What is the pathogenesis of cutaneous manifestations in hepatitis C virus (HCV) infection?

Updated: Mar 26, 2021
  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD  more...
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The causes of extrahepatic dermatologic manifestations of hepatitis C virus (HCV) infection relate to the nature of the virus, the method of infection, host responses to HCV infection, and myriad feedback considerations. HCV is a flavivirus with a positive sense single-strand RNA (ssRNA); the ends of the RNA are conserved. HCV RNA encodes 3300 amino acids. The polyprotein encoded is cleaved by host and viral proteases to yield at least 9 polypeptide proteins, core peptides, and viral envelope proteins E1 and E2 (which encode for glycoprotein spikes set in the host cell membrane derived envelope).

Six nonstructural (NS) proteins, termed NS2, NS3, NS4a, NS4b, NS5a, and NS5b, include RNA polymerase, cyclase, and other proteins necessary for viral replication. Hypervariable regions of the E2 envelope protein are responsible for quasi-species generation. Some nonessential sequences of NS genes also create variability in antigenic structure. Mutation of NS3 sections results in escape mutants that conserve essential viral functions while interfering with host T-cell function by down-regulating interleukin 2 and interferon gamma function and up-regulating interleukin 10. [15]

The chronicity of infection also relates to inoculum size, with high rates and worse disease in patients who have undergone transfusions and organ transplantation. The resulting persistent infection and immune stimulation create the many immunologic epiphenomenon, such as LP, mixed cryoglobulinemia, and thyroiditis. A generation of factors unfavorable to apoptosis control functions may favor malignant transformation in chronic hepatitis C infection.

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