Nature Microbiology Editorial: Connecting the dots from viral infection to disease, 2023

Sly Saint

Sly Saint

Senior Member (Voting Rights)
Methodological advances have helped identify viruses as causative agents of disease but this is complicated by heterogeneity in patient outcomes and long-term symptoms.

Viruses that infect animals and plants are now well known as aetiologies of disease. However, unlike bacterial pathogens, viruses were not always easily identified as causative agents owing to their small sizes and their reliance on host cells. About 50 years after bacterial pathogens were identified, the first evidence linking viruses to specific diseases was reported. In the late nineteenth century, Dmitri Ivanovsky reported tobacco mosaic virus infection of plants, while animal infection with foot-and-mouth disease virus was described by Friedrich Loeffler and Paul Frosch. Around the same time, Carlos Finlay reported the first virus shown to cause disease in humans, yellow fever virus, and found that it was transmitted to humans by mosquitoes1. Together, these findings laid the foundations for contemporary virology.

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Furthermore, research groups have used multi-omics approaches and large cohorts to study how virus infection can drive long-term symptoms, such as those reported for long COVID. These symptoms are similar to those experienced in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS has been tentatively connected to infection with Epstein–Barr virus but a solid evidence base is lacking. Neurological symptoms such as memory loss, impaired concentration and fatigue have been reported both in patients with ME/CFS and patients with long COVID7. Symptoms vary across patients and so determining the role of a virus in these aetiologies is difficult. In a longitudinal study with a cohort of 309 patients, Su et al. used a deep multi-omics approach to reveal an association between SARS-CoV-2 RNA levels, Epstein–Barr virus viraemia, and specific auto-antibodies with risk for developing long COVID8.

This extensive analysis indicates that several variables are relevant for long COVID development and so disentangling the specific role of a virus in long-term disease is extremely complex, but large cohort studies can be helpful. Comorbidities, infection history and genetic predisposition can also complicate analyses. Therefore, multi-centre collaborations are needed to enable well-documented, large, longitudinal cohort studies. Ideally, these large cohorts would include a diverse set of participants (considering race and/or ethnicity, geographical location, sex, age, pregnancy status, socioeconomic status) in order to unravel the complexities of virus-induced diseases, such as long COVID and ME/CFS.
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more at link.
https://www.nature.com/articles/s41564-023-01452-5
 
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Pathogenic viruses are a serious public health concern
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Uh, no, I don't think we can say that anymore. Which makes this:
so our ability to link pathogens and disease is becoming increasingly important
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especially damning. Having just abandoned everything having to do with COVID is just incredible mass failure. It's completely unprecedent for an expert profession to just give up like this, about something they know is important.

So much politics.
 
"How to unravel the complexities of virus-induced diseases, such as Long Covid and ME/CFS."

This is an excellent editorial, and I wish I knew who its authors were.

In a nutshell: linking viruses to long-term disease is complex, but with careful and smart research, it can be done.

Two examples of the problems linking viruses to diseases:

1. Distinguishing cells that are engulfing/destroying viruses from those that are truly infected.

For instance, macrophages play a key role in engulfing and destroying viruses. As a result, these cells include virus proteins and nucleic acid, but this doesn't mean an individual or a tissue is infected. However, there are biomolecular methods that can identify exactly what is happening.

2. Understanding the link between infection and symptoms.

Herpes Simplex viruses, HSVs, can cause severe brain infection and some patients continue to suffer from neurological symptoms despite treatment with antivirals. Careful research helped tease out what was happening, along with the observation that that anti-inflammatory drugs can alleviate post-HSV symptoms.

"In this case, while HSV infection is the trigger, prolonged inflammation is the cause of the symptoms."

The editorial concludes that disentangling the specific role of a virus in a long-term disease is extremely complex, but large cohort studies can be helpful.

It gives the example of both long Covid and ME/CFS, saaying that both have been linked to the Epstein-Barr virus, for ME/CFS, the evidence is not definitive (I'm not sure that's quite fair), while a large longitudinal study in the long Covid using multi-omics approach provided stronger links that Epstein-Barr virus is a risk for developing long Covid.

I hope this editorial is a sign that more virologists are taking Long Covid and MEcfs seriously.

A view from @chillier would be welcome.
 
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