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ARS Home » Northeast Area » Wyndmoor, Pennsylvania » Eastern Regional Research Center » Food Safety and Intervention Technologies Research » Research » Publications at this Location » Publication #277698

Title: High pressure inactivation of human norovirus-like particles: evidence that the capsid of human norovirus is highly pressure resistant

item LOU, FANGFEI - The Ohio State University
item HUANG, PENGWEI - Children'S Hospital - Cincinnati, Ohio
item NEETOO, HUDAA - University Of Delaware
item Gurtler, Joshua
item Niemira, Brendan
item CHEN, HAIQIANG - University Of Delaware
item JAING, XI - Children'S Hospital - Cincinnati, Ohio
item LI, JIANRONG - The Ohio State University

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/6/2012
Publication Date: 7/22/2012
Citation: Lou, F., Huang, P., Neetoo, H., Gurtler, J., Niemira, B.A., Chen, H., Jaing, X., Li, J. 2012. High pressure inactivation of human norovirus-like particles: evidence that the capsid of human norovirus is highly pressure resistant. Meeting Abstract. IAFP Annual Meeting., Providence, Rhode Island, July 22-25, 2012., Volume 1, Page 1.

Interpretive Summary:

Technical Abstract: High pressure processing (HPP) is a promising non-thermal technology to inactivate foodborne viruses. However, the effectiveness of HPP on inactivating human norovirus (HuNoV), the leading cause of acute gastroenteritis, is unknown because it cannot be propagated in cell culture. Therefore, developing a new model system to understand the survival of HuNoV is urgently needed. The objective of this study is to evaluate the stability of capsid of HuNoV to HPP using virus-like particles (VLPs) as a model. HuNoV VLPs were treated at pressures ranging from 500 to 900 MPa at 4 deg C for various holding times (from 1 to 60 min). The effectiveness of HPP on disrupting HuNoV capsid was evaluated by analyzing the integrity of VLP structure, and the binding to its functional receptors, histo blood group antigens (HBGAs). We found that pressurization at 500-600 MPa, the pressure capable of completely inactivating HuNoV surrogates (such as murine norovirus, MNV; and feline calicivirus, FCV) in 2 min, was not sufficient to disrupt the structure and function of HuNoV VLPs even with a holding time of 60 min. The disrupting efficacy of HPP increased with the pressure level. The time required for the complete disruption of HuNoV VLPs at 700, 800, and 900 MPa was 30, 10, and 2 min, respectively. Moreover, HuNoV VLPs were more resistant to HPP in their ability to bind the type A than the types B and O HBGAs. Additionally, the 23-nm VLPs appeared to be much more stable than the 38-nm VLPs. While HuNoV VLP is highly resistant to HPP, a level of 800-900MPa is capable of effectively disrupting HuNoV capsid within a short holding time. The apparent high resistance of HuNoV capsid to HPP also indicates that the HuNoV VLPs represents a better model than MNV and FCV to study the survival of HuNoV under various conditions. Better models will facilitate the use of HPP to inactivate pathogenic viruses, thereby improving the safety of shellfish and other foods.