Viruses belonging to Anelloviridae or Circoviridae as a possible cause of chronic fatigue, Grinde, 2020

John Mac · Dec 15, 2020

Though the title says chronic fatigue the article is about chronic fatigue syndrome

Abstract
Chronic fatigue often starts with an acute viral infection—as witnessed in the case of SARS-CoV-2—but indirect consequences of these infections are presumably the actual cause of the condition. As recently reviewed in this journal, the culprit could be a virus already present in the patient. The review covers several types of viruses, but concludes that the question is still open. The focus is on well known, pathogenic viruses for which there are ample diagnostic tools. I argue that there is one lesser-known group of viruses, the related anello- and circoviruses, which ought to be investigated. More or less everyone harbours at least one strain of these viruses in the blood, while not in the spinal fluid. They normally replicate at a low level, but their activity increases in an immune suppressed host; and there are cases where they do reach the brain. The initial infection could facilitate their access to the brain.

Possible causes of chronic fatigue
There are several lines of investigation as to the aetiology of chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis. The arguably two most common are: one, immune system abnormalities such as chronic immune activation or autoimmunity; and two, as recently reviewed in the Journal of Translational Medicine, chronic viruses [1]. In both cases, several correlates are found, but none appears to give a satisfactory explanation for the condition. There are two problems with these correlates. For one, the parameters investigated tend to be limited to those with easily available diagnostic tools; and two, a correlate may be due to indirect effects of the actual causative factor. For example, if the aetiology is infectious, there would be an expected impact on in immunological parameters. On the other hand, if the immune surveillance is somehow compromised, there would be an expected increase in the titre (and detection rate) of chronic viruses.

What is generally accepted is that the condition in many cases (perhaps 50%) starts with an infection [2]. This is typically in the form of a viral-like flu with presumed viremia. The infection, however, is considered a triggering factor rather than the actual cause. A condition similar to CFS was noted as sequela in connection with the SARS epidemic, and again in connection with Covid-19 [3]. The observation accentuates the importance of finding the true culprit, but also offers an opportunity for research.
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https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-020-02666-5

Snow Leopard · Dec 15, 2020

There have been a few groups who have used a broad-based look for infections, not just specific human viruses, but using pan-viral microarrays like the Virochip which can detect fragments of viruses belonging to other families (it should in principle detect zoonotic viruses). I would have expected such studies to note if there were unusual findings with respect to Anelloviridae or Circoviridae.

The author doesn't talk about specific mechanisms about how these viruses could induce the illness beyond a general mention of crossing the blood-brain barrier and causing tissue damage.

borko2100 · Dec 15, 2020

The observation that perhaps half the cases of CFS starts with a severe infection, suggests that this infection facilitates an event that can also take place in its absence. Viral infections can suppress the immune system, for example, by reducing the production of interferons. This could lead to an increased titre of other viruses present in the patient. Viral infections can also compromise the blood brain barrier (BBB). Combined, these effects are likely to facilitate an access to the brain of viruses already present in the blood.
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This theory could explain why many people seem to get permanently worse after a crash. Namely blood barrier gets compromised temporarily (stress, another virus, etc.), this allows more virus to enter the brain, then viral load in the brain increases and settles down to a higher level than before the crash. This higher viral load then leads to new and / or more severe symptoms than before.

James Morris-Lent · Dec 16, 2020

Snow Leopard said: ↑

The author doesn't talk about specific mechanisms about how these viruses could induce the illness beyond a general mention of crossing the blood-brain barrier and causing tissue damage.
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Tissue damage being characteristically and conspicuously absent in the condition. Ugh.

Kalliope · Dec 16, 2020

interesting that the author is from the Norwegian Institute of Public Health. Never heard of him before, but he has a Wikipedia page.
https://en.wikipedia.org/wiki/Bjørn_Grinde

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