■ Healthcare
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vaccine will take time. Also, the original SARS-
CoV emerged in 2003, and generating a vaccine
to that virus has proven to be challenging.
Q. You specialize in understanding and characteriz-
ing virus-host interactions and viral antagonism of
host immune responses. What can you tell us about
the virus-host interactions of COVID-19?
A. Typically, when viruses infect a cell, the cell
activates its innate immune response to at-
tempt to eradicate viruses. The human body
essentially marshals its resources to fight
against what is, in essence, the invasion of a
foreign entity. These responses include inflam-
mation, inducing cell death to destroy both
the cell and the virus, and activating antiviral
proteins such as interferon. It can, in some
ways, be considered a “shotgun” approach,
with the initial immune response scattering
its shot and killing everything in the vicinity
of the threat.
All these efforts are in place to try and con-
tain the infection. Eventually, in what can be
thought of as “the next wave” of defense, the
adaptive immune response is activated to de-
stroy any viruses that were not killed in the ini-
tial response. The adaptive response includes B
cells producing antibodies to target and neu-
tralize remaining viruses in the body.
For viruses, the most important part of the
adaptive immune response or “next wave” is the
activity of cells called cytotoxic T-cells. These
cells are the hunters/killers of the immune re-
sponse and take more of a “rifle” approach, ac-
tively hunting down cells infected with viruses
and eradicating those particular cells, thereby
containing the virus.
In addition, the adaptive response creates
memory immune cells, which remain after the
body clears the virus and can activate the im-
mune response much faster on a second expo-
sure. These memory immune cells are the basis
of vaccines and why it is so important to be im-
munized against infectious agents.
Viruses, however, are not in the habit of going
quietly. Viruses have evolved complex strategies
to prevent the body’s immune response from
activating. In the case of the original SARS-CoV,
we know that it blocks the activation of sever-
al key immune pathways. By modulating the
host’s immune response, SARS-CoV was able
to ensure a successful infection by escaping the
body’s defenses.
It’s also important to note that things can go
wrong on the defense as well. Sometimes the
immune system overresponds to infection. I al-
ways tell my students to think of the immune
system working best in the so-called Goldilocks
zone. Too little of an immune response and the
28 COMMERCE www. commercemagnj.com
virus is not cleared. Too much and the body’s
own immune response damages the body trying
to clear the virus.
Q. What can you tell us about host immune respons-
es in humans to COVID-19?
A. There’s a lot we don’t know at the moment.
It’s likely that in some individuals, the immune
response is not strong enough to kill the virus,
and as the virus replicates it destroys the lungs,
leading to severe complications and possibly
even death. In others, it seems to be that the
virus induces a cytokine storm. Cytokines are
produced by immune cells to communicate and
coordinate responses to infectious agents.
In these patients, too much cytokines results
in an immune response that damages the pa-
tient’s own body, leading to severe complica-
tions. This scenario may be responsible for a
number of the severe cases and even mortality
among those who seem to otherwise healthy.
To use the Goldilocks analogy, this would be a
case of the porridge being too hot. The cytokine
storm is not unique to SARS-CoV 2.
This event has been noted in other great pan-
demics including the 1918 Spanish Flu, Avian
Influenza, and the original SARS-CoV. The rea-
sons why some individuals have an over-active
immune response against severe human coro-
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