Andy Walsh: Recognizing the Discovery of Hepatitis C

From @AndyWalsh:

I thought the timeline was interesting to compare to our present circumstances. By the 1960s, we had recognized that blood transfusion recipients had higher rates of liver cancer and other liver diseases, and by the 1970s it was clear that not all of that risk could be explained by hepatitis B infections. But it wasn’t until 1989 that the hepatitis C virus was isolated and identified, leading to the availability of screening tests in the 1990s. Antiviral treatments are available; early options from the 1980s were developed to treat other viruses and presently available therapies can achieve 95% cure rates with fewer side effects than previous options. However, there is no licensed vaccine.

Compared to that multi-decade journey, it is astonishing that we are less than one year from the first human SARS-CoV-2 infections and already have an identified pathogen and multiple vaccine candidates and therapeutic options in final phases of clinical testing. There are some biological differences at play; for example, hepatitis C virus mutates at a higher rate and so there are seven distinct strains circulating, complicating vaccine development. At the same time, we are benefiting from substantial improvements in the tools of virology and molecular biology to get where we are so quickly. So in celebrating this prize, we can be doubly grateful that our blood supply is safer and that we no longer have to wait decades to identify new viruses.

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I would be interested to know what are the mutation rates of both viruses.
Also, it seems that there are also several distinct strains of SARS-Cov2 that are circulating, so vaccine development may be challenging for this virus too.

The majority (all?) of the vaccines are focused on the spike protein, so as long as there aren’t any significant variants within that gene it shouldn’t be a problem. Small changes in the spike protein also shouldn’t be a problem since a vaccine should illicit antibody production specific to multiple sections of the protein.

Using a strict definition of ‘strain’ – a genetic variant that causes a different phenotype – there are only two known strains of SARS-CoV-2. There’s substantial evidence that vaccines under development should work for both.

The substitution rate for HCV is somewhat higher than for SARS-CoV-2, but that’s not the main reason that the former has much greater genetic diversity. Rather, it’s because it’s been circulating in humans for much longer.