COVID-19 Aspirin Inhibits Antibody Production In Human Cells

[Sucrates]

You've probably seen statements (some false) that some anti-inflammatories might exacerbate COVID-19.
I wonder if anyone could comment on the real world effects of the mechanisms in this study, particularly aspirin and tylenol.
Ibuprofen and other widely used non-steroidal anti-inflammatory drugs inhibit antibody production in human cells

"However, aspirin is also used as an anti-inflammatory agent (1200 mg/day) in which case, in vivo therapeutic levels are between 100– 2000 µM [30]."

 

[InChristAlone]

You wouldn't NEED antibiodies with aspirin, because it decreases inflammation.
"The people dieing at a very high rate of the virus are already suffering from circulatory disease, heart disease, hypertension and stroke, they already have an active angiotensin system and the virus finds an environment already going in that direction. It happens that the ace angiotensin converting enzyme #2 its a dereceptor for the virus the virus attaches to that and in the process entering the cell and becoming infective and ace2 is the enzyme that undoes the work of ace in the cells and ace produce angiotensin and ace2 then destroys angiotensin so what the virus does in binding to ace2 seems to be inactivating the inactivator of angiotensin that leaves ace free to make angiotensin which then doesn't have any way out and it accumulates causing all of the dry cough high fever and increased hypertension and stroke and so on. " ~Ray Peat

 

[Hairfedup]

Hmm. I too wonder. Been on Aspirin 300mg for around 2 weeks now, healed up the vast majority of my SIBO/Barret's symptoms - COVID isn't what its cracked up to be so I doubt Imma come off the Aspirin anytime soon.

 

[LucyL]

That's a huge difference between aspirin at 100 µM and 500 µM. Seems odd. I think it should be considered with the studies from this thread
Aspirin is antiviral

 

[schultz]

I'd take aspirin personally. I'm not sure I'd recommend it to someone though as I am not 100% sure it wouldn't cause some intestinal issue. I've never had an issue with it myself though and I've probably consumed more than a kilogram of the stuff in my lifetime.

I wouldn't take acetaminophen or ibuprofen. Both of them can cause liver damage.

 

[SOMO]

Too many antibodies = Immune system wiped out/exhausted

Too many antibodies = Immune system OVER-activation.

Too many antibodies = more opportunity for autoimmune reactions

 

[jb116]

Yup, it's what we want in context with good metabolic rate.

 

[Tristan Loscha]

It is likely true,and should be watched.
It isnt just about inhibiting inflammation,
if it were,the benefit of the strong cortisol-agents
would be more clear.

 

[Sucrates]

It is likely true,and should be watched.

What is likely true?

 

[Giraffe]

Sensitive and Specific Detection of Low-Level Antibody Responses in Mild Middle East Respiratory Syndrome Coronavirus Infections

This study was published in October 2019.

"Antibody responses varied among PCR-confirmed MERS-CoV cases; case-patients with mild and asymptomatic infections showed low or undetectable seroconversion, in contrast to severe infections that resulted in robust responses (5,17,31). The low-level antibody responses produced following nonsevere infections led to failure in detecting such responses in some patients by a routinely used ELISA and neutralization assays (5,17,32). This result may have impeded estimation of prevalence of virus infections in surveillance studies. We were able to detect nonneutralizing antibody responses among previously infected mild and asymptomatic cases that were previously unidentified; this finding indicates that MERS-CoV prevalence could be higher than current estimates and that using sensitive platforms could lead to more precise calculation of incidence rates."

 

[Tristan Loscha]

What is likely true?

..i meant to agree with the title and idea of the thread:


'Covid-19 Aspirin inhibits antibody production in human cells'


and then i added this:

"It is likely true,and should be watched.
It isnt just about inhibiting inflammation,
if it were,the benefit of the strong cortisol-agents
would be more clear."

 

[Tristan Loscha]

Sensitive and Specific Detection of Low-Level Antibody Responses in Mild Middle East Respiratory Syndrome Coronavirus Infections

This study was published in October 2019.

"Antibody responses varied among PCR-confirmed MERS-CoV cases; case-patients with mild and asymptomatic infections showed low or undetectable seroconversion, in contrast to severe infections that resulted in robust responses (5,17,31). The low-level antibody responses produced following nonsevere infections led to failure in detecting such responses in some patients by a routinely used ELISA and neutralization assays (5,17,32). This result may have impeded estimation of prevalence of virus infections in surveillance studies. We were able to detect nonneutralizing antibody responses among previously infected mild and asymptomatic cases that were previously unidentified; this finding indicates that MERS-CoV prevalence could be higher than current estimates and that using sensitive platforms could lead to more precise calculation of incidence rates."

interesting.

 

[S.Seneff]

In Italy, Going Back to Work May Depend on Having the Right Antibodies

 

[Sucrates]

..i meant to agree with the title and idea of the thread:


'Covid-19 Aspirin inhibits antibody production in human cells'


and then i added this:

"It is likely true,and should be watched.
It isnt just about inhibiting inflammation,
if it were,the benefit of the strong cortisol-agents
would be more clear."

Thanks

 

[Sucrates]

In Italy, Going Back to Work May Depend on Having the Right Antibodies

It's going to be very interesting once we get large-scale random antibody testing.

