Overview of Hepatitis C and Skin

Connie M. Chung; Julia R. Nunley


Dermatology Nursing. 2006;18(5):425-430. 

In This Article


Hepatitis C virus, an RNA virus belonging to the Flaviviridae family, was first identified in 1989 as the primary cause of "non-A, non-B hepatitis" (Choo et al., 1989). With the only known natural host being humans, HCV is transmitted primarily through direct contact with infected blood or blood products (Pawlotsky, 2004). Exposure to tainted blood exists in a variety of contexts including intravenous drug use, blood transfusion (before 1992), solid organ transplantation from an infected donor, occupational exposure, tattoos, snorting cocaine through shared straws, high-risk sexual behavior, and maternal-infant transmission (Boyer et al., 2002). In the United States, the most common risk factor is intravenous drug use (Pearlman, 2004). Sexual transmission rates are very low; however, sexual promiscuity, co-infection with human immunodeficiency virus, or co-infection with herpes simplex type-2 increases the likelihood of sexual transmission (Pearlman, 2004; Poynard, Yuen, Ratziu, & Lai, 2003).

There are six distinct genotypes of HCV and multiple subtypes. Most of the clinical consequences of the different genotypes are identical although their response to therapy is dissimilar. Genotype 1 is the most common in the United States and is unfortunately the least responsive to therapy; genotypes 2 and 3 are much more amenable to therapy (Boyer et al., 2002; Lauer & Walker, 2001). The current standard treatment regimen is the combination of pegylated interferon and ribavirin (Boyer et al., 2002). Overall, about 60% of individuals who adequately complete this course of therapy successfully eradicate the virus and attain a sustained viral response (SVR); these individuals are essentially cured (Russo, Zacks, & Fried, 2003). However, the actual SVR rate for genotype 1 is closer to 55% whereas that of genotypes 2 and 3 is nearly 80% to 90% (Boyer et al., 2002). Studies have shown that liver histology and function improve and remain stable in those who obtain an SVR and the risk of developing hepatocellular carcinoma becomes almost zero (Tanikawa, 2004; Teoh & Farrell, 2004). Recent data suggest that even non-responders may have some benefit to therapy as well (Fargion, Fracanzani, & Valenti, 2004).


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