Genome-wide identification of interferon-sensitive mutations enables influenza vaccine design-Reference-Cited by-全球学者库

Genome-wide identification of interferon-sensitive mutations enables influenza vaccine design

Published:2018-01-19 Issue:6373 Volume:359 Page:290-296
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Du Yushen¹²^ORCID,Xin Li³,Shi Yuan¹^ORCID,Zhang Tian-Hao¹⁴^ORCID,Wu Nicholas C.⁴^ORCID,Dai Lei¹,Gong Danyang¹,Brar Gurpreet¹^ORCID,Shu Sara¹^ORCID,Luo Jiadi¹⁵⁶^ORCID,Reiley William⁷,Tseng Yen-Wen¹,Bai Hongyan³,Wu Ting-Ting¹^ORCID,Wang Jieru¹⁵^ORCID,Shu Yuelong³⁸,Sun Ren¹²⁴^ORCID

Affiliation:

1. Department of Molecular and Medical Pharmacology, University of California, Los Angeles, CA 90095, USA.

2. Cancer Institute, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, School of Medicine, Zhejiang University, Hangzhou 310058, China.

3. National Institute for Viral Disease Control and Prevention, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Chinese Center for Disease Control and Prevention, Key Laboratory for Medical Virology and Viral Diseases, Ministry of Health of the People's Republic of China, Beijing 102206, China.

4. Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA.

5. Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15224, USA.

6. Department of Pathology, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410005, China.

7. Trudeau Institute, Saranac Lake, NY 12983, USA.

8. School of Public Health (Shenzhen), Sun Yat-sen University, Guangdong 510275, China.

Abstract

Avoiding interferon avoidance Interferon (IFN) expression is a mammal's first response to viral infection. Many viruses have thus evolved mechanisms to evade IFN. Du et al. developed a method to systematically ablate IFN evasion genes from live, attenuated influenza virus (see the Perspective by Teijaro and Burton). A combination of mutants was assembled to construct a virus that triggered transient IFN responses in mice but that was unable to replicate effectively. The transient IFN responses led to robust antibody and memory responses that protected against subsequent challenge with different influenza viruses. This approach could be adapted to improve other RNA virus vaccines. Science , this issue p. 290 ; see also p. 277

Funder

National Institutes of Health

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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