Can enterovirus RNA be found in the blood?

Pyrrhus

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Can enterovirus RNA be found in the blood?
The literature indicates that, after the acute phase of an enteroviral infection, the virus can only be found in tissues, but not in the blood. But are there any exceptions to this rule, perhaps for some specific groups of patients?

1) One small study that looked at whole blood (not just blood plasma) found no significant enteroviral RNA in ME patients:

Whole blood human transcriptome and virome analysis of ME/CFS patients experiencing PEM following CPET (Bouquet et al., 2019)
https://forums.phoenixrising.me/thr...-pem-following-cpet-bouquet-et-al-2019.84824/


2) Nonetheless, there have been at least two researchers who found enterovirus RNA in the blood of some patients:
  1. Dr. Antonio Toniolo co-cultured whole blood from post-polio patients with cells "permissive" for enterovirus. After co-culturing the cells, he detected enterovirus RNA. There are no reports that anyone has tried to replicate Toniolo's findings, but it is rumored that Dr. Maureen Hanson has tried.
  2. Dr. John K. Chia, who is a clinician who also dabbles in research, used a cutting-edge RNA stabilizing agent - added to the patient's blood immediately at time of collection - and found evidence of enterovirus in the blood of ME patients.

3) In the field of Type I Diabetes, researchers appear to have been successful with a subset of patients who have a mutation in their gene for MDA5. (MDA5 is a key cellular sensor that cells depend on to detect when they are infected with a virus.)

Detection of enterovirus RNA in peripheral blood mononuclear cells correlates with the presence of the predisposing allele of the type 1 diabetes risk gene IFIH1 and with disease stage (Sioofy-Khojiny et al., 2022)
https://doi.org/10.1007/s00125-022-05753-y

Aims/hypothesis: Enteroviral infection has been implicated consistently as a key environmental factor correlating with the appearance of autoimmunity and/or the presence of overt type 1 diabetes, in which pancreatic insulin-producing beta cells are destroyed by an autoimmune response. Genetic predisposition through variation in the type 1 diabetes risk gene IFIH1 (interferon induced with helicase C domain 1), which encodes the viral pattern-recognition receptor melanoma differentiation-associated protein 5 (MDA5), supports a potential link between enterovirus infection and type 1 diabetes.

Methods: We used molecular techniques to detect enterovirus RNA in peripheral blood samples (in separated cellular compartments or plasma) from two cohorts comprising 79 children or 72 adults that include individuals with and without type 1 diabetes who had multiple autoantibodies. We also used immunohistochemistry to detect the enteroviral protein VP1 in the pancreatic islets of post-mortem donors (n=43) with type 1 diabetes.

Results: We observed enhanced detection sensitivity when sampling the cellular compartment compared with the non-cellular compartment of peripheral blood (OR 21.69; 95% CI 3.64, 229.20; p<0.0001). In addition, we show that children with autoimmunity are more likely to test positive for enterovirus RNA than those without autoimmunity (OR 11.60; 95% CI 1.89, 126.90; p=0.0065). Furthermore, we found that individuals carrying the predisposing allele (946Thr) of the common variant in IFIH1 (rs1990760, Thr946Ala) are more likely to test positive for enterovirus in peripheral blood (OR 3.07; 95% CI 1.02, 8.58; p=0.045). In contrast, using immunohistochemistry, there was no correlation between the common variant in IFIH1 and detection of enteroviral VP1 protein in the pancreatic islets of donors with type 1 diabetes.

Conclusions/interpretation: Our data indicate that, in peripheral blood, antigen-presenting cells are the predominant source of enterovirus infection, and that infection is correlated with disease stage and genetic predisposition, thereby supporting a role for enterovirus infection prior to disease onset.
 

Pyrrhus

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In the field of Type I Diabetes, researchers appear to have been successful with a subset of patients who have a mutation in their gene for MDA5. (MDA5 is a key cellular sensor that cells depend on to detect when they are infected with a virus.)
I found this particularly interesting as I have a couple of mutations in my gene for TLR3. One of those mutations has been linked to a somewhat higher susceptibility to certain RNA viral infections.

Both MDA5 and TLR3 are key cellular sensors that detect viral double-stranded RNA (dsRNA)...
 

Marylib

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Maybe I should run the genetic genie thing again. Back when I was healthy, I ran into problems with my blood sugar. At one point I was told that I was at risk for type 2 diabetes and that I should get plenty of exercise...Unfortunately, that is not happening. But the blood sugar is okay. So much of ME seems to be some kind of diabolical adjustment that keeps you barely alive after infections.