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Inactivation of Hepatitis C Virus Infectivity by Human Breast Milk
Stephanie Pfaender1,
Julia Heyden1,
Martina Friesland1,
Sandra Ciesek2,
Asim Ejaz3,
Joerg Steinmann4,
Jochen Steinmann5,
Angelika Malarski6,
Heribert Stoiber3,
Georgios Tsiavaliaris7,
Werner Bader8,
Gerhard Jahreis6,
Thomas Pietschmann1 and
Eike Steinmann1
+ Author Affiliations
1Institute for Experimental Virology, TWINCORE Centre for Experimental and Clinical Infection Research; a joint venture between the Medical School Hannover (MHH) and the Helmholtz Centre for Infection Research (HZI), Feodor-Lynen-Str. 7, Hannover 30625, Germany
2Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Germany
3Institute of Virology, Medical University, Innsbruck
4Institute of Medical Microbiology, University Hospital Essen, Essen, Germany
5MikroLab GmbH, Bremen, Germany
6Department of Nutritional Physiology, Institute of Nutrition, Friedrich Schiller University, Jena, Germany
7Institute for Biophysical Chemistry, Hannover Medical School, Hannover, Germany
8KRH Klinikum Nordstadt Frauenklinik, Hannover, Germany
Correspondence: PD Dr Eike Steinmann, Institute for Experimental Virology, TWINCORE, Centre for Experimental and Clinical Infection Research; a joint venture between the Medical School Hannover (MHH) and the Helmholtz Centre for Infection Research (HZI), Feodor-Lynen-Str 7, 30625 Hannover, Germany ([email protected]).
Abstract
Background. Hepatitis C virus (HCV) is spread through direct contact with blood, although alternative routes of transmission may contribute to the global burden. Perinatal infection occurs in up to 5% of HCV-infected mothers, and presence of HCV RNA in breast milk has been reported. We investigated the influence of breast milk on HCV infectiousness.
Methods/Results. Human breast milk reduced HCV infectivity in a dose-dependent manner. This effect was species-specific because milk from various animals did not inhibit HCV infection. Treatment of HCV with human breast milk did not compromise integrity of viral RNA or capsids but destroyed the lipid envelope. Fractionation of breast milk revealed that the antiviral activity is present in the cream fraction containing the fat. Proteolytic digestion of milk proteins had no influence on its antiviral activity, whereas prolonged storage at 4°C increased antiviral activity. Notably, pretreatment with a lipase inhibitor ablated the antiviral activity and specific free fatty acids of breast milk were antiviral.
Conclusions. The antiviral activity of breast milk is linked to endogenous lipase-dependent generation of free fatty acids, which destroy the viral lipid envelope. Therefore, nursing by HCV-positive mothers is unlikely to play a major role in vertical transmission.
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