Evaluation of a strain Long human respiratory syncytial virus with M2–2 gene deletion in intranasally vaccinated BALB/c mice

By
Ri-gan Shu
Jie Jun
Yun-xuan Zheng
Dan-ning Yue
Hao Hu
Hua-wei Xu
Xiao-lei Zhao
Hong-ru Wang
Xi-man Liu
Yi-peng Zhang
He Wang
Jie-mei Yu
Yan-peng Zheng
Xiang-lei Peng
Yuan-hui Fu
Jin-sheng He
June 8, 2026
0 min

Frontiers In Immunology

Overview

This study evaluates a recombinant RSV strain lacking the M2-2 gene, demonstrating reduced viral replication and enhanced immune responses in BALB/c mice. The findings support the potential of this strain as a candidate for live-attenuated vaccines against RSV.

Background

Incorporate statistics on RSV morbidity and mortality to emphasize the public health need.

Data Highlights

Strain	Lung Viral Load	Body Weight Loss
RLΔM2-2	Significantly lower	Less pronounced
RLΔM2-2112	Higher	More pronounced

Key Findings

The recombinant strain RLΔM2-2 showed reduced replication in HEp-2 and Vero cells compared to the parental strain.
In BALB/c mice, RLΔM2-2 resulted in lower lung viral loads and less body weight loss than RLΔM2-2112.
Intranasal immunization with RLΔM2-2 induced robust systemic and pulmonary immune responses.
The immune response included preF-specific antibodies and RSV-specific CD8+ T-cell responses with a Th1-biased profile.
Vaccination with RLΔM2-2 conferred protection against subsequent RSV challenges without enhanced respiratory disease.

Clinical Implications

The findings suggest that the M2-2 deletion strategy may enhance the safety and efficacy of RSV live-attenuated vaccines. This approach could lead to the development of effective immunization options for infants and young children, addressing a critical gap in current RSV prevention strategies.

Conclusion

The study supports the potential of the M2-2 deletion strategy in developing safe and effective RSV vaccines. Further evaluation of this recombinant strain is warranted to advance RSV vaccine development.