Cobalamins are stored in high concentrations in the human liver and thus ar
e available to participate in the regulation of hepatotropic virus function
s. We show that cyanocobalamin (vitamin B12) inhibited the H(IV internal ri
bosome entry site (IRES)-dependent translation of a reporter gene in vitro
in a dose-dependent manner without significantly affecting the cap-dependen
t mechanism. Vitamin B12 failed to inhibit translation by IRES elements fro
m encephalomyocarditis virus (EMCV) or classical swine fever virus (CSFV),
We also demonstrate a relationship between the total cobalamin concentratio
n in human sera and HCV viral load (a measure of viral replication in the h
ost), The mean viral load was two orders of magnitude greater when the seru
m cobalamin concentration was above 200 pM (P < 0.003), suggesting that the
total cobalamin concentration in an HCV-infected liver is biologically sig
nificant in HCV replication.