COVID-19: not all patients develop protective antibodies

2020-08-04 – MEDICINE & SCIENCE

 

(Vienna, 05 August 2020) A laboratory test that has now been developed by a study group from MedUni Vienna is able to determine whether COVID-19 patients develop protective antibodies after having the disease. The main finding of the test is as follows: the scientists from MedUni Vienna's Institute of Pathophysiology and Allergy Research discovered that only around 60% of patients who have had COVID-19 and recovered from it develop protective antibodies and, for the first time, they were able to show that some antibodies even "assist" the virus by augmenting its to the cells of the host. The results have recently been published in the leading journal "Allergy".

 

Researchers from MedUni Vienna's Center for Pathophysiology, Infectiology and Immunology led by Rudolf Valenta developed an ELISA laboratory test to identify patients who had developed protective antibodies after having COVID-19. This showed that only 60% of patients convalescing from COVID-19 developed antibodies that inhibit the interaction of the SARS-CoV-2 receptor-binding domain (RBD) with ACE2. The ACE2 (Angiotensin Converting Enzyme 2) receptor for SARS-CoV-2 occurs predominantly in the respiratory tract and other organs affected by the virus. "The positive outcome is that we now have a test that can identify antibodies and show whether people who have already been infected have protective immunity or not."

However, the research team also discovered that certain immunocomplexes consisting of RBD and patient antibodies, have a higher binding rate to ACE2. This is a hitherto unknown mechanism that enables the virus to dock onto cells more easily. "This is the first study to show elevated binding to ACE2 by immunocomplexes comprising RBD and patient antibodies," explains Principal Investigator Rudolf Valenta. Potentially, this can make it even easier for the virus to infect cells." Further research is now needed to find out exactly what this means in terms of immunity and for vaccine development.

 

Read more: https://www.meduniwien.ac.at/web/en/about-us/news/detailsite/2020/news-im-august-2020/covid-19-not-all-patients-develop-protective-antibodies/

 

Link to published study: https://onlinelibrary.wiley.com/doi/epdf/10.1111/all.14523

The plot thickens.

just want to post so i can find this again when i am

in a better mood to contemplate

So... potentially some vaccines may actually "assist" COVID-19 infection? Fascinating.

That's probably because they have t-cell fighting off the disease and giving immunity or probably other kind of immune system function to fight off the disease that doctors still don't understand. There are tests for t-cell immunity. These are discussed by Swedish doctor Soo Aleman and Anders Tegnell in 2 separate videos.

 

Swedish Doctor: T-cell immunity and the truth about Covid-19 in Sweden:

 

https://www.youtube.com/watch?v=CwQpg62Kflg

 

Swedish Covid-19 chief Anders Tegnell: judge me in a year:

 

https://www.youtube.com/watch?v=xh9wso6bEAc

 

On 8/7/2020 at 7:11 PM, Puccini said:

However, the research team also discovered that certain immunocomplexes consisting of RBD and patient antibodies, have a higher binding rate to ACE2. This is a hitherto unknown mechanism that enables the virus to dock onto cells more easily.

 

On 8/8/2020 at 7:42 PM, timendres said:

So... potentially some vaccines may actually "assist" COVID-19 infection? Fascinating.

 

Maybe.  The basuc idea is not new. Antibody dependent enhancement, ADE, was discussed as a potential problem for  SARS-1 vaccines Jan 10 2012 (BMC Proceedings). They compared SARS to viruses like Dengue Fever where ADE can produce more severe second infections. Another, recent paper, June 7 2020 (here: NCBI-NIH) makes a comparison between Dengue, SARS-2, and ADE in detail. 

 

From the recent paper:

"Here, we review the possible antibody‐dependent enhancement (ADE) occurrence, known for dengue infections, when there is a second infection with a different virus strain. Consequently, pre-existing antibodies do not neutralize infection, but enhance it, possibly by triggering Fcγ receptor‐mediated virus uptake."

 

"No clinical data exist indicating such mechanism for SARS‐CoV‐2, but previous coronavirus infections or infection of SARS‐CoV‐2 convalescent with different SARS‐CoV‐2 strains could promote ADE, as experimentally shown for antibodies against the MERS‐CoV or SARS‐CoV spike S protein."

 

They both suggest vaccine developers need to consider this as they rush to get a vaccine out first.