 

[S.Seneff]

J Infect Dis. 1990 Dec;162(6):1277-82.
Adverse effects of aspirin, acetaminophen, and ibuprofen on immune function, viral shedding, and clinical status in rhinovirus-infected volunteers.
Graham NM1, Burrell CJ, Douglas RM, Debelle P, Davies L.
Author information
1
Department of Community Medicine, University of Adelaide, South Australia.
Abstract
A double-blind, placebo-controlled trial was conducted to study the effects of over-the-counter analgesic/antipyretic medications on virus shedding, immune response, and clinical status in the common cold. Sixty healthy volunteers were challenged intranasally with rhinovirus type 2 and randomized to one of four treatment arms: aspirin, acetaminophen, ibuprofen, or placebo. Fifty-six volunteers were successfully infected and shed virus on at least 4 days after challenge. Virus shedding, antibody levels, clinical symptoms and signs, and blood leukocyte levels were carefully monitored. Use of aspirin and acetaminophen was associated with suppression of serum neutralizing antibody response (P less than .05 vs. placebo) and increased nasal symptoms and signs (P less than .05 vs. placebo). A concomitant rise in circulating monocytes suggested that the suppression of antibody response may be mediated through drug effects on monocytes and/or mononuclear phagocytes. There were no significant differences in viral shedding among the four groups, but a trend toward longer duration of virus shedding was observed in the aspirin and acetaminophen groups.
DOI::10.1093/infdis/162.6.1277

Medications. The study medications were presented in identi-
cal capsules containing aspirin (500 mg), acetaminophen (500 mg),
ibuprofen (200 mg), or placebo (McNeil Consumer Products, Fort
Washington, PA). Daily doses of the medications were 4 g of aspi-
rin (four doses of two capsules), 4 g of acetaminophen (four doses
of two capsules), or 1.2 g ofibuprofen (three doses oftwo capsules
and one dose of two placebo capsules). The placebo recipients re-
ceived four doses of two capsules. To maintain compliance, dosing
was observed by a study nurse, and spot urine samples were tested
for study drug levels on days 0 and 5. Acetaminophen and ibuprofen
doses were designed to be comparable with recommended over-
the-counter doses. A relatively high dose of aspirin was chosen to
maximize the probability of detecting any real effects on immune
function and virus shedding. This approach was believed to be ap-
propriate in view of the findings of Stanley et al. [1] and the funding-
restricted sample size.

DISCUSSION
The specific antibody response to challenge by many re-
spiratory viruses occurs late and exerts relatively little influ-
ence on the control of acute infections [22-24]. Protection
from specific antibody is therefore conferred only against sub-
sequent challenge with the same virus serotype. In the con-
trol of acute, established viral infections, the role of nonspecific
proteins, such as interferon, are much more important [24].
In our present study, aspirin and acetaminophen were sig-
nificantly associated with suppression of the serum neutraliz-
ing antibody response to the study challenge virus, RV2. The
effect of ibuprofen on antibody level was weaker and did not
differ significantly from that of placebo.
In healthy adults, the clinical consequences of the level of
immunosuppression observed in this study may not be worri-
some, particularly if other components of the immune re-
sponse to rhinovirus infection (e.g., interferon antiviral
activity) remain unimpaired. However, in groups relatively
immunosuppressed or at increased risk for acute respiratory
infections, the effects of these drugs are potentially more
problematic. For example, children, particularly those in de-
veloping countries, are more susceptible to acute respiratory
infections than were the adults in this study. If widely used
over-the-counter medications significantly suppress immune
function, there may be a real risk of increasing the severity
of infection. A recent study showing that acetaminophen
lengthened the duration of varicella infectionsin children lends
empirical support to this hypothesis [19]. Ifspecific antibody
production is suppressed, this might attenuate the humoral
response to subsequent rechallenge with the same agent. How-
ever, this remains speculative, and further research is needed
to determine if other parts of the immune response to respi-
ratory viruses are affected by over-the-counter antipyretics/
analgesics and whether children, the immunosuppressed, or
other at-risk groups would be adversely affected in a clini-
cally significant manner.
In addition to a previous reported association between acet-
aminophen and clinical severity of varicella infection in chil-
dren [19], there was evidence in our study that aspirin and
acetaminophen might adversely influence clinical status.
These two drugs were associated with increased turbinate
edema and nasal obstruction in comparison with placebo. This
level of increased clinical severity in a URI would present
few problems for most healthy adults and could be quickly
reversed with pseudoephedrine. However, nasal obstruction
might be more important in infants, where sucking and breast-
feeding could be impaired. In developing countries in par-
ticular, impairment of sucking or feeding in infants can have
serious consequences. Nonetheless, given that Stanley et al.
[1] did not report similar findings, these results should be
treated with some caution until further data are available to
confirm or refute them.
Aspirin, acetaminophen, and ibuprofen did not significantly
increase virus shedding in comparison with placebo, but as
shown in table 2, duration ofshedding in the aspirin and acet-
aminophen groups tended to be slightly longer (P = .34).
Duration of shedding was also associated with an attenuated
antibody response (P = .038). Nevertheless, these findings
do not support a strong effect of aspirin on virus shedding
as reported elsewhere [1]. A weaker effect, ifpresent, