Sequential activation of DNA viruses by the RNA virus SARS-CoV-2 in patients with long COVID syndrome, 2023, Gyongyosi et al.

[SNT Gatchaman]

Sequential activation of DNA viruses by the RNA virus SARS-CoV-2 in patients with long COVID syndrome
Gyongyosi, M; Hasimbegovic, E; Lukovic, D; Zlabinger, K; Spannbauer, A; Samaha, E; Bergler-Klein, J; Hengstenberg, C; Mucher, P; Haslacher, H; Breuer, M; Strassl, R; Riesenhuber, M; Nitsche, C; Zelniker, T A

Background: Reactivation of Epstein-Barr virus (EBV) has been suggested to play role in long lasting multiorgan symptoms several months after the initial COVID-19 illness.

Purpose: The aim of our prospective study was to 1) to evaluate the reactivation of DNA viruses of EBV, Cytomegalovirus, Herpes simplex, Varicella zoster and Parvovirus-B19 by SARS-CoV-2 in patients with the diagnosis of long-COVID syndrome, 2) to investigate the effect of supposed virus reactivation on clinical conditions and long COVID syndromes.

Methods: Patients with long COVID syndrome were prospectively included into the Vienna PostCoV Registry between March 15th 2021 and September 30th 2021. - The time between COVID-19 infection and first clinical visit was 219 ± 98 days (7 ± 3 months). Clinical symptoms were documented and patients were divided into symptoms-oriented subgroups with dominantly respiratory, cardiovascular or neuropsychologic complaints. Qualitative and quantitative viral IgG and IgM titer of the selected DNA viruses of n=105 patients were compared with age and sex-matched healthy (non-infected, non-vaccinated, n=105) controls, who had neither spike- nor nucleocapsid antibodies, nor clinical history of COVID-19 disease.

Results: Long Covid patients had significantly higher cumulative number of IgM positivity of the DNA viruses (18.1% vs 6.7%, p=0.02), and significantly elevated quantitative EBV IgG (420 ± 296 vs 339 ± 282 mg/dL, p=0.033) and Parvo-B19 IgM (0.28 ± 0.29 vs 0.03 ± 0.12 mg/dL, p<0.001) titer as compared to healthy controls. Significantly more patients with long COVID symptoms had an EBV IgG titer above the detection limit as compared with healthy controls (40% vs 28%, p=0.018), suggesting EBV virus reactivation and chronic EBV infection. EBV IgG titer was significantly higher in patients with dominant respiratory symptoms, while elevated Parvo-B19 IgM titer was observed in patients with dominant cardiovascular complaints. In patients with long-COVID syndrome the quantitative EBV IgG titer increased with the time between infection and blood sampling (logarithmic correlation, p=0.011), suggesting the subclinical continuous EBV activation by the SARS-CoV2 RNA virus, while the quantitative Parvo-B19 IgM titer decreased linearly during the observation period.

Conclusions: In this study of patients with long-COVID syndrome, SARS-CoV-2 infection apparently activated certain types of DNA viruses (EBV, and Parvo-B19), as demonstrated by the significantly higher incidence of cumulative IgM positivity, and elevated EBV IgG and parvovirus-B19 IgM titers, in long-COVID patients compared to healthy controls.

Link | PDF (European Heart Journal)

 

[SNT Gatchaman]

Only abstract and figures but probably worth noting. (I don't know if this is simply a conference slide/abstract or if a full article is pending.)

 

[rvallee]

Seems more appropriate to say that some infections, including COVID-19, provide an opportunistic environment for certain latent pathogens, such as EBV. The idea that SARS-CoV-2 specifically enables EBV to do that is slim to nil, whereas the environment provided by a 'stressed', in the sense that there demands on it in the context of finite capacity, immune response to a pathogen is already a known issue. The viruses simply respond to protein signals, and likely do to immune responses, when the body is less capable of dealing with them. This makes evolutionary sense, and nothing in biology makes sense except in the context of evolution.

But the general idea is very hard to accept, even though it's so commonly said that 'stress' will do just that, allow opportunistic latent pathogens to re-emerge. 'Stress', of course, is known to be associated with... markers of an immune response. Then of course you have things like secondary bacterial pneumonia, a common outcome of respiratory viral infections. The immune system doesn't just respond to infections, it does so much more than that, there seems to be a problem of framing and old contexts. There is an 'inflammatory' response to exercise, for example, because it's the immune system that repairs the damage. And the normal cycle of apoptosis involves basic innate immune processes.

There is really a need for a perspective shift on what the immune system is and does, especially in how much of what it does has been appropriated to some generic notion of 'stress', rather than being the body's defense and maintenance system and that that the overarching notion of stress is ultimately the sum of many, many micro-'stresses' at the cellular level.

It's also so much more than pathogens. Humans breathe in so much air pollution every single day, ingest and come into contact with more. All things our immune systems deal with. In addition to cancerous cells and much more. And since exercise also 'stresses' the immune system, makes demands on it, it would make sense of what is incorrectly termed 'burnout' being essentially the sum of many micro-'stresses' on the body's ability to maintain itself. Also likely most forms of fatigue.

It's such a shame that there is no such actual thing as real holistic medicine, able to take in the full body into account as an organism, rather than a small set of organs doing their own things in isolation. But, noooo, instead we have freaking 19th century quackery squatting the place and obsessing over getting people to exercise, even when what they need is rest. Pffft.