Chapter
1:
COVID-19
pathogenesis
poses
paradoxes
difficult
to
explain
with
traditional
physiology.
For
instance,
since
type
II
pneumocytes
are
considered
the
primary
cellular
target
of
SARS-CoV-2;
as
these
produce
pulmonary
surfactant
(PS),
possibility
that
insufficient
PS
plays
a
role
in
has
been
raised.
However,
opposite
predicted
high
alveolar
surface
tension
is
found
many
early
patients:
paradoxically
normal
lung
volumes
and
compliance
occur,
profound
hypoxemia.
That
‘COVID
anomaly’
was
quickly
rationalised
by
invoking
vascular
mechanisms–mainly
because
surprisingly
preserved
hypoxemic
cases.
quick
rejection
damage
only
occurred
actual
mechanism
gas
exchange
long
presumed
be
non-problematic,
due
diffusion
through
surface.
On
contrary,
we
provide
physical
chemical
evidence
occurs
an
process
expansion
contraction
three-dimensional
structures
its
associated
proteins.
This
view
explains
anomalous
observations
from
level
cryo-TEM
whole
individuals.
It
encompasses
results
premature
infants
deepest
diving
seals.
Once
understood,
COVID
anomaly
dissolves
straightforwardly
explained
covert
viral
3D
structure
PS,
direct
treatment
implications.
As
natural
experiment,
SARS-CoV-2
virus
itself
helped
us
simplify
clarify
not
nature
dyspnea
relationship
compliance,
but
also
fine
detail
including
such
features
water
channels
which
had
heretofore
entirely
unexpected.
Chapter
1:
COVID-19
pathogenesis
poses
paradoxes
difficult
to
explain
with
traditional
physiology.
For
instance,
since
type
II
pneumocytes
are
considered
the
primary
cellular
target
of
SARS-CoV-2;
as
these
produce
pulmonary
surfactant
(PS),
possibility
that
insufficient
PS
plays
a
role
in
has
been
raised.
However,
opposite
predicted
high
alveolar
surface
tension
is
found
many
early
patients:
paradoxically
normal
lung
volumes
and
compliance
occur,
profound
hypoxemia.
That
‘COVID
anomaly’
was
quickly
rationalised
by
invoking
vascular
mechanisms–mainly
because
surprisingly
preserved
hypoxemic
cases.
quick
rejection
damage
only
occurred
actual
mechanism
gas
exchange
long
presumed
be
non-problematic,
due
diffusion
through
surface.
On
contrary,
we
provide
physical
chemical
evidence
occurs
an
process
expansion
contraction
three-dimensional
structures
its
associated
proteins.
This
view
explains
anomalous
observations
from
level
cryo-TEM
whole
individuals.
It
encompasses
results
premature
infants
deepest
diving
seals.
Once
understood,
COVID
anomaly
dissolves
straightforwardly
explained
covert
viral
3D
structure
PS,
direct
treatment
implications.
As
natural
experiment,
SARS-CoV-2
virus
itself
helped
us
simplify
clarify
not
nature
dyspnea
relationship
compliance,
but
also
fine
detail
including
such
features
water
channels
which
had
heretofore
entirely
unexpected.
Chapter
1:
COVID-19
pathogenesis
poses
paradoxes
difficult
to
explain
with
traditional
physiology.
For
instance,
since
type
II
pneumocytes
are
considered
the
primary
cellular
target
of
SARS-CoV-2;
as
these
produce
pulmonary
surfactant
(PS),
possibility
that
insufficient
PS
plays
a
role
in
has
been
raised.
However,
opposite
predicted
high
alveolar
surface
tension
is
found
many
early
patients:
paradoxically
normal
lung
volumes
and
compliance
occur,
profound
hypoxemia.
That
‘COVID
anomaly’
was
quickly
rationalised
by
invoking
vascular
mechanisms–mainly
because
surprisingly
preserved
hypoxemic
cases.
quick
rejection
damage
only
occurred
actual
mechanism
gas
exchange
long
presumed
be
non-problematic,
due
diffusion
through
surface.
On
contrary,
we
provide
physical
chemical
evidence
occurs
an
process
expansion
contraction
three-dimensional
structures
its
associated
proteins.
This
view
explains
anomalous
observations
from
level
cryo-TEM
whole
individuals.
It
encompasses
results
premature
infants
deepest
diving
seals.
Once
understood,
COVID
anomaly
dissolves
straightforwardly
explained
covert
viral
3D
structure
PS,
direct
treatment
implications.
As
natural
experiment,
SARS-CoV-2
virus
itself
helped
us
simplify
clarify
not
nature
dyspnea
relationship
compliance,
but
also
fine
detail
including
such
features
water
channels
which
had
heretofore
entirely
unexpected.