Coronavirus Immunity - Part 1
Coronavirus Immunity - Part 1
Introduction
Observations in coronavirus infected lab mouses brought us new conclusions about the immunity response. Here we learn that T cells (T CD8+ cells, specifically) have extraordinary ability to move, especially when in the presence fo CD4+T cells. As such, they can transfer to CNS and develop the ability to either replicate and travel further to distant organs where are up to develop new pathologies. In the wild type of mice, T cells can be silenced and have low or no effect which can be seen by the level of demyelination.
Unlike the recovery of wild-type mice, mice unable to secrete Ab exhibit increased mortality associated with the re-emergence of the infectious virus within the CNS.
A protective role of T cells during persistence is disputed by viral recrudescence in mice devoid of B cells.
The MHV A59 strain, which infects both the liver and CN fails to reactivate in the liver in the absence of humoral immunity.
Why are wild type mice capable of lower viral impact/better response?
Can it be explained by diverse wild type mice genetic in comparison with lab mouses or we can find more about it following new finding of T and B cells response after the infection?
So far, research shows that viral infection stays visible up to two years after the initial contact. This data was for the previously know coronavirus types. The new one, discovered just lately, at the end of the year 2019, it yet to be specified. Many people infected by the new coronavirus type, show no to little clinical abnormalities.
Detected was ongoing primary CNS demyelination, “similar to pathological changes associated with multiple sclerosis”. (C. C. BERGMANN ET AL.)
One strain of the coronavirus A59, clearly leads to these pathological changes. What was the innate CNS inflammatory response behind this?
As in this new strain, prominent adaptive response peaks 7-10 days post-infection.
“Although survivors exhibit little or no clinical abnormalities, histological examination shows ongoing primary CNS demyelination, similar to the pathological changes associated with multiple sclerosis. Viral antigen and more prominently RNA remain detectable exclusively within the CNS up to 2 years p.i. “ (C. C. BERGMANN ET AL .)
Before they can be noticed in CNS, T cells are detectable in other places, mostly spleen and ClN (cervical lymph nodes). Spleen is regulating red and white blood cells and it is a place where used
“T cells, most prominently the CD8+ subset, provide the most critical anti-viral functions. T-cells from the inflamed CNS of previously immunized mice exhibit increased enzyme B production, as well as enhanced cytolysis at a single-cell level.” (C. C. BERGMANN ET AL .)
After the clearance of the virus, most of the T cells disappear but those who resist and stay show viral presence since there is also ongoing demyelination present. What triggers our attention is the replication competitive form of the virus in CNS.
Reference: “Coronavirus Immunity - From T cells to B cells”; Cornelia C. Bergman, Chndran Ramakrishna, J. M. Gonzales, S. I. Tschen, and Stephen A. Stohlman
(The esearch was supported by the National Institutes of Health Grants NS18146 and AI47249).
link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7124054/pdf/978-0-387-33012-9_Chapter_61.pdf
