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Not good if true -- small study group of 74 ... 
also could be Chinese propaganda

Antibody levels in recovered COVID-19 patients decline quickly: research

Levels of an antibody found in recovered COVID-19 patients,
fell sharply in 2-3 months 
after infection for both symptomatic and asymptomatic patients, 
according to a Chinese study 
raising questions about the length of any immunity against the novel coronavirus.

The research, published in Nature Medicine on June 18,
highlights the risks of using COVID-19 ‘immunity passports’ 
and supports the prolonged use of public health interventions 
such as social distancing and isolating high-risk groups, researchers said.

Health authorities in some countries such as Germany are debating the ethics and practicalities 
of allowing people who test positive for antibodies to move more freely than others who don’t.

The research, which studied 37 symptomatic patients and 37 asymptomatic patients, 
found that of those who tested positive for the presence of the IgG antibody, 
one of the main types of antibodies induced after infection, 
over 90% showed sharp declines in 2-3 months.

The median percentage decrease was more than 70% for both symptomatic and asymptomatic patients.

For neutralising serum antibodies, 
the median percentage of decrease for symptomatic individuals was 11.7%, 
while for asymptomatic individuals it was 8.3%.

The study was conducted by researchers at Chongqing Medical University, 
a branch of the Chinese Center for Disease Control and Prevention and other institutes.

Jin Dong-Yan, a virology professor at the University of Hong Kong, 
who was not part of the research group, 
said the study does not negate the possibility that other parts of the immune system could offer protection.

A Study on Infectivity of --->  Asymptomatic SARS-CoV-2 Carriers <---

An ongoing outbreak of coronavirus disease 2019 (COVID-19)
has spread around the world.
It is debatable whether asymptomatic COVID-19 virus carriers are contagious.

We report here a case of the asymptomatic patient,
and present clinical characteristics of 455 contacts,
which aims to study the infectivity of asymptomatic carriers.

Material and methods:
455 contacts
who were exposed to the asymptomatic COVID-19 virus carrier,
became the subjects of our research.
They were divided into three groups:
35 patients,
196 family members
and 224 hospital staffs.
We extracted their epidemiological information, clinical records,
auxiliary examination results and therapeutic schedules.

The median contact time for patients was four days
and that for family members was five days.
Cardiovascular disease accounted for 25% among original diseases of patients.
Apart from hospital staffs,
both patients and family members were isolated medically.
During the quarantine,
seven patients plus one family member appeared new respiratory symptoms,
where fever was the most common one.
The blood counts in most contacts were within a normal range.
All CT images showed no sign of COVID-19 infection.
No severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections <---
was detected <---
in 455 contacts by nucleic acid test. <---

In summary, all the 455 contacts were excluded from SARS-CoV-2 infection,
and we conclude,
that the infectivity of some asymptomatic SARS-CoV-2 carriers might be weak.

Zen and the art of debunkery MUST READ!!!  Arrow Arrow Arrow

Notice how china virus is like an improv skit ...only based on malignancy instead of a benign offering.

JUNE 29, 2020
Arrow Existing drugs can prevent SARS-CoV-2 from hijacking cells
[Image: 2-existingdrug.jpg]SARS-CoV-2 viruses on a cell with filopodia. Credit: Elizabeth Fischer, Microscopy Unit NIH/NIAID
An international team of researchers has analyzed how SARS-CoV-2, the virus that causes COVID-19, hijacks the proteins in its target cells. The research, published in the journal Cell, shows how the virus shifts the cell's activity to promote its own replication and to infect nearby cells. The scientists also identified seven clinically approved drugs that could disrupt these mechanisms, and recommend that these drugs be immediately tested in clinical trials.

The collaboration included researchers at EMBL's European Bioinformatics Institute (EMBL-EBI), the Quantitative Biosciences Institute's Coronavirus Research Group in the School of Pharmacy at University of California San Francisco (UCSF), the Howard Hughes Medical Institute, the Institut Pasteur, and the Excellence Cluster CIBSS of the University of Freiburg.
Viruses are unable to replicate and spread on their own: they need an organism—their host—to carry, replicate, and transmit them to further hosts. To facilitate this process, viruses need to take control of their host cell's machinery and manipulate it to produce new viral particles. Sometimes, this hijacking interferes with the activity of the host's enzymes and other proteins.
Once a protein is produced, enzymes can change its activity by making chemical modifications to its structure. For example, phosphorylation—the addition of a phosphoryl group to a protein by a type of enzyme called a kinase—plays a pivotal role in the regulation of many cell processes, including cell-to-cell communication, cell growth, and cell death. By altering phosphorylation patterns in the host's proteins, a virus can potentially promote its own transmission to other cells and, eventually, other hosts.
The scientists used mass spectrometry, a tool to analyze the properties of a sample by measuring the mass of its molecules and molecular fragments, to evaluate all host and viral proteins that showed changes in phosphorylation after SARS-CoV-2 infection. They found that 12% of the host proteins that interact with the virus were modified. The researchers also identified the kinases that are most likely to regulate these modifications. Kinases are potential targets for drugs to stop the activity of the virus and treat COVID-19.
[b]The extraordinary behavior of infected cells[/b]
"The virus prevents human cells from dividing, maintaining them at a particular point in the cell cycle. This provides the virus with a relatively stable and adequate environment to keep replicating," explains Pedro Beltrao, Group Leader at EMBL-EBI.
SARS-CoV-2 not only impacts cell division, but also cell shape. One of the key findings from the study is that infected cells exhibit long, branched, arm-like extensions, or filopodia. These structures may help the virus reach nearby cells in the body and advance the infection, but further study is warranted.
"The distinct visualization of the extensive branching of the filopodia once again elucidates how understanding the biology of virus-host interaction can illuminate possible points of intervention in the disease," says Nevan Krogan, Director of the Quantitative Biosciences Institute at UCSF and Senior Investigator at Gladstone Institutes.
[b]Old drugs,  Sheep new treatments[/b]
"Kinases possess certain structural features that make them good drug targets. Drugs have already been developed to target some of the kinases we identified, so we urge clinical researchers to test the antiviral effects of these drugs in their trials," says Beltrao.
In some patients, COVID-19 causes an overreaction of the immune system, leading to inflammation. An ideal treatment would relieve these exaggerated inflammatory symptoms while stopping the replication of the virus. Existing drugs targeting the activity of kinases may be the solution to both problems.
The researchers identified dozens of drugs approved by the Food and Drug Administration (FDA) or ongoing clinical trials that target the kinases of interest. Seven of these compounds, primarily anticancer and inflammatory disease compounds, demonstrated potent antiviral activity in laboratory experiments.
"Our data-driven approach for drug discovery has identified a new set of drugs that have great potential to fight COVID-19, either by themselves or in combination with other drugs, and we are excited to see if they will help end this pandemic," says Krogan.
"We expect to build upon this work by testing many other kinase inhibitors while identifying both the underlying pathways and additional potential therapeutics that may intervene in COVID-19 effectively," says Kevan Shokat, Professor in the Department of Cellular and Molecular Pharmacology at UCSF.

Explore further
Coronavirus and cancer hijack the same parts in human cells to spread: Existing cancer drugs could fight COVID-19

[b]More information:[/b] Mehdi Bouhaddou et al, The Global Phosphorylation Landscape of SARS-CoV-2 Infection, Cell (2020). DOI: 10.1016/j.cell.2020.06.034
[b]Journal information:[/b] Cell [/url]

Provided by [url=]European Molecular Biology Laboratory

Quote:Zen and the art of debunkery MUST READ!!!  Arrow Arrow Arrow
Along the vines of the Vineyard.
With a forked tongue the snake singsss...

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