Mr. Brunetto et al., HEPATITIS-C VIRUS-INFECTION AND LIVER-DISEASE - PECULIAR EPIDEMIOLOGIC AND CLINICOPATHOLOGICAL FEATURES, FEMS microbiology reviews, 14(3), 1994, pp. 259-265
Hepatitis C virus (HCV) infection is associated with a wide spectrum o
f liver disease ranging from asymptomatic carriage to severe forms of
chronic hepatitis. HCV is not invariably pathogenic and generic hetero
geneity of HCV could be a major cause of such a variability. In clinic
al practice this means that presence and replication of the virus do n
ot invariably imply a virus-induced liver damage. IOM antibodies that
are the best diagnostic tools for the other forms of viral hepatitis a
re not sensitive and specific enough for hepatitis C, therefore we hav
e to look for alternatives. Detection of anti-HCV does not help to dis
tinguish past from present infections and only anti-HCV seroconversion
in previously negative patients can indicate a recent HCV infection.
However, the Significant association between serum anti-C100-3 and HCV
-RNA suggests that anti-HCV can be considered an indirect marker of HC
V infectivity. In anti-HCV-negative infections and early acute hepatit
is cases HCV-RNA detection will represent a valid diagnostic alternati
ve. In patients undergoing antiviral therapy monitoring anti-HCV by im
munoblotting assays and HCV-RNA by quantitative assays represent a val
id tool to predict response that invariably has occurred in patients w
ho had undetectable serum HCV-RNA and/or decreasing anti-HCV titres. A
ssays that detect multiple anti-HCV antibodies all together appear uns
uitable for monitoring because they miss the disappearance of single a
ntibodies. Anti-C22 appears the most frequent and earliest to be detec
ted and usually it has the highest titre. Anti-C100 titres decrease ea
rlier than anti-C33 and anti-C22 in patients with chronic HCV hepatiti
s who respond to antiviral therapy. The natural course of HCV infectio
n appears to be characterized by three consecutive phases: disease, as
ymptomatic carrier and recovery. If transition from the first to the l
ast occurs very slowly or the disease phase persists for years it may
warrant in susceptible hosts severe forms of liver disease.