AAs a scientist working every day on the immunology of Covid-19 and the long Covid, I am well aware that, as we head into autumn and back to school, the UK faces further confusion and disharmony from the covid Where do we go next? It’s not over? And why keep talking about mitigation when we now have so many other concerns?
Any discussion of our current Covid situation must take into account the legacy of disability and misery associated with prolonged Covid. In my opinion, there is now some good news among the old bad. Over the past few months, figures from the Office for National Statistics show the estimated number of people with long-term Covid starting to fall, from a high of 2 million in May to around 1.8 million. I understand that this means that some are gradually recovering. And while long Covid after Omicron BA.5 infection is clearly happening, new cases of long Covid are appearing at a lower frequency. Colleagues in Singapore, a country with a large spike in Omicron infections after a relatively mild early pandemic, mention talk of quiet Covid clinics with no patients.
There are also some signs that we may be getting closer to defining and treating Covid-19 more precisely. Many studies have been set up around the world to recruit groups with long covid to compare with “rapid recoveries” (people who recovered quickly and completely from covid) to try to find differences in levels of antibodies, hormones , immune cells or others. things that can be measured with a blood test. These so-called “defining biomarkers” can be game-changers. They can help health services define and refer cases, provide more extensive evidence for employers and courts, and also point towards identifying therapies and treatments.
One of the first such studies was reported this month in a preprint by Akiko Iwasaki, David Putrino and colleagues at Yale. They report a clear biomarker that delineates differences in the long-covid group, with signs including low serum cortisol (a hormone involved in controlling the stress response) and evidence of reactivation of latent Epstein- Barr. This is still not an absolute diagnostic test for long-term Covid, but it expands our knowledge of what exactly happens behind the symptoms, as well as signaling possible treatments.
Despite some bursts of good news, it’s worth repeating that Covid remains a largely untreated source of despair, especially for those more than two-year-old “first wave” carriers who can’t return to work and, in many cases, getting little work from employers. The cruel irony of this is obvious for a patient group in which our much-lauded “frontline heroes” are massively overrepresented.
Long Covid remains a very real risk, but the best way to avoid it is to avoid getting infected (or re-infected) in the first place. The initially successful launch of the vaccine in the UK in 2020-21 is ancient history in terms of the current battle. The BA.5 subvariant has so many immune-evasive mutations that it is a distant relative of the ancestral strain of Sars-CoV-2 against which the first vaccines were generated. In any case, most people’s neutralizing antibody levels have largely declined to baseline (or similar to unvaccinated) levels, even if they are triple vaccinated. Hence the enormous burden of innovative infections and reinfections. There is a strong consensus on the urgent need to strengthen the fall.
Immunologists and vaccine producers have engaged in considerable debate about the complexities of ensuring that the next generation of variant-specific boosters are the best they can be. Internationally, approaches have diverged. The UK has acquired doses of a bivalent booster, meaning it targets two strains, which carries the original and ancestral sequence of Sars-CoV-2, as well as the BA.1 sequence, the Omicron variant that was with us in late 2021. Meanwhile, in the US, the government has ordered 170 million doses of a bivalent vaccine targeting the original and ancestral sequence of Sars-CoV-2 and the currently relevant BA.5 sequence.
Trial data for these approaches are still scarce. The current sense is that the boost against BA.1 may not provide strong cross-protection against BA.5. But data on BA.5-specific reinforcers are also minimal. How important are these details? A team in Sydney, led by Miles Davenport, analyzed data from eight other studies to model the effectiveness of variant-specific reinforcers. The data there is reassuring. The original first-generation booster is even predicted to increase protection against symptomatic infection over a six-month period from 50% to 85.6%. New variant-modified boosters, generally 1.5 times more potent in terms of Omicron neutralization, will provide greater than 90% protection.
There will likely be some differences between the boosters once more studies are completed. But this complexity should never erode the public’s confidence that you (and the clinically vulnerable around you) will be safer this fall and winter with a booster, any booster, than without.
There should be no doubt about a comprehensive strengthening program. Indeed, we must remember that UK vaccine uptake, at 80%, is behind other European countries such as France, Italy and Portugal, with lower vaccine uptake skewed towards lower socio-economic groups in which Covid-19 is often more severe. We need to increase vaccine uptake in the unvaccinated, along with a strong message from the government and the Joint Committee on Vaccination and Immunization that protection and normalization now depend on the widespread and efficient deployment of new boosters. Those following the data and also mindful of protecting the clinically extremely vulnerable will also wear masks and maximize ventilation.
Danny Altmann is Professor of Immunology at Imperial College London, Trustee of the Medical Research Foundation and Long Covid Support, and co-author of The Long Covid Handbook
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