Effect of monovalent COVID-19 vaccines on viral interference between SARS-CoV-2 and several DNA viruses in patients with long-COVID syndrome

[Osaca]

Effect of monovalent COVID-19 vaccines on viral interference between SARS-CoV-2 and several DNA viruses in patients with long-COVID syndrome

Abstract​

Epstein–Barr virus (EBV) reactivation may be involved in long-COVID symptoms, but reactivation of other viruses as a factor has received less attention. Here we evaluated the reactivation of parvovirus-B19 and several members of the Herpesviridae family (DNA viruses) in patients with long-COVID syndrome. We hypothesized that monovalent COVID-19 vaccines inhibit viral interference between SARS-CoV-2 and several DNA viruses in patients with long-COVID syndrome, thereby reducing clinical symptoms. Clinical and laboratory data for 252 consecutive patients with PCR-verified past SARS-CoV-2 infection and long-COVID syndrome (155 vaccinated and 97 non-vaccinated) were recorded during April 2021–May 2022 (median 243 days post-COVID-19 infection). DNA virus–related IgG and IgM titers were compared between vaccinated and non-vaccinated long-COVID patients and with age- and sex-matched non-infected, unvaccinated (pan-negative for spike-antibody) controls. Vaccination with monovalent COVID-19 vaccines was associated with significantly less frequent fatigue and multiorgan symptoms (p < 0.001), significantly less cumulative DNA virus–related IgM positivity, significantly lower levels of plasma IgG subfractions 2 and 4, and significantly lower quantitative cytomegalovirus IgG and IgM and EBV IgM titers. These results indicate that anti-SARS-CoV-2 vaccination may interrupt viral cross-talk in patients with long-COVID syndrome (ClinicalTrials.gov Identifier: NCT05398952).

https://www.nature.com/articles/s41541-023-00739-2

 

[SWAlexander]

the Herpesviridae family

Right. Covid reawaken HSV 1 and 2 Aug. 2021

 

[SWAlexander]

Will it ever end?​

T Cell Cross-reactivity in Autoimmune-like Hepatitis Triggered by COVID-19​

Over 1,000 cases of pediatric hepatitis of unknown etiology have been reported worldwide since the first case was reported in the UK. To date, the etiology of pediatric hepatitis remains unknown and controversial. Adenovirus was first suspected to be the cause as it was present in the blood samples of the majority of cases. Partial cases have also been tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1]. However, it is still unclear how these viruses contribute to pediatric hepatitis. In the case of a pediatric patient with SARS-CoV-2 infection, the liver biopsy showed acute submassive hepatocyte necrosis, accompanied by a significant increase in T cell infiltration [2]. Furthermore, CD8 T-cell dominant hepatitis induced by coronavirus disease 2019 (COVID-19) vaccination has also been recently reported [3]. Although it is known that T cell receptors (TCRs) can discriminate between self- and non-self-antigens, it is now well-accepted that TCRs exhibit cross-reactivity toward similar and even distinct antigen peptides [4]. Thus, we hypothesized that following SARS-CoV-2 infection or vaccination, T cells carrying TCRs that recognize self-antigens undergo clonal expansion, which could eventually result in the onset of autoimmune-like hepatitis
https://www.sciencedirect.com/science/article/pii/S2949928323000093