The good news is that the AstraZeneca vaccine is still thought to be effective against the more severe forms of disease caused by the South African variant of SARS-CoV-2; and that various manufacturers are already well on their way to producing vaccines designed to work effectively against the variant.

In the medium term, what matters most is preventing more serious forms of Covid-19; and it is thought the AstraZeneca vaccine will do this.

While it has been widely reported that the AstraZeneca vaccine is “less effective” against the South African variant, we must remember that, in full, this should read “less effective than it is against previous variants”. It is by no means clear if it is more or less effective against the variant than other vaccines.

If South Africa has large stocks of other vaccines, and can proceed with its vaccination programme without the cessation of its use of the AstraZeneca vaccine causing delays, the decision is inconsequential for the country. But if this will cause delays, it will mean avoidable deaths and cases of severe disease.

Within months we hope to see availability of new vaccines, tailored to the South African variant. The genome of the variant spike protein is known, and the technology to “plug in” the genes for it into mRNA and vector vaccines is well-established.

One remaining uncertainty is how regulators will treat such “tweaked” vaccines. Will they treat them like seasonal flu? Or will they require full-scale phase III trials before they will approve them?

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The information we have is very limited, but the trial seems to have been restricted to HIV negative younger people (mean age 31), about 1000 in the placebo arm and 1000 in the active vaccine group. In this age group and with these numbers, the effect on severe disease is going to be hard to estimate. Without seeing results in detail, it isn’t possible be sure how firm these conclusions are.

However, if the press reports are correct it does seem of concern that protection against disease was not shown. The findings of the Novavax vaccine trial of 60% efficacy in the prevention of disease of any severity in HIV negative volunteers in South Africa might also suggest that vaccines will need to be updated in line with emerging mutations of the virus.

Although the most obvious explanation for the apparent reduced efficacy is the emergence of variants, the role of anti-adenovirus cross-reactive immunity should also be examined. The Oxford/AZ vaccine is a disabled simian adenovirus and should not be affected by prior exposure to other adenoviruses, but this needs checking.

Vaccines that are effective against the more severe forms of disease may not affect milder forms, so there is optimism that severe disease will still be prevented by vaccines based on the original spike protein despite mutations. In addition, many of the vaccines now proven to be effective can be relatively easily redesigned to express emerging forms of the viral protein.

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Evidence suggests the Oxford AZ vaccine protects against disease caused by the predominant Covid variants circulating in the UK. It remains highly likely that the vaccine will also protect against severe disease caused by the South African variant.