We do know vaccinations and infections reduce risks of LC. We also know that strain evolution has also reduced the risk of LC- with WA1 and Alpha this was >20%, Delta was more like 10% and now Omicron is less than 5% going on to develop LC. So both increases in immunity either via vax or infection help reduce risks, as well as the strain evolution resulting in less LC.Quote:
Originally Posted by bodywhomper
https://www.science.org/content/arti...get-long-covid
(People who catch Omicron are less likely to get Long Covid.
Vaccination, virus biology may be driving down risk)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9212672/
(Risk of long COVID associated with delta versus omicron variants of SARS-CoV-2)
Also- this is not a new post-viral infection phenomena as similar/overlapping symptoms can occur after a number of different viral and bacterial infections, and is likely a major contributor to ME/Chronic Fatigue Syndrome (25 of 29 symptoms overlap- see below). Also likely that reactivation of dormat life long viruses (EBV, CMV, etc) you are carrying after Sars-S infection are contributing to symptoms.
from the review https://www.nature.com/articles/s41577-023-00904-7
Quote:
Box 3 Lessons from and for ME/CFS and the case of ‘long SARS’
It is hard to discuss or present data on long COVID without being challenged about the relationship of findings to mechanisms in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), not least by patient groups who understandably feel that their condition has endured decades of neglect in terms of biomedical research prioritization. In light of clear overlaps with long COVID, there now exists an opportunity for cross-hybridization, with much to be learnt from the long, past experience and investigations in ME/CFS, and from the new momentum of long COVID investigations over the past few years. The symptom overlap is self-evident, encompassing the key features of post-exertional fatigue, neurocognitive symptoms, dysautonomia and postural orthostatic tachycardic syndrome. A systematic review found that 25 of 29 CFS symptoms were reported by at least one long COVID study18, whereas another study compared genes common between the two conditions in a number of ways, including pathway and network analysis148. This study found common hub proteins, such as IL-6 and IL-1β, between the two conditions. Another review focused on their similarities through the link of TGFβ signalling and circadian rhythms148. There is resonance in the post-acute viral infection symptomology across the two conditions19. ME/CFS has commonly been described as a post-viral condition that may ensue following a range of infections, including pandemic H1N1 influenza149, Varicella zoster virus150, enteroviruses and SARS-CoV-117. Overlap in the immunopathological analyses is particularly interesting. It is noteworthy that raised CCL11, which has credentials as a long COVID serum biomarker functionally linked to neurocognitive symptoms, is also a biomarker of ME/CFS151. Revisiting the ME/CFS data also raises the possibility of investigating some of the implicated biomarkers, such as CXCL10 and leptin, in more detail in long COVID152. Furthermore, the ME/CFS data set may offer a reference framework to consider a role for Epstein–Barr virus reactivation in long COVID, noting that CFS can ensue from infectious mononucleosis associated with an enhanced imprint of T cell activation153.
