There are a percentage of people who develop long Covid type symptoms after vaccination, with no evidence of links to active infection. How can that be possible?
Research is now indicating that long Covid is primarily a disease of the gut, associated with persistent immune activation and damage to gut microflora leading to the unique pattern of symptoms.
Our recent “Long Covid Coalition Conference” was honoured to have Dr Leo Galland present on the links to alterations in the gut microbiota.
Interested to see his presentation, click here >
Watch the YouTube video here >
Research thoughts into the links with vaccination and long Covid
People who have pre-existing gut issues (characterised by bloating, diarrhoea and constipation) are likely to have an element of inflammatory changes in their bowel mucosa.
If the immune reaction to COVID-19 vaccination triggers an IgA/IgG response in the gut mucosa, this could lead to further alterations in the gut microbiota. Severe COVID-19 is already correlated with faecal microbiome changes and it could be possible that this is driven by IgA rather than the virus.
Dr Leo Galland already indicated in his presentation that lower levels of Faecalibacterium prausnitzii bacteria in the gut are associated with a higher risk of long Covid.
Our research into COVID-19 has pointed to combination of serum ACE-2 with viral spike protein as the primary cause of the autoimmune response. This could potentially also occur with vaccination and trigger an IgA/IgG response against ACE-2.
If the gut becomes further depleted of protective bacteria and there is already underlying inflammation, this could become exacerbated post vaccine. Additionally, ACE-2 is required for efficient function of specific amino acid transporters in the intestine (BOAT1 transporters).
These thoughts remain theoretical but there has to be an immune explanation for why some people become chronically unwell with long Covid after the vaccine.
Managing these patients could be complex as it requires the immune reaction in the gut to stabilize before symptoms improve. There may be a way to bypass the affected transporters that are impacted in the gut to help relieve symptoms in the interim.
The work continues.
Immune response may damage ACE2:B0AT1 complex, but not necessarily gut flora (gut endothelia is separate barrier from gut flora). Long covid like symptoms are evident after the vaccination due to B0AT1 disfunction and ACE2:S1:Abs immune complex prolonged presence in the host.
Vaccine designs prescribed dosage that avoids significant damages to the gut ACE2:B0AT1 complex, and any damage is recycled by endosomal cathepsins usually without any systemic evidence. It is harder for immune system to resolve damaged gut ACE2:B0AT1 when bound with S1, then sACE2 (soluble ACE2) bound to S1. Since ADAM17 access to ACE2 is sterically blocked by the presence of B0AT1, ACE2 of the tetramer complex does not release soluble sACE2 ectodomains in the gut (Sharma et al 2020). And clearance of ACE2:B0AT1:S1:Abs complex is delayed in comparison to sACE2:S1 clearance from the circulation.
But it could be argued that long covid is not 100% gut dependent. Mitochondrial dysfunction in other cell lines cause long-term post covid symptoms as well. In stricto sensu mitochondrial damage is regarded as Covid-19 complication and not a form of long covid that is regarded as prolonged activation of immune response. But without mitochondrial homeostasis with JAK-STAT pathway a patient can’t fully recover from Covid-19 complication.