HEPATITIS / YOUNOSSI
FIGURE 1. Genomic
organization of hepatitis C virus. C = core; E = envelope; NS =
nonstructural; UTR = untranslated regions; IRES = internal ribosome entry
site. Adapted with kind permission from Fang JWS, et al.52
Hepatitis C
Epidemiology.
Approximately 3.9 million Americans (1.8% of the population) and over
170 million people worldwide have evidence of HCV infection.1
Of the 3.9 million Americans infected with HCV, 2.7 million are
chronically infected.41 Because institutionalized individuals
were not represented in these surveys, these numbers very likely
underestimate the true prevalence of HCV. Minority populations are
typically overrepresented among HCV-positive patients, adding to the
healthcare burden of populations least likely to have access to adequate
and effective medical care. Chronic HCV infection leads to 8,000 to 10,000
deaths annually. The frequency of patients presenting with complications
associated with HCV infection is expected to triple within the next 20
years, corresponding to a 61% increase in incidence of cirrhosis, a 68%
increase in the incidence of HCC, a 279% increase in decompensated liver
disease, and a 528% increase in the demand for liver transplantation.42–48
HCV is a complex, single-stranded RNA virus that belongs to the Flaviviridae family.49–51 Although HCV has not yet been cultivated in cell culture, details of its molecular structure have been revealed in recent years (Figure 1).52
The envelope glycoproteins are coded for by the hypervariable region of the HCV genome, and the high mutation rates associated with these protein structures may be responsible for viral escape from the host immune responses. Variability of these protein structures is reflected in the existence of several HCV variants with different geographic distribution and response to therapy.53–56 At least 6 different HCV genotypes, as well as subtypes within genotypes, have been identified by nucleotide sequencing.57–59 In addition, variants may arise within a host that are not sufficiently distinct to be termed genotypes. These variants are referred to as quasispecies,60–64 the generation of which may relate to infectivity, chronicity, and resistance to therapy.61,62,65–69
The HCV is now known to have caused most cases of non-A, non-B hepatitis prior to identification of HCV and was the major cause of transfusion-associated hepatitis until screening of the blood supply became feasible in the early 1990s.70–72 Currently, the risk of transfusion-associated HCV is less than 1 unit per 103,000 units transfused.73 Injection drug users continue to account for over half of the new infections reported annually, with other parenteral exposures such as tattooing, body piercing, and needlestick accidents accounting for the other cases.74–76 Despite these known risk factors, 30% to 40% of patients with acute HCV deny specific exposure associated with acquiring the infection in the 6 months prior to the onset of illness.20 The risk of transmission of HCV via sexual activity for patients with a steady partner appears to be low,76–79 and transmission by sexual or household exposures accounts for less than 10% of cases. The likelihood of perinatal transmission is approximately 5%, with a very low risk of chronic infection developing in the infant.80,81
Volume 67 Supplement 1
Cleveland Clinic Journal of Medicine
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