Gentle People:
Here is something else that I have learned so far and it seems to contain conflicting information. Judge for yourselves.
1. According to the Japanese, the SARS-CoV-2 protein basically blocks the human cell from recognizing that a virus is present. Human interferons: Type I and type III IFNs, establish the cellular state of viral resistance, as well as activate the adaptive immune responses to viruses (
Successful viral pathogens, however, have evolved mechanisms to escape both immune recognition and suppress the functions of IFNs and ISGs. Many viral proteins are dedicated to modulating the host IFN response. These mechanisms have been extensively investigated for SARS-CoV and MERS-CoV ( It has been proven that many viruses block interferon from signalling for help and when Interferon is not expressed, it consequently does not signal B cells and T cells to arrive and fight the virus. The virus is then uninhibited and infects every cell in the host body...
2. Conflicting with this concept is the idea that a cytokine storm response is created by the SARS-CoV-2. A cytokine storm occurs when too many T cells gather to fight an infection and do more damage than good. When too many killer T cells enter the lungs, they can destroy both the virus and the cells in the lungs. The Japanese claim they did not find T cells in the lungs of their patients. This would be possible if interferon was inhibited by the SARS-CoV-2 from signalling the B and T cells.
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In another new study, scientists in Japan last week identified how SARS-CoV-2 accomplishes its genetic manipulation. Its ORF3b gene produces a protein called a transcription factor that has “strong anti-interferon activity,” Kei Sato of the University of Tokyo and colleagues found the transcription factor to be stronger than the original SARS virus or influenza viruses. The SARS-CoV-2 protein basically blocks the human cell from recognizing that a virus is present, in a way that prevents interferon genes from being expressed. Interferon genes call for help from human B cells and T cells while slowing down the SARS virus. Without interferon genes, no call for help is issued and the virus continues to infect the cells.
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The more than 100 COVID-19 vaccines in development mainly focus on another immune response: antibodies. Antibody proteins are made by B cells and ideally latch onto SARS-coV-2 and prevent it from entering cells. (They do, that is, if they are triggered by interferon to locate the SARS-CoV-2. )
T cells thwart infections in two different ways. 1. Helper T cells spur B cells into making antibody proteins and other immune defenders into action, and 2. killer T cells target and destroy infected cells. The severity of disease can depend on the strength of the killer T cell response, which if too strong, may trigger a cytokine storm response and do more harm than good. It can kill rather than cure.
For reasons that are not completely understood, too many immune cells can be sent to the infection site and when this happens a particular type of molecule in the body, known as a cytokine, is activated. The immune cells at the infection site signal more immune cells to flood the area. This creates a cytokine storm where far too many immune cells are activated to fight the infection. The reaction ends up inflaming the tissue surrounding the infection and both the virus and the human cell...die!
When the infection is in the lungs a severe inflammation created by the cytokine reaction can cause permanent damage and doctors who place an oxygen tube into an already damaged lung may be doing more harm than good. A prolonged cytokine storm will eventually shut down breathing completely as infected lung cells lose the capacity to transfer oxygen to blood cells. This is usually when a doctor will use a ventilator to place an oxygen tube into a damaged lung of a patient. A cytokine storm is what makes the reaction so deadly in certain epidemic strains such as bronchitis and other varieties of influenza, Pneumonia, sepsis, and possibly rheumatoid arthritis are susceptible to triggering a cytokine storm.
Using bioinformatics tools, a team led by Shane Crotty and Alessandro Sette, immunologists at the La Jolla Institute for Immunology, predicted which viral protein pieces would provoke the most powerful T cell responses. They then exposed immune cells from 10 patients who had recovered from mild cases of COVID-19 to these viral snippets.
All of the patients carried helper T cells that recognized the SARS-CoV-2 spike protein, which enables the virus to infiltrate our cells. They also harbored helper T cells that react to other SARS-CoV-2 proteins. And the team detected virus-specific killer T cells in 70% of the subjects, they report today in Cell. “The immune system sees this virus and mounts an effective immune response,” Sette says.
The results jibe with those of a study posted as a preprint on medRxiv on 22 April by immunologist Andreas Thiel of the Charité University Hospital in Berlin and colleagues. They identified helper T cells targeting the spike protein in 15 out of 18 patients hospitalized with COVID-19.
Duration of contamination on objects and surfaces
The more than 100 COVID-19 vaccines in development mainly focus on another immune response: antibodies. Antibody proteins are made by B cells and ideally latch onto SARS-coV-2 and prevent it from entering cells. (They do, that is, if they are triggered by interferon to locate the SARS-CoV-2. )
T cells thwart infections in two different ways. 1. Helper T cells spur B cells into making antibody proteins and other immune defenders into action, and 2. killer T cells target and destroy infected cells. The severity of disease can depend on the strength of the killer T cell response, which if too strong, may trigger a cytokine storm response and do more harm than good. It can kill rather than cure.
For reasons that are not completely understood, too many immune cells can be sent to the infection site and when this happens a particular type of molecule in the body, known as a cytokine, is activated. The immune cells at the infection site signal more immune cells to flood the area. This creates a cytokine storm where far too many immune cells are activated to fight the infection. The reaction ends up inflaming the tissue surrounding the infection and both the virus and the human cell...die!
When the infection is in the lungs a severe inflammation created by the cytokine reaction can cause permanent damage and doctors who place an oxygen tube into an already damaged lung may be doing more harm than good. A prolonged cytokine storm will eventually shut down breathing completely as infected lung cells lose the capacity to transfer oxygen to blood cells. This is usually when a doctor will use a ventilator to place an oxygen tube into a damaged lung of a patient. A cytokine storm is what makes the reaction so deadly in certain epidemic strains such as bronchitis and other varieties of influenza, Pneumonia, sepsis, and possibly rheumatoid arthritis are susceptible to triggering a cytokine storm.
Using bioinformatics tools, a team led by Shane Crotty and Alessandro Sette, immunologists at the La Jolla Institute for Immunology, predicted which viral protein pieces would provoke the most powerful T cell responses. They then exposed immune cells from 10 patients who had recovered from mild cases of COVID-19 to these viral snippets.
All of the patients carried helper T cells that recognized the SARS-CoV-2 spike protein, which enables the virus to infiltrate our cells. They also harbored helper T cells that react to other SARS-CoV-2 proteins. And the team detected virus-specific killer T cells in 70% of the subjects, they report today in Cell. “The immune system sees this virus and mounts an effective immune response,” Sette says.
The results jibe with those of a study posted as a preprint on medRxiv on 22 April by immunologist Andreas Thiel of the Charité University Hospital in Berlin and colleagues. They identified helper T cells targeting the spike protein in 15 out of 18 patients hospitalized with COVID-19.
Abstract
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a rapidly unfolding pandemic, overwhelming health care systems worldwide1. Clinical manifestations of Corona-virus-disease 2019 (COVID-19) vary broadly, ranging from asymptomatic infection to acute respiratory failure and death2, yet the underlying physiological conditions and mechanisms for this high variability are still unknown. Also, the role of host immune responses in viral clearance and its involvement in pathogenesis remains unresolved. For SARS-CoV (2002/03), however, CD4+ T cell responses are generally associated with positive outcomes3,4, while cellular immune responses to SARS-CoV-2 have not yet been investigated. Here we describe an assay that allows direct detection and characterization of SARS-CoV-2 spike glycoprotein (S)-reactive CD4+ T cells in peripheral blood. We demonstrate the presence of S-reactive CD4+ T cells in 83% of COVID-19 patients, as well as in 34% of SARS-CoV-2 seronegative healthy donors, albeit at lower frequencies. Strikingly, in COVID-19 patients S-reactive CD4+ T cells equally targeted both N-terminal and C-terminal parts of S whereas in healthy donors S-reactive CD4+ T cells reacted almost exclusively to the Cterminal part that is a) characterized by higher homology to spike glycoprotein of human endemic "common cold" coronaviruses, and b) contains the S2 subunit of S with the cytoplasmic peptide (CP), the fusion peptide (FP), and the transmembrane domain (TM) but not the receptor-binding domain (RBD). S-reactive CD4+ T cells from COVID-19 patients were further distinct to those from healthy donors as they co-expressed higher levels of CD38 and HLA-DR, indicating their recent in vivo activation. Our study is the first to directly measure SARS-CoV-2-reactive T cell responses providing critical tools for large scale testing, in depth epitope mapping and characterization of potential cross-reactive cellular immunity to SARS-CoV-2. The presence of pre-existing SARS-CoV-2-reactive T cells in healthy donors is of high interest but larger scale prospective cohort studies are needed to assess whether their presence is a correlate of protection or pathology. Results of such studies will be key for a mechanistic understanding of the SARS-CoV-2 pandemic, adaptation of containment methods and to support vaccine development.
Competing Interest Statement
The authors Jürgen Schmitz, Stefan Miltenyi, Florian Kern, Ulf Reimer, Holger Wenschuh are employed at non-academic cooperations.
Funding Statement
Duration of contamination on objects and surfaces
Although the virus was greatly reduced, viable SARS-CoV-2 was measured for this length of time:
- Plastic: up to 2-3 days
- Stainless Steel: up to 2-3 days
- Cardboard: up to 1 day
- Copper: up to 4 hours
[source]
Floor
"The rate of positivity was relatively high for floor swab samples (ICU 7/10, 70%; GW 2/13, 15.4%), perhaps because of gravity and air flow causing most virus droplets to float to the ground.
In addition, as medical staff walk around the ward, the virus can be tracked all over the floor, as indicated by the 100% rate of positivity from the floor in the pharmacy, where there were no patients.
Furthermore, half of the samples from the soles of the ICU medical staff shoes tested positive. Therefore, the soles of medical staff shoes might function as carriers. The 3 weak positive results from the floor of dressing room 4 might also arise from these carriers. We highly recommend that persons disinfect shoe soles before walking out of wards containing COVID-19 patients." [source]
