We also need pathologies included. The Wüst Lab biopsy findings are plausible contributors and similar to CVB pathology.

Of course, Steve.

It's not as different as it's portrayed and can be grouped as Pisoniviricetes-induced disease, Pisoniviricetes being the viral class that includes the orders Picornavirales and Nidovirales responsible for ME, COVID and many more diseases. What's missing is any serious attempt to deal with the class.

(PDF) A Comparative Review of Systemic and Neurological Symptomatology in 12 Outbreaks Collectively Described as Chronic Fatigue Syndrome, Epidemic Neuromyasthenia, and Myalgic Encephalomyelitis PDF | Outbreaks of illnesses of unknown etiology typified by a chronic relapsing course of constitutional symptoms and nervous system involvement have... | Find, read and cite all the research you nee...

Here Briggs and Levine describe subgroups seen in outbreaks. Other descriptions of the acute disease are described in ME outbreak literature and other research on the specific viruses involved. MECFS is a broader, more complicated mix of long-term outcomes.
www.researchgate.net/publication/...

The viruses mentioned in Ramsay's 1976 article are the founders of the phylum to which SARS2 belongs, Pisuviricota (picornavirus supergroup), and have similar infectious outcomes. This is why some of LC looks like ME. They can also occur together.

Kordi 2025
pubmed.ncbi.nlm.nih.gov/39907434/

The clinical syndrome variously called benign myalgic encephalomyelitis, Iceland disease and epidemic neuromyasthenia - PubMed The clinical syndrome variously called benign myalgic encephalomyelitis, Iceland disease and epidemic neuromyasthenia

The viruses mentioned in that article are a clue.

Acheson (1959) wrote that ameningitic myalgic lympho-reticular encephalomyelopathy was a more accurate albeit less practicable name (ME being the practicable, abridged name).
pubmed.ncbi.nlm.nih.gov/13637100/

www.meresearch.org.uk/research/oth...

Special problems of children with myalgic encephalomyelitis/chronic fatigue syndrome and the enteroviral link Since 1997, it has been known that myalgic encephalomyelitis/chronic fatigue syndrome constitutes the biggest cause of long‐term sickness leading to absence from school, in both staff and pupils. The ...

Having a TYMES Trust involvement might make the works of Colby, Dowsett and related authorships relevant.

pmc.ncbi.nlm.nih.gov/articles/PMC...
www.tandfonline.com/doi/abs/10.1...

This one had some help to get the "don't look for the virus" kind of complicated. Once you reassemble the pieces, it's even more complicated, but much easier to see how the pieces fit together.

T-Cell Receptor Sequences Identify Combined Coxsackievirus- Streptococci Infections as Triggers for Autoimmune Myocarditis and Coxsackievirus- Clostridia Infections for Type 1 Diabetes - PubMed Recent research suggests that T-cell receptor (TCR) sequences expanded during human immunodeficiency virus and SARS-CoV-2 infections unexpectedly mimic these viruses. The hypothesis tested here is tha...

Outside of ME, there is also some some possibility that other pathogens may matter selectively according to location.
pubmed.ncbi.nlm.nih.gov/38339075/

They are, but these affect people differently according to viral strain and the host's age & sex. Teen girls are in the first peak of ME. In utero affects development and survival even more than the neonatal myocarditis/sepsis, while men are at higher risk of dropping dead during strenuous exercise.

The original holds true for many. Others come in at various points along the way. EV-Bs are the older, smaller cousins of SARS2 and just as nasty.

The original ME was deemed most likely to be [Enterovirus betacoxsackie (EV-B), the current name for Coxsackie Bs, Echoviruses, and some others]. The modern variations of ME/CFS include EVs, HHVs, and other infections as well as non-infectious onsets. In both cases, it can involve metabolic effects.

And as the polio receded, the ME became more visible until someone decided it shouldn't be.

Yet, the definition is built into the name: long-term coronavirus-induced disease, a category, just as heart disease is.

Host-specific sensing of coronaviruses and picornaviruses by the CARD8 inflammasome This study describes an innate immune mechanism for sensing coronavirus and picornavirus infection by detecting the activity of virus-encoded proteases. Genetic variants among mammalian hosts affect w...

One interesting finding from elsewhere:
journals.plos.org/plosbiology/...
"we find that a single nucleotide polymorphism (SNP) in humans reduces CARD8’s ability to sense coronavirus 3CLpros and, instead, enables sensing of 3C proteases (3Cpro) from select picornaviruses."

The latter are generally the people who created or were influenced by the Waddell-Aylward-Wessely-et al BPS models and see LC as PVFS/PIFS/CFS 2.0, just as they did the other Pisoniviricetes that induce ME, cardiovascular diseases, diabetes and many other conditions.

Prior to the SARS-CoV-2 pandemic, the acronym COVID stood for coronavirus-induced disease (a category that included any and all coronavirus-induced diseases). Using this definition, Long Covid would include all the long-term coronavirus-induced diseases and their component signs, symptoms, etc.

You'd hope so. Some seem to consider it optional.

And then there's the problem of virologists et al using outdated taxonomies, missing the new(ish)ly found genetic similarities between pathogens and being mystified by SARS2 not acting like flu, but mysteriously developing multiple IACC/ME-like signs, symptoms, syndromes and diseases… picorna-like.

It has its good days but most of what I've seen still has echoes from the wrong end of the 1980s.

It reads like old, mild CFS material of the Fukuda era. Nary a pwME was described in this piece, and certainly none severe.

The spike is the key to the room, not the room occupant, their pet or the contents of their luggage. There's too much focus on the key and not enough on the other factors.

I suspect that if the event were held somewhere other than the home of psychobehavioural attitudes, it would be. This is "sheep in wolf skin" going into the den of the leader of the pack to challenge the carnivorous.

True, the UNSW members of COFFI may be too "busy" to attend, but it's important that they are not the only voice on campus. A UNSW professor is advertising the event in X/Twitter.

I've not seen much of that data. Have seen some of the prevalence reporting showing multiple Pisoniviricetes in play over the last 5 years. How many 3C(L) proteases, etc does one have to collect to be truly "healthy"?

Not simple, but very Hickie et al 2006, not EV-ME.

You could say the same about CVBs: multiple diseases, pathways to disability, risk of death, few treatments, no cures. And a target of gaslighting from the same gaslighters.

Just another Pisoniviricetes virus out on a jaunt. (Yep, some of the others do it, too.)

Much more. Coronaviruses are related to enteroviruses (polio, cardiovascular diseases, neurological diseases, diabetes, sudden death, miscarriage, birth defects, developmental abnormalities, neonatal sepsis, ALS,…) and inducing much the same range of conditions, sometimes alongside other classmates.

Also, PIFS/PVFS after Ross River is generally self-limiting. Ignoring recovery may also prolong recovery.