Steroid's COVID-19 benefits confirmed; spotlight on immune cells
Send a link to a friend
[July 25, 2020]
By Nancy Lapid
(Reuters) - The following is a brief
roundup of some of the latest scientific studies on the novel
coronavirus and efforts to find treatments and vaccines for COVID-19,
the illness caused by the virus.
Full dexamethasone trial results released
The full results of a large randomized clinical trial in Britain - the
gold-standard of tests - looking at the steroid dexamethasone confirm
the benefits in its use in COVID-19 patients that were hinted at in
early findings issued last month. The results, released on Friday in the
New England Journal of Medicine, showed benefits for people with
advanced or moderate disease. Overall, 2,104 COVID-19 patients were
randomly assigned to receive dexamethasone and 4,321 to receive usual
care. Four weeks later, dexamethasone had reduced the risk of death by
36% among patients who needed mechanical ventilation when they entered
the study, and by 18% among those who were receiving oxygen without
mechanical ventilation. The drug did not improve survival among patients
who were not using oxygen or mechanical ventilation. In an editorial,
Dr. H. Clifford Lane and Dr. Anthony Fauci from the U.S. National
Institute of Allergy and Infectious Diseases said the results show the
crucial importance of large, well-designed, carefully run, randomized
controlled trials. Even during a pandemic, they said, when it might be
tempting to simply "give all therapies a chance," in order for patients'
outcomes to improve "there will need to be fewer small or inconclusive
studies and more studies such as the dexamethasone trial." (https://bit.ly/2ODqKpC;
https://bit.ly/2CGrZlo)
Immune cells may recognize the coronavirus years later
Researchers in Singapore are not worried that antibodies to the novel
coronavirus fade quickly. More important, they said, is that immune
system cells called T cells and B cells "remember" the virus and can
trigger an immune response. As reported on Wednesday in the journal
Nature, the researchers looked for "memory" T cells in 36 COVID-19
survivors, 23 survivors of the 2003 coronavirus that caused SARS, and 37
people who never had either illness. All COVID-19 survivors had T cells
that recognized the novel coronavirus. The SARS survivors all had T
cells that remembered the 2003 virus - and their T cells also recognized
the new coronavirus. Furthermore, more than half of those who were never
infected with either coronavirus had protective T cells, suggesting they
may have encountered other coronaviruses in the past, and there may be
some pre-existing immunity to the new coronavirus in the general
population. "We find the present discussion about 'antibodies are fading
away' a little pointless," three of the researchers told Reuters in a
joint email. "What is important is that a level of B and T cell memory
remain to be present to quickly start an effective immune response able
to stop viral spread," said Anthony Tanoto Tan of Duke-NUS Medical
School, along with colleagues Nina Le Bert and Antonio Bertoletti. T
cells can kill infected cells to slow the virus down, and they also help
instruct B cells to produce antibodies, the researchers said.
[to top of second column]
|
A computer image created by Nexu Science Communication together with
Trinity College in Dublin, shows a model structurally representative
of a betacoronavirus which is the type of virus linked to COVID-19,
better known as the coronavirus linked to the current outbreak,
shared with Reuters on February 18, 2020. NEXU Science
Communication/via REUTERS
Low interferon levels identify high-risk COVID-19
Low blood levels of a type of interferon (IFN) could identify
COVID-19 patients at high risk for severe pneumonia and acute
respiratory distress syndrome. Interferons are naturally occurring
proteins that help the body's immune system fight infection. In a
study published on Monday in the journal Science, researchers found
that severely and critically ill COVID-19 patients had severely
impaired production of IFN type I, persistent virus in the blood and
an excessive inflammatory response. They said the findings support
the potential value of treating these patients early on with IFN,
combined with anti-inflammatory drugs or steroids such as
dexamethasone in the most severely ill people. They also found that
low plasma levels of type-I IFN were seen before patients began to
deteriorate and require intensive care. "Levels of circulating Type
1 IFN could even characterize each stage of disease, with the lowest
levels observed in the most severe patients," they said in a news
release. (https://bit.ly/2WzyAoP)
Heart disease may underlie mysterious blood findings in COVID-19
patients
Severe COVID-19 predominantly affects the lungs, but elevated blood
levels of troponin, a protein released during heart injury, also are
common. To learn more, cardiologists in London performed
cardiovascular magnetic resonance scans in COVID-19 survivors who
had at least mildly elevated troponin levels while hospitalized.
Among 29 people with no obvious reason for elevated troponin, such
as a heart attack, they found two patterns of myocarditis, or heart
muscle inflammation. In patients with one pattern, heart function
seemed unaffected. These patients should undergo cardiology
follow-up to monitor for any potential long-term consequences, Dr.
Dan Knight of the Royal Free Hospital told Reuters. The other
pattern, seen in roughly a third of patients, was associated with
reduced blood supply to the heart, or ischemic heart disease. Many
patients in this group "had important coronary artery disease which
was previously unknown but required further treatment" that would
not have been offered had troponin levels not been investigated,
Knight said. The main message, Knight added, is that when troponin
levels are elevated in COVID-19 patients with no apparent reason,
further workup could reveal undiagnosed heart disease.
(Reporting by Nancy Lapid; Editing by Will Dunham and Sonya
Hepinstall)
[© 2020 Thomson Reuters. All rights
reserved.] Copyright 2020 Reuters. All rights reserved. This material may not be published,
broadcast, rewritten or redistributed.
Thompson Reuters is solely responsible for this content.
|