The hepatitis C virus (HCV) is known as the “silent epidemic” because many patients are unaware of their infection status and many cases go unrecognized and untreated for many years. Gaining a better understanding of how patients were infected could help clinicians in determining who to screen and treat.
Adding to the Mystery
The exact origin of the HCV is unknown, as are the mechanisms responsible for its pandemic spread in many parts of the world. Various dating and statistical methodologies have been employed to arrive at a “best guess” of HCV being several hundred years old, but the dramatic increase in the number of cases worldwide seems to have occurred after World War II.1
It has been speculated that nonhuman primates were somehow responsible for the spread of HCV to humans—similar to HIV—but no HCV or HCV-like viruses have been found in nonhuman primates. Adding to the mystery, nonprimate hepaciviruses (NPHVs) have been discovered in both horses and dogs.
In the few percent of horses found to be viremic with NPHV in a 2012 study,2 polymerase chain reaction–determined viral loads were comparable to what is observed in humans. The horses also showed some laboratory evidence of liver inflammation (elevated levels of γ-glutamyl transferase), but they did not appear to have any clinical symptoms referable to the liver.
In dogs, the NPHV was isolated from respiratory specimens in association with respiratory symptoms.3 In humans, HCV is not found in respiratory secretions, nor does it cause respiratory disease.
The Spread of a Blood-borne Virus
The HCV virus, a blood-borne virus, is inefficiently spread sexually in the absence of blood exposure. Much of the spread worldwide after World War II was a result of blood transfusions with HCV-contaminated blood or blood products, injection drug use and, in much of the world, the use of nonsterile medical equipment on multiple patients.
In the United States, about 1% of the population is infected with HCV, the third hepatitis virus discovered, after Hepatitis A virus (HAV) and hepatitis B virus (HBV). The existence of a “non-A, non-B” hepatitis virus associated with blood transfusions was known from the early 1970s. At that time, there were assays that detected HAV and HBV but not HCV.
1. Simmonds P. The origin of hepatitis C virus. Curr Top Microbiol Immunol. 2013;369:1-15.
2. Lyons S, Kapoor A, Sharp C, et al. Nonprimate hepaciviruses in domestic horses, United kingdom. Emerg Infect Dis. 2012;18:1976-1982.
3. Kapoor A, Simmonds P, Gerold G, et al. Characterization of a canine homolog of hepatitis C virus. Proc Natl Acad Sci USA. 2011;108:11608-11613.
4. HCV Epidemiology in the United States. Hepatitis C Online. Accessed February 21, 2017.
5. Treatment of HCV Genotype 1. Hepatitis C Online. Accessed February 21, 2017.
6. Shire NJ, Sherman KE. Epidemiology of hepatitis C virus: a battle on new frontiers. Gastroenterol Clin N Am. 2015;44:699-716.
7. Martin NK, Vickerman P, Foster GR, et al. Can antiviral therapy for hepatitis C reduce the prevalence of HCV among injecting drug user populations? A modelling analysis of its prevention utility. J Hepatol. 2011;54:1137-1144.