hey guys welcome back to another video this one's going to be on covid 19 in autoimmunity so long
covid and multi-system inflammatory disease these are scientifically mysterious complications of
covid 19 and covid 19 by itself is a mysterious disease in a lot of ways despite us already
knowing a lot about it scientists are working hard to unravel the cause and effect of the interaction
between the sars cov2 virus and the immune system covid causes several symptoms that may
point to a phenomenon called autoimmunity as a potential cause of long covid now this includes
pulmonary fibrosis meaning scarring of the lungs unfortunately i'm seeing the same picture unfold
in so many of my patients in the pulmonary clinic where they've had covid 19 and now they have a
lot of scarring in their lungs as a result of that and covid can cause other issues like brain
changes we've all heard about the brain fog it can cause skin rashes excessive blood clotting
inflamed blood vessels and more autoimmunity is when the immune system mounts an attack on
its own healthy cells and tissues mistaking them for foreign or virally infected cells
now under normal conditions the immune system can discriminate between self and foreigners meaning
it can differentiate between the body's proteins and foreign antigens but sometimes in some people
the immune system can mistakenly identify its own proteins as foreign antigens and it launches
its attack on itself now when these autoantibodies react against self antigens the outcome can be
inflammation and damage to tissues this is what happens with autoimmune diseases such as type 1
diabetes graves disease multiple sclerosis and more this is also what happens with idiopathic
pulmonary fibrosis where people get scarring in their lungs much in the same way that happens
with covid in fact there are a lot of autoimmune conditions that can result in scarring in the
lungs or pulmonary fibrosis this includes things like lupus scleroderma polymyositis rheumatoid
arthritis and ankylosing spondylitis the vast majority of people who get covid will have
disease that is isolated to the upper respiratory tract but in 20% of people who get the infection
it'll go deep into the lung parenchyma and have the potential to cause more severe disease meaning
covid pneumonia which sometimes blossoms into ards acute respiratory distress syndrome
the question of autoimmunity as a potential cause of more severe covert disease that was brought
up when autopsies of people who died of covid 19 revealed an inconsistency between the viral load
in the degree of lung damage this disconnect led to researchers to surmise that the immune system
is more responsible than the virus for causing the extensive and often irreparable lung damage
a study that hasn't yet been peer reviewed enrolled 147 hospitalized patients with covid 19
in three medical centers they measured autoantibodies that were associated with
connective tissue diseases for example lupus they also measured other antibodies like anticytokine
antibodies and antiviral antibodies now compared to a healthy control group autoantibodies were
more commonly found in people who had covid 19. researchers found auto antibodies in half
of hospitalized covid patients compared to less than 15 percent who were healthy and
uninfected now in some the auto antibodies didn't change throughout the course of illness
however in 20% the autoantibodies increased as the disease progressed it takes several weeks for
autoantibodies to build up which may explain the delay in developing symptoms of severe covid 19
there is a study done at rockefeller university in new york that enrolled almost a thousand
patients with severe covid about 10 percent had antibodies that blocked the action of type
1 interfering molecules which is a protein that helps the immune system fight pathogens
these auto antibodies were more common in men at 12.5 percent compared to women at 2.6 percent this
may explain why men are more likely to have more severe disease the researchers in the study are
now screening 40 000 people to see what proportion of uninfected people carry these antibodies
and their distribution by age ancestry and gender now this data will be compared to the distribution
and percentage of each factor in people with severe covid researchers in another study
supported the finding of increased autoantibodies in covid patients the antibodies they found were
directed towards b cells a type of immune cell that produces antibodies and interferon although
the researchers noted that they found no covid 19 specific autoantibodies that distinguish
covid 19 patients from uninfected controls the levels of autoantibodies were correlated with
known markers of inflammation and the correlations became more extreme as the disease worsened other
researchers and yet to be peer-reviewed study found that anti-annexin antibodies were elevated
among hospitalized covenanting patients with the highest levels in those who died antibodies that
inhibit anexin's activity can cause widespread blood clotting cellular death and swelling in
lung tissue the authors concluded that these anti-annexan antibody levels predicted mortality
have other viruses been implicated in forming auto antibodies well case reports from as early
as 1984 show autoantibodies against interferon after a viral infection with varicella zoster viruses that
have been proposed as triggers for autoimmune disorders include parvovirus b19 epstein-barr
virus cytomegalovirus herpesvirus 6 hepatitis a hepatitis c and rubella so the epstein-barr virus
which causes mononucleosis or mono has been linked to many autoimmune disorders including lupus
streptococcus pyogenes the bacteria that causes strep throat can prompt an autoimmune
reaction called rheumatic fever in addition to glomerulonephritis which is a kidney condition
rheumatic fever can cause permanent heart damage after attacking heart cells aka
myocytes helicobacter pylori is a bacteria that can cause infection of the stomach and this
bacterial infection is thought to be a trigger for developing immune thrombocytopenic purpura aka itp
itp is an autoimmune attack on platelets which are responsible for blood clotting at least
partially responsible for blood clotting sars cov2 has been linked to several autoimmune disorders
there's been a case report of a 65 year old female with covid 19 in addition to another
case report of a pediatric patient and they each developed itp recently i did a video on a
doctor in florida who died as a result of bleeding because of thrombocytopenia meaning low platelets
his platelet level went all the way down to zero this happened shortly after he got the first
dose of the pfizer vaccine did this vaccine cause this or instead did he get the sars cov2 infection
and that caused the low platelets or was there another undiagnosed condition that was flying
under the radar such as leukemia that led to low platelets and led to his outcome it's easy
to jump to conclusions but based on the timing it seems like it was related to the vaccine but
there's no way to know for sure right now that's why an autopsy is necessary but even then doing an
autopsy doesn't necessarily guarantee that we'll get a definitive answer but getting back to sars cov2
there are case reports of people developing other autoimmune diseases like guillain-barre
syndrome a progressive ascending minute rises up symmetric paralysis guillain-barre syndrome is a
relatively rare immune mediated disease that may be triggered by respiratory viruses or vaccination
anti-phospholipid antibodies have been found in many patients of the covid 19 anti-phospholipid
antibody syndrome is the major cause of strokes in people with systemic autoimmune disorders
these antibodies are normally found in about 0.5 percent of the population
they've also been found in many but not all patients who've had covid 19 and blood clots the
findings of increased auto antibodies in patients with severe covid are intriguing but critics
point out that the control group in many of these studies were healthy uninfected people not people
infected with another virus and the findings of autoantibodies were not always consistent
with clinical findings further studies comparing the effects of auto antibodies in covid 19 with
autoantibody production and influenza may help determine a pattern of auto antibody production
that is more classic in covid 19 cytokine storms are an overreaction by the immune system
and are more systemic in short term in contrast autoantibodies are more targeted in long term
dexamethasone which is a corticosteroid along with the arthritic drugs tocilizumab and sarilumab
they've been used to modulate an overactive immune response in a clinical trial tocilizumab and
sarilumab improved outcomes for critically ill patients on a ventilator in the intensive care
unit these medications require careful timing to interrupt an over-reactive immune system
without interfering with a normal immune system fighting the covid 19 infection covid is often
a biphasic illness with an initial phase that is primarily respiratory symptoms caused by the virus
and then the immediate immune response with innate immunity and sometimes that's later followed up
with a secondary inflammatory phase researchers have found that medications that are helpful in
one stage can actually be harmful if administered at the wrong time for example remdesivir an
antiviral medication has not been beneficial in the later stages of covid 19. so there
are two arms of the immune system on one hand you have the non-specific innate immune system
and then you have the specific adaptive immune system whenever you're infected with a pathogen
that is new to your immune system you rely on the innate immune system to fight the pathogen
interferons are proteins that are part of that initial innate response interferon beta is one
of the first cytokines produced and drives innate immune response in the lung this connection
illustrates the importance of the finding that sars cov2 may inhibit interferon activity and
those who develop more severe covid there has been a randomized double-blind placebo-controlled pilot
study in nine uk hospitals in which they enrolled 98 patients 50 to the control group and then 48 to
the treatment group in the treatment group they gave nebulized inhaled interferon the two groups
were then well matched demographically and the results showed that the treatment group seemed
to improve more quickly compared to the control group although the results were not statistically
significant and the larger trial is now in the works could autoantibodies be formed to help
halt an immune system that is out of control well the two factors that determine the outcome
of a covid 19 infection are the viral load and the quality and quantity of the immune response
a high viral load can do more damage before the immune system can bring it under control an immune
system with a poor antibody or cellular response can't mount a response fast enough or strong
enough to limit the infection's damage now on the other hand an immune response that is not well
regulated will lead to tissue damage secondary to that inflammation a study showed that the
autoantibodies were still present seven months after infection leading researchers to stress the need
to determine whether there's a link between auto antibodies and long covid these studies they raise
many questions but they can also be avenues to new treatment options so that's going to be all
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