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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 #237927
Title: Inactivation of HAV and norovirus surrogates within raw shellfish and other foods

Author
item Kingsley, David

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/25/2009
Publication Date: 5/8/2009
Citation: Kingsley,D. 2009. Inactivateion of HAV and norovirus surrogates within raw shellfish and other foods [abstract]. University of Bari,Italy. p.1.

Interpretive Summary:

Technical Abstract: High pressure processing can inactivate hepatitis A virus, (HAV) and the human norovirus surrogates, feline calicivirus (FCV) and murine norovirus (MNV), in foods such as oysters, strawberries, and green onions. A 5-min 400-Megapascals (MPa) treatment at 5 degrees C and a 1–min 400-MPa treatment at 9 degrees C are sufficient to inactivate 4.05 and 3.15 log10 Plaque-forming units (PFU) of MNV and HAV within oysters, respectively. For virus inactivation within strawberry puree and on the surface of green onions, a 5-min 375-MPa treatment at room temperature was sufficient to inactivate 4.32 and 4.75 log10 PFU of HAV, respectively. Recent studies have a 5-min, 400-MPa treatment of 1000 PFU of MNV within oyster extract was sufficient to protect STAT-1 -/- mice from infection after oral ingestion. Since human norovirus cannot be readily propagated in vitro, a human volunteer study is now being performed to evaluate the potential for high pressure to inactivate human norovirus directly within oysters. Evaluation of the effect of temperature on high pressure inactivation on HAV and human norovirus surrogates has been performed. Both surrogates, FCV and MNV, display markedly enhanced pressure-induced inactivation at colder temperatures, while the same temperature is protective for HAV when compared to inactivation at 20 degrees C. For example, a 4-min 200-MPa treatment of FCV inactivated 5.0 log10 PFU at -10 degrees C, but only 0.3 log10 PFU at 20 degrees C, while for MNV, a 5-min 350-MPa treatment inactivated 1.79 log10 PFU at 20 degrees C, but inactivated 5.56 log10 PFU at 5 degrees C. For HAV, a 1-min 400-MPa treatment at -10 degrees C only reduced the titer of HAV by 1.0 log10 PFU, but the same treatment at 20 degrees C resulted in a 2.5 log10 PFU reduction. Increasing salt and sugar concentration reduces the efficiency of high pressure inactivation for HAV and FCV. We find that low pH dramatically enhances the ability of high pressure to inactivate HAV.