SARS-CoV-2 Viral Load and Cytokine Dynamics Profile as Early Signatures of Long COVID Condition in Hospitalized Individuals, 2025, Domínguez et al.

SARS-CoV-2 Viral Load and Cytokine Dynamics Profile as Early Signatures of Long COVID Condition in Hospitalized Individuals
Jacobo Alonso Domínguez; Inés Martínez Barros; Irene Viéitez; Mercedes Peleteiro; Beatriz Calderón-Cruz; José A. González-Nóvoa; Alexandre Pérez González; Virginia Leiro Fernández; Aida López López; Eva Poveda López

BACKGROUND
The global pandemic caused by SARS-CoV-2 has resulted in millions of people experiencing long COVID condition, a range of persistent symptoms following the acute phase, with an estimated prevalence of 27%–64%.

MATERIALS AND METHODS
To understand its pathophysiology, we conducted a longitudinal study on viral load and cytokine dynamics in individuals with confirmed SARS-CoV-2 infection. We used reverse transcriptase droplet digital PCR to quantify viral RNA from nasopharyngeal swabs and employed multiplex technology to measure plasma cytokine levels in a cohort of people with SARS-CoV-2 infection. Our study included individuals with long COVID condition and those without, all of whom had at least three nasopharyngeal and plasma samples collected within 55 days after diagnosis of SARS-CoV-2 infection.

RESULTS
Individuals affected with long COVID symptoms had delayed viral clearance and lower viral loads at diagnosis compared to those without symptoms. Additionally, cytokine analysis revealed variations in IL-18, MIG, and IP-10 levels, with delayed normalization in individuals affected by long COVID syndrome. Correlation analysis indicated associations between viral load and IP-10 and interrelations among cytokines IL-1β, IL-18, MIG, and IP-10.

CONCLUSION
Our study provides insights into the association between nasopharyngeal viral load, cytokine dynamics, and the development of long COVID syndrome, providing an early signature of this condition.

Link | PDF (Influenza and Other Respiratory Viruses) [Open Access]

 

This sounds like the people who get lumbered with a chronic covid aftermath are those who succumb to less of the virus overwhelming them in the first place and also take longer to get rid of these smaller numbers of virus, also taking longer to normalise levels of their cascading pro-inflammatory cytokines - whipping up a storm sooner on less provocation and for longer

Unless there is some undetected difference in the covid virus being assayed

if so that might mean its not a variation in any body, but it is an indistinct varation in the virus setting off covid with a chronic aftermath (provoked by smaller numbers of a slightly variegated virus) if not so easily detected by the immune system and its researchers

Spoiler: I guess a virus....... and is PEM an acute-on-chronic illness

I guess a virus does not have a body but can travel between host cells, and I guess a bacteria is a variable body like I am so there may be a vrariable bacterial body compounding with a variable virus compounding with a variable mammal body, for all I know.

I am not certain that its a variation in any body allowing this sneaky virus to render some not all of its survivors liable to recurrent, chronic, and acute-on chronic illness and while about it: might we start thinking of PEM as an acute-on-chronic illness because that is a well-known recognisable liability ?

And is PEM a flare and can it become a relapse and can that become an extremely protracted most severe decline, and was it defined before or after NG206 outlined to me the ME/CFS pattern of [ flare / relapse / decline ] progressions: as happen if I fail to manage (or am not allowed to manage) the flare / failing which the relapse / failing which the decline ... if not managed in the time give .... or if not manageable in the time goiven

Since unlike some I am able to vary the condition so I have the flares etc etc in common with those people who have those suspected or diagnosed cases of Long Covid which do not get stuck invariably

I don't know if anti-viral assistance at the start of Covid reduces this liablity which fails to fully recover afterwards if surviving at all. Or might an antiviral even exacerbate the liability as can happen with antibiotics and even happens when prescribed with cognisant precision (for type, amount and duration) resulting in recurrent infections etc

I don't know how come us unfortunate people became so susceptibly liable

But how come a neurologist, 2 rheumatologists and a market analyst all told me (since the pandemic began) that there was so far, at that time, no evidence of any reliable method to measure cytokines, has that been sorted by now, or were they all just being sniffy as usual about the multitudinous discarded theories & methods spawned by research in the process of substantiating their bread and butter for them?

I was vastly disappointed at the time, that my cytokines could not be reliably tested

 

Interesting that CXCL10 = IP-10 has been highlighted in several other Long Covid threads.
https://www.s4me.info/search/36265054/?q=cxcl10&o=date