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1) 🇺🇸 A new paper in Nature shows that viral reactivation is common in COVID-19, associated with severity and not primarily a consequence of immunosuppression. The association with Long Covid, however, was far from clear.

2) This was a major study with 1,154 participants hospitalized with COVID-19 across 20 US hospitals between May 2020 and March 2021. Viruses were detected in blood, nasal swabs, and lung and airway fluid (in patients who were intubated).

3) Samples were collected multiple times so we can see a trajectory of viral reactivation. EBV reactivation, for example, started high but quickly declined, whereas Anelloviridae reactivation showed a slower decline.

4) The measurements were taken prior to the definition of Long Covid, but the study does include patient-reported outcomes (PROs) from which they made 4 LC subgroups.

5) The paper notes, however: "Upon evaluating viral reactivation during the acute stage of COVID19, no significant relationship was found with PRO groups." So there was no link between viral reactivation during acute infection and Long Covid.

6) It's only when they looked closer at viral detection during the convalescent period (after the acute infection) that they found a link with Anelloviridae being more prevalent in the LC subgroup physical function.

7) Anelloviruses were an unexpected finding in the Lipkin study of viruses in ME/CFS. In that paper, however, patients had a lower prevalence of anelloviruses compared to controls. Here, they report that Anelloviridae transcripts were more prevalent among patients.

8 ) For herpesviruses, the authors note: "we did not find a higher rate of EBV transcripts in the acute phase of COVID-19 for patients who developed long COVID, this result raises the question of why increased EBV antibody titres have been frequently observed in long COVID."

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EBV reactivates any time the immune system is even slightly compromised: other infections, as well as stressors (exams, spaceflight) have been shown to very significantly increase EBV titers.