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].”
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.”
“In patients with SLE and persistently positive aPL, we recommend HCQ for the primary prevention of thrombosis”
In other words, the evidence that HCQ helps continues to build.