Hepatitis C Virus mutations 'outrun' immune systems

Unlike its viral cousins Hepatitis A and B, Hepatitis C Virus has eluded the development of a vaccine and infected more than 170 million people worldwide. Approximately 700,000 people die each year from the infection. The creation of a vaccine seems far more difficult that those of its brethren, Hepatitis A Virus and B Virus. Research has now identified a biological mechanism that appears to play a big role in helping Hepatitis C Virus evade both the natural immune system and vaccines[1].
The study found that some mutations occur outside of the viral sites that are typically targeted by antibody responses. Those mutations could also account for the difficulty of making an effective vaccine.

The research discovered that the effectiveness of the antibodies varied, with some viral strains very inhibited by the antibodies and others hardly affected at all. To find out what was causing the variation, the researchers next tapped into the genomes of the Hepatitis C Virus, but found nothing.

The researchers then expanded their search to the proteins on the surface of Hepatitis C Virus. They found that, while mutations in the binding site were not associated with resistance, other mutations in the surface proteins away from the binding site correlated with viruses that persisted despite antibody treatment.

These are the mutations the researchers believe may allow the viruses to avoid being blocked by antibodies altogether. If you think of it like a race, the antibody is trying to bind to the virus before it can enter the cell. These mutations may allow the virus to get into the cell before it even encounters the immune system.

[1] El-Diwany et al: Extra-epitopic hepatitis C virus polymorphisms confer resistance to broadly neutralizing antibodies by modulating binding to scavenger receptor B1 in PloS Pathogens – 2017

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