Get boosted - especially if you had the AstraZeneca vaccine11 Dec 2021 | Reading time: 2 min
The omicron COVID-19 variant is spreading rapidly, making up 40% of cases in London.
It might be milder than delta, but the evidence isn’t clear. Nonetheless, we don’t know if long COVID is less likely with omicron than with other strains. That should be a big concern for younger people who are less at risk of hospitalisation and death, but are at a ~3% risk of developing long COVID if they’re infected1. Half of those people have chronic fatigue. This is something worth making an effort to avoid.
Even with two doses of the Pfizer vaccine, your protection against omicron is significantly lower than against previous variants - your antibodies are potentially 10–20x less neutralising than against the delta variant.
But if you had the AstraZeneca vaccine, you functionally have no (detectable) antibody protection against omicron:
Across 5 preliminary live virus studies (3 international and 2 UK), there was a 20- to 40-fold reduction in neutralising activity by Pfizer 2-dose vaccinee sera for Omicron compared to early pandemic viruses. There was at least 10 fold loss of activity when compared to Delta; in both UK studies this was over 20 fold. A greater reduction in activity was seen for AZ 2-dose sera, and for a high proportion of such sera, neutralising activity fell below the limit of quantification in the assay.
(You still likely have T-cell immunity, which reduces the severity of the disease if you do get infected.)
Some good news - getting boosted works even if you didn’t have Pfizer originally:
An mRNA booster dose resulted in an increase in neutralising activity irrespective of primary vaccination type, including an increase in the proportion of samples that were above the limit of quantification. This is true regardless of which vaccine was used for the primary course.
Get a booster shot as soon as you can.
See this blog post from the ONS: “in April 2021 we published results using one of the three approaches, based on tracking continuous symptoms. One of the more striking findings from the latest release is the revision to the 12-week prevalence estimate using this approach, from 14% back in April to 3% now. This fall in the prevalence estimate is largely because we know more about participants’ long-term symptoms today than we did then.” ↩