How immunity work against Covid
How
lungs immune cells (immunity) can contribute to a virus attack
In
COVID-19 and many other diseases caused by virus attacks, the immune cells in
the lungs contribute to the aggravation of the attack. In a new study,
researchers described how different types of immune cells (immunity) develop in the lungs
and what lies behind them in acute lung disease.
And
the structure of the lungs exposes them to viruses and bacteria from both air
and blood. This study looked at what happens to certain immune cells (immunity) called
macrophages during a virus attack. Macrophages are immune cells ( immune system) that protect
the lungs and lungs from similar attacks. But in some cases, the gross stage of
lung cancer can also contribute to serious lung disease diseases such as COPD
and Covid-19.
In the study, classical monocytes show that they migrate to the airways and lung tissue and are reconstructed into macrophages that protect the health and function of the lungs. We also identified a specific type of monocyte, HLA-DRI, which is the intermediate immune cell (immunity)between the blood monocyte and the airway macrophage.
These
HLA-DRI monocytes release blood circulation and migrate to the lung tissue.
Non-classical monocytes, however, develop in the macroscopic phases in many
blood vessels of the blood lungs and do not migrate to the lung tissue.
In
infection with the coronavirus SARS-COV-2 novel, researchers hope to replace
protective, anti-inflammatory macrophages with blood monocytes by
anti-inflammatory lung macrophages. “The presence of these blood
monocyte-derived macrophages has been linked in other studies to how seriously
ill a person in Covid-19 is and how much damage can be done to the lungs.
Patients
with severe Covid-19 also have low HLDR monocytes in their blood because they
migrate from the blood to the lungs. Given their important role in rapid
inflammatory responses, our results suggest that future therapies should focus
on inflammatory macrophages and monocytes to reduce lung lung damage and
mortality from acute COVID-19.
How
to measure aerosols with a particle counter, after accounting for dust
Novel
coronavirus is spread mainly by aerosols, or small droplets produced by
coughing or sneezing that may carry the virus. Aerosol filtration in public
places, therefore, may provide a certain level of infection risk, but
performing that measure usually requires specialists and specialized equipment.
Now,
scientists have come up with an even clearer way: use a calculator for
commercially available particles. The study was published in Physics of Fluids,
a journal from the American Institute of Physics. Many particle counters are
available on the market. While the study used a device advertised as the Fluke
985, the researchers said similar results were obtained with other particle
counters. Readings obtained by hand-held particle counters, however, will
include background dust without aerosols.
How
can you separate these dust particles from aerosols from people who breathe,
talk, sneeze, and cough?
Investigators
have overcome this with a simple removal. We can measure the amount of dust
particles in the absence of aerosols and take into account whether people
produce aerosols by talking or coughing. It's just a simple site like the
University of Amsterdam.
While
the device used comes with channels of different sizes - 0.3, 0.5, 1.0, 2.0,
5.0, and 10.0 microns (1 micron half a meter) - the amount of dust is so good
that aerosols in that range cannot be really measured. More than 98% of the
dust, in fact, is contained in the first two channels (smallest particles) of
size 0.3 and 0.5 microns.
The
study did not look at the particles in these aerosol test channels. But there
is a limited range where you can get aerosols. To confirm, the researchers
compared their ratings with those from specific laboratory techniques.
Aerosol
filtration is usually measured using a process called laser diffraction, in
which a laser beam passing through a sample illuminates particles of varying
sizes. The results from this special procedure and the method used in the
study, the researchers found, are well matched.
Beware
the UK mutant
Fast-spreading
UK-type variants of SARS-CoV-2 could also develop independently in India. Ignorance
cannot be pleasure. One basic element of disease surveillance is adequate coverage
and density to catch events before they spread widely. Much more genome sequencing
is critical.
The
year 2020 will be marked by the emergence of a new virus - SARS coronavirus 2
(SARS-CoV-2) and the Covid-19 pandemic. With just a few days to go, 2020 is
expected to be closed with 84 million Covid-19 cases and more than 1.8 million
deaths.
Despite
this darkness, this has also been a year of hope, with the development, testing
and approval of policies at a rapid pace. For the first time, the human
epidemic will be controlled by vaccines in real time.
One
of the greatest threats to human progress is the virus. Two recent events
remind us of why viruses can become such powerful enemies. With the discovery
of 58 people tested for the new coronavirus in Antarctica, the epidemic has
reached all continents. Then there is the emerging virus in the United Kingdom,
which is threatening to close the world again - a country that has just begun
to recover from closures and travel bans.
Mutation
or the genome of SARS CoV-2 is a ribonucleic acid (RNA) made up of more than
30,000 units (called nucleotides). Among the families of RNA viruses,
coronaviruses have the largest genome. Most RNA viruses contain approximately
10,000 nucleotides.
When
genomes replicate - any genome, whether DNA or RNA, from very small viruses to
humans - there is a random mutation. While high-tech materials are capable of
correcting these defects, viruses and especially RNA, do not. Many mutations
are dangerous, and those viruses have never been detected. Mutations that
provide only a specific selected benefit lead to the emergence of new viruses.
Evolution also requires the pressure to choose.
With
the virus, this could be its ability to be better infected and replicate to
higher numbers or protect the immune system. The low probability of these
events is compensated by high levels of viral replication. For example, each
cell infected with the coronavirus produces about a thousand new virus cells in
less than 12 hours.
What happens is that compared to the original strains of SARS-CoV-2, the viruses of this family have collected 23 mutations in 5 genes? Of these, there are six identical variations and six similar; the first also converts amino acids on that site into protein.
Importantly, of the 17 different mutations, eight are in
spike proteins - a protein that allows the virus to attach and enter cells.
Modification of N501Y in one of the key communication residues in the spike
receptor domain (RBD) of the spike protein increases its affinity with the ACE2
receptor.
Modification
of the P681H at the clearing site between S1 and S2 spike protein sites
promotes the entry of potentially viable cells, and increases the transmission
of animal species of infection. The N501Y mutation is also associated with
increased infection and violence in animal models.
Both
of these changes have been observed independently in the past, but have come
together in the UK on a variety of viruses. The result is a virus that spreads
faster than before. Reason for Concern… There is widespread concern that this
mutation could prevent the current test from detecting the virus, kill it, or
allow it to prevent further classification of vaccines.