Inactivation of hepatitis C virus infectivity by human breast milk.
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.


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.
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, Hannover 30625, Germany.
Stephanie
S
Pfaender
Julia
J
Heyden
Martina
M
Friesland
Sandra
S
Ciesek
Asim
A
Ejaz
Joerg
J
Steinmann
Jochen
J
Steinmann
Angelika
A
Malarski
Heribert
H
Stoiber
Georgios
G
Tsiavaliaris
Werner
W
Bader
Gerhard
G
Jahreis
Thomas
T
Pietschmann
Eike
E
Steinmann
D045744:Cell Line, Tumor; D004355:Drug Stability; D019286:Endopeptidase K / Q000494:pharmacology; D005230:Fatty Acids, Nonesterified / Q000737:chemistry / Q000302:isolation & purification / Q000494:pharmacology; D061353:Food Storage; D016174:Hepacivirus / Q000187:drug effects* / Q000472:pathogenicity; D006526:Hepatitis C / Q000635:transmission / Q000821:virology; D006801:Humans; D018445:Infectious Disease Transmission, Vertical; D008049:Lipase / Q000037:antagonists & inhibitors; D008895:Milk, Human / Q000737:chemistry / Q000201:enzymology / Q000502:physiology* / Q000821:virology; D008954:Models, Biological; D019562:Viral Load / Q000187:drug effects; D014771:Virion / Q000187:drug effects; D038301:Virus Inactivation / Q000187:drug effects*
D005230:Fatty Acids, Nonesterified; D008049:Lipase; D019286:Endopeptidase K
antiviral; breast milk; free fatty acids; hepatitis C virus (HCV); transmission