) is an RNA virus belonging to the paramyxovirus family, which include clinically important viruses such as Nipah, Hendra, Mumps, and Measles. HPIV3 causes lower respiratory illnesses such as pneumonia, bronchiolitis and croup in infants and young children. ISGylation is a ubiquitin-like modification controlling various aspects of host response during infections. It was still unknown whether paramyxoviruses can trigger ISGylation during infection and the role of ISGylation, if any, during infection. We now show that HPIV3 can induce ISGylation in both myeloid immune (macrophages) and non-myeloid stromal (epithelial cells) cells. Interestingly, using ISGylation deficient lung epithelial cells, we demonstrate ISGylation playing an antiviral role during infection. Mechanistically, ISGylation restricted HPIV3 budding, possibly by impairing HPIV3 Matrix protein mediated budding from epithelial cells. Topic Categories Viral Immunology (VIR)

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Publication Details

Journal
The Journal of Immunology
Published
2025-11-01
DOI
https://doi.org/10.1093/jimmun/vkaf283.1118
Primary Topic
Virology and Viral Diseases
Type
article
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article

Role of ISGylation during Human Parainfluenza Virus Type 3 Infection 3302

Santanu Bose, Lindsay Grace Miller, Sudiksha Pandit, Michael A. Hoffman
The Journal of Immunology
Virology and Viral Diseases
article

Role of ISGylation during Human Parainfluenza Virus Type 3 Infection 3302

Santanu Bose, Lindsay Grace Miller, Sudiksha Pandit, Michael A. Hoffman
article en

Abstract

Abstract Description Human parainfluenza virus type 3 (HPIV3) is an RNA virus belonging to the paramyxovirus family, which include clinically important viruses such as Nipah, Hendra, Mumps, and Measles. HPIV3 causes lower respiratory illnesses such as pneumonia, bronchiolitis and croup in infants and young children. ISGylation is a ubiquitin-like modification controlling various aspects of host response during infections. It was still unknown whether paramyxoviruses can trigger ISGylation during infection and the role of ISGylation, if any, during infection. We now show that HPIV3 can induce ISGylation in both myeloid immune (macrophages) and non-myeloid stromal (epithelial cells) cells. Interestingly, using ISGylation deficient lung epithelial cells, we demonstrate ISGylation playing an antiviral role during infection. Mechanistically, ISGylation restricted HPIV3 budding, possibly by impairing HPIV3 Matrix protein mediated budding from epithelial cells. Topic Categories Viral Immunology (VIR)

The Journal of ImmunologyVol. 214(Supplement_1)
University of Wisconsin–La Crosse (US), Washington State University (US)
Openalex Percentile: Top 54%
Virology and Viral Diseases
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