A recent study published in Immunity has revealed that the Pfizer/BioNTech mRNA vaccine is much better than natural infection at revving up killer T cells to fight future SARSCoV-2 infection. The vaccine has shown an exceptional ability to spur the proliferation and activation of killer T cells directed at SARSCoV-2. However, this ability is lowered when an individual is infected with the virus before getting vaccinated.
The study emphasizes the importance of those hoping to avoid the health risks associated with COVID-19 getting vaccinated before contracting the disease. Though vaccination after having had COVID-19 does somewhat boost the number and battle-readiness of killer T cells, it does not provide as much protection as vaccination preceding infection.
Furthermore, the study highlights that killer T cells’ lost punch after a bout of COVID-19 could weaken the immune response to a new SARS-CoV-2 assault later, increasing the chances that the virus will persist in overlooked infected cells and possibly contributing to the development of long COVID. Killer T cells are immune cells that inspect cells’ surfaces for infectious pathogens and kill infected cells. If killer T cells are not abundant enough or do not get sufficiently activated, then the virus gets extra time to commandeer that cell’s productive machinery and spread to other cells.
It is important to note that the study investigated how the Pfizer/BioNTech vaccine works, and no equivalent analysis was performed on other vaccines like Moderna.
COVID-19 continues to have significant worldwide health and economic effects. Understanding the relationship between SARS-CoV-2, infected host cells, and the pathophysiology of the disease is urgent.
Recent research suggests that transposable elements (TEs) play a crucial role in the host’s response to COVID-19 and the development of illness. A study posted to the bioRxiv preprint server examines the effect of SARS-CoV-2 on the expression profiles of TEs in virus-exposed or infected cells.
The study found that LTR69 subfamily of endogenous retroviruses was upregulated by SARS-CoV-2 infection. LTR69 can regulate host gene expression, thus contributing to the outcome of COVID-19.
It is important to note that additional research is required to confirm these findings since this study was still undergoing peer review during its publication.
A recent study led by University of Melbourne Professor Katherine Kedzierska shows that hematology patients generate strong cellular immune responses against SARSCoV-2 after vaccination, on par with healthy individuals. The research team found that hematology patients highly benefit from receiving three doses of vaccination, irrespective of their B-cell numbers and antibody response.
After vaccination, T-cells are generated, and the vaccines boost the levels of T-cells that kill viral-infected cells. The signatures of T-cells generated after vaccination in hematology patients are very similar to healthy individuals that are either infected or vaccinated.
The study shows that it is safe and beneficial for heavily immunocompromised hematology patients, who are vulnerable to severe COVID-19 infection, to receive vaccination against SARS-CoV-2. The research provides key insights for future immunization strategies with vaccines such as influenza which predominantly induce B-cell immune responses.
In conclusion, these studies shed further light on the importance of vaccination in protecting against future COVID-19 infections, as well as highlighting the role of transposable elements and cellular immune responses in the host’s response to SARS-CoV-2 infection. Further research is required to confirm these findings and guide future vaccination strategies.
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