Coronavirus Immunity - Part 2
From the previous research, in the case of Ab deficient mouse data present that virus is in replication form, rather competent than silent in CNS. To stay hidden, the virus was maintained by the sustained intrathecal Ab. These days majority of tests rely on specific IgS ASC which accumulate in the CNS but could be detected and show the presence of the virus. Detected virus-specific IgG ASC are sustained in CNS usually 1 week after clearance of the infectious virus.
There is a difficulty in finding exact data about the still-active form of the virus or just rested but cleared infectious virus presence. Following the peak in virus-specific IgG ASC in the CNS, data show further growth in the presence of the virus in the secondary lymphoid organ. This probably happens before they become integrated into the CNS. Maybe that is a clue to follow- finding the virus in lymphoid nodes and organs and stopping further replication. But its nature is more than progressive and even fast detection doesn’t guarantee that exact medicine will reach in time. Unfortunately, many patients suffer from many motor activity disturbances, some of them similar to multiple sclerosis and after review, data show that “virus-specific ASC are retained in the CNS at high frequencies for at least 3 months post-infection. This implicates “ASC-specific survival factors in the CNS during viral persistence.”(1)
When compared with the lab mouse in a controlled environment, the other mouse which was immunocompromised, developed little demyelination. This pointed out better resistance even tough uncontrolled virus replication was present. Once again, the question about the resistance to the virus was raised. During the infection, overexpression of chemokine is a common answer and when it happens in CNS, the result is progressive demyelination. Here were noticed the activity of the bystander cells. In the beginning, it seems like their function was not relevant but then it was noticed that bystander cells were recruited by chemokine. Unfortunately, activation of the bystander cells within the CNS after microbial activity “may influence subsequent CNS inflammation and/or enhance pathogenesis.”(1)
Depending on the tissue, the virus has a very different effect and differential susceptibility to T-cell effector function. When reactivated in the absence of antibody, the virus is not silenced entirely. We can see its reactivation within CNS even if there is no T cell immunity. (1)
Lastly, retention of both T cells and ASC in the CNS during persistence suggests myelin loss is associated with an ongoing immune response, sustained by low-level oligodendroglial infection.” Here is once again confirmed unfortunate circumstance of the virus infection- loss of motor function or worse. Because of this, many rehabilitation centers are activated solely to help patients to recover. This type of strain is known for the UK coronavirus case, mostly. New studies show the different activities of virus strains in different world parts. After all, its presence in CSN certainly causes an ongoing immune response and often myelin loss.
reference:
Cornelia C. Bergmann, Chandran Ramakrishna, J. M. Gonzales, S. I. Tschen, and Stephan A. Stohlman “Coronavirus Immunity; From T cells to B cells’, 2006.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7124054/pdf/978-0-387-33012-9_Chapter_61.pdf
