Z Gastroenterol 2013; 51 - P_5_53
DOI: 10.1055/s-0032-1332167

Inactivation of Hepatitis C Virus by Human Breastmilk

S Pfaender 1, J Heyden 1, M Friesland 1, S Ciesek 2, A Ejaz 3, J Steinmann 4, C Rohrer 5, H Stoiber 3, G Tsiavaliaris 6, W Bader 7, G Jahreis 5, T Pietschmann 1, E Steinmann 1
  • 1TWINCORE, Centre for Experimental and Clinical Infection Research, Institute for Experimental Virology, Hannover, Germany
  • 2Hannover Medical School, Department of Gastroenterology, Hepatology and Endocrinology, Hannover, Germany
  • 3Medical University, Institute of Virology, Innsbruck, Austria
  • 4University Hospital Essen, Institute of Medical Microbiology, Essen, Germany
  • 5Friedrich-Schiller University, Department of Nutritional Physiology, Jena, Germany
  • 6Hannover Medical School, Research Centre for Structural Analysis, Hannover, Germany
  • 7KRH Klinikum Nordstadt Frauenklinik, Hannover, Germany

Aims: Chronic Hepatitis C virus (HCV) infection causes severe liver disease and affects more than 130 million individuals with up to 4 million new infections each year. The virus is spread through direct contact with blood, although alternative routes of transmission may contribute to the global burden of hepatitis C. 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 to assess the risks of HCV transmission via this route.

Methodology/Principal Findings:

Infectivity of HCV from different viral strains in the presence of breast milk of various donors was determined by limiting dilution assays, viral antigen detection. Human breast milk reduced HCV infectivity of all seven viral genotypes in a dose dependent manner. The antiviral effect of breast milk was species-specific since milk from various animals did not inhibit HCV infection. Notably, infant formula milk did not reduce HCV infectiousness. Treatment of HCV with human breast milk did not compromise integrity of viral RNA or capsids, but destroyed the lipid envelope of virus particles. Fractionation of breast milk components by ultracentrifugation revealed that the antiviral activity is present in the cream fraction containing the milk fat. Proteolytic digestion of milk proteins had no influence on its antiviral activity whereas prolonged storage at 4°C and temperatures above increased antiviral activity. Notably, pretreatment of milk with a lipase inhibitor ablated the antiviral activity and specific free fatty acids enriched during storage of human breast milk were antiviral against HCV.

Conclusions/Significance:

Taken together, these data indicate that human breast milk inhibits HCV infectiousness. 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, and should not be prevented unless other factors result in mammary tissue damage.