A WSJ article from earlier this week, about “COVID Long Haulers” is generating a lot of discussion.
One point it makes: “Another possibility [for the cause of chronic COVID] is that the virus causes some people’s immune systems to attack and damage their own organs and tissues, researchers said. A June study found roughly half of 29 hospitalized ICU patients with Covid-19 had one or more types of autoantibodies.”
Also getting some attention in MSM (mainstream media) this week is this recent paper published in Science Translational Medicine:
Prothrombotic autoantibodies in serum from patients hospitalized with COVID-19
“Antiphospholipid syndrome is an acquired and potentially life-threatening thrombophilia in which patients develop pathogenic autoantibodies targeting phospholipids and phospholipid-binding proteins (aPL antibodies). … These findings suggest that half of patients hospitalized with COVID-19 become at least transiently positive for aPL antibodies and that these autoantibodies are potentially pathogenic [e.g. drive thrombosis].”
https://stm.sciencemag.org/content/early/2020/11/02/scitranslmed.abd3876
Is mitigating the autoantibody problem one potential reason hydroxychloroquine (HCQ) helps in COVID-19?
Maybe that’s what’s already been suspected but the Science paper helps backup the use of HCQ.
For instance the literature on SLE includes these observations:
“data indicate that hydroxychloroquine may play a role in decreasing APL antibody levels in APL positive patients and maintaining low APL levels in APL negative patients.”
https://ard.bmj.com/content/69/Suppl_2/A10.3
“In patients with SLE and persistently positive aPL, we recommend HCQ for the primary prevention of thrombosis”
https://ashpublications.org/hematology/article/2016/1/714/21142/What-is-the-role-of-hydroxychloroquine-in-reducing
In other words, the evidence that HCQ helps continues to build.