Proteomic methods reveal cyclophilin A function as a host restriction factor against rotavirus infection
Related Experiment Video
Updated: May 15, 2026
Assays for the Specific Growth Rate and Cell-binding Ability of Rotavirus
Published on: January 28, 2019
Haiyang He1, Zhirong Mou, Wanling Li
1Institute of Immunology, Third Military Medical University, Chongqing, P. R. China.
Insights
Cyclophilin A (CYPA) is identified as a host protein that restricts rotavirus (RV) infection. Increased CYPA expression in the gut reduces RV replication and protects against diarrhea in young children.
Area of Science:
- Virology
- Immunology
- Gastroenterology
Background:
- Rotavirus (RV) is a leading cause of severe diarrhea in children globally.
- RV infection globally suppresses host protein expression but can upregulate specific host proteins.
- Understanding these host-pathogen interactions is crucial for developing interventions.
Purpose of the Study:
- To globally identify host proteins upregulated during early human rotavirus (HRV) infection.
- To investigate the role of Cyclophilin A (CYPA) in HRV infection and host susceptibility.
Main Methods:
- Proteomic analysis to identify upregulated host proteins during HRV infection.
- In vitro experiments to study CYPA recruitment, interaction with viral protein VP2, and its effect on viral replication.
- In vivo studies using BALB/c mice to correlate CYPA expression with resistance to RV diarrhea.
Main Results:
- Ten host proteins were identified as upregulated during early HRV infection.
- Cyclophilin A (CYPA) was found to be recruited to the viroplasm and interact with HRV protein VP2.
- Increased CYPA expression inhibited HRV replication by repressing viral protein expression.
- Elevated CYPA levels in mouse enterocytes correlated with resistance to RV-induced diarrhea.
Conclusions:
- CYPA acts as a novel host restriction factor against rotavirus infection.
- CYPA confers protection against RV infection and may influence host susceptibility to RV diarrhea.
Abstract:
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 VP2; 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.
