The past months have been very busy on the Long Covid research front, both for our research planning as well as Long Covid research in general. Here we’ll walk you though our status and some of the recent findings and their implications.
To begin with, we are seeing a large number of research studies being published on Long Covid every day. To stay up to date on all the latest research, please visit our Long Covid research library. Some of the latest studies have expanded our understanding of Long Covid epidemiology and contributing factors, but unfortunately, there is not a lot that is actionable or useful on a patient level so far. We still do not have any proven therapeutics, diagnostics or understanding of what causes Long Covid (outside of the obvious general causal factor, COVID-19!). There are more and more clinical trials that are beginning or already underway and hopefully we will have more patient-actionable information soon.
What we have seen recently is several thorough studies showing the likelihood of getting Long Covid after an acute COVID-19 infection. We’ve had a range of these studies in the past, but we are now getting very good studies that have control groups and allow for a more accurate assessment of the risks. What we see is that 7–10% are likely to develop Long Covid lasting longer than 6 months, with similar or slightly lower rates in children and higher rates seen following reinfections. This has also allowed the determination that antiviral treatment early in the acute infection can reduce the likelihood of developing Long Covid by around 27%. Similarly, vaccination helps reduce the risk of developing Long Covid by roughly 50%, though the exact extent of the reduction is not clear. Unfortunately there is still a lack of data on the impact of the most recent COVID-19 boosters on existing Long Covid symptoms and it is not known if the boosters can prevent or reduce the symptom worsening that many Long Covid patients report upon reinfection.
There have also been several studies published recently that continue to expand on existing disease hypotheses. We’ve seen further data on muscle and mitochondria dysfunction in Long Covid that can affect energy availability and may cause fatigue or post-exertional symptom exacerbation. One recent study found evidence for reduced levels of the neurotransmitter serotonin in Long Covid, as well as the persistent reprogramming of immune cells, both of which could have broad effects on the body. There is more evidence for clotting abnormalities in Long Covid, including the presence of microclots in muscle tissue, though we still don’t know if this is a cause or an effect of the disease. We are also seeing more examples of persistent virus, especially in the gut, though again, it’s not clear if this is in all Long Covid patients, how long the virus can persist for and if this is the driver for continued disease. Whilst we are not there yet, we are getting closer to a real understanding of the disease. We have also seen some of the first pre-print data on the relatively rare occurrence of Long Covid after COVID-19 vaccination.
One other area of research that has seen a lot of progress recently has been the study of lactate. As a reminder, our hypothesis of an underlying mechanism of Long Covid disease revolves around the excess production of lactate and the associated acidosis. Unfortunately lactate is not normally measured in the clinic and the levels of lactate in the body can change rapidly, making assessment of hyperlactatemia and acidosis difficult in the context of Long Covid. However, several studies have recently developed and validated continual blood or sweat lactate sensors. Some of these are also in product development (e.g. smartwatches and sensors) and it is likely that we will see some of these become commercially available soon. This could greatly help our ability to track and monitor lactate in patients over the course of the day and in different activities, to better understand and possibly treat patient disease.
This is also a critical aspect of the Long Covid clinical research that we have been developing. In our acidosis hypothesis publication we proposed ways of assessing acidosis and lactate levels in patients to validate our hypothesis. We also aim to see if lactate can be used as a diagnostic marker for Long Covid and if acidosis can be treated to improve patient outcomes. Through your generous contributions we have been able to initiate this research by developing collaborations with academic clinical research units. We are nearing the final planning stages of this research and hope that we will be able to formally announce the study by this summer. Through this research we should be able to clearly ascertain if acidosis is associated with Long Covid, begin to understand more about the mechanism and potentially start exploring some treatment options.
We look forward to updating you on all the details soon!
