Premium
Proteomic methods reveal cyclophilin a function as a host restriction factor against rotavirus infection
Author(s) -
He Haiyang,
Mou Zhirong,
Li Wanling,
Fei Lei,
Tang Yan,
Zhang Ji,
Yan Ping,
Chen Zhengqiong,
Yang Xia,
Shen Zigang,
Li Jintao,
Wu Yuzhang
Publication year - 2013
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.201100579
Subject(s) - cypa , cyclophilin a , downregulation and upregulation , biology , rotavirus , diarrhea , host factor , host (biology) , virology , immunology , microbiology and biotechnology , virus , gene , genetics , medicine
Rotavirus ( RV ) infection is the main cause of acute dehydrating diarrhea in infants and young children below 5 years old worldwide. RV infection causes a global shutoff of host proteins as many other viruses do. However, previous studies revealed that RV could selectively upregulated the expression of some host proteins that then played important roles in RV infection. To globally explor such host proteins that were upregulated in early human rotavirus ( HRV ) infection, proteomic methods were used and a total of ten upregulated host proteins were unambiguously identified. Cyclophilin A ( CYPA ), a peptidyl‐prolyl cis‐trans isomerase, was among these upregulated host proteins. Following infection, CYPA was recruited to the viroplasm and interacted with HRV structural protein VP 2; CYPA reduced host susceptibility to HRV infection and inhibited replication of HRV by repressing the expression of viral proteins. Furthermore, we found that the increased expression of CYPA in enterocytes of small intestine correlated to the period when BALB /c mice became resistant to RV diarrhea. Together, we identified CYPA as a novel host restriction factor that confered protection against RV infection and might contribute to host susceptibility to RV diarrhea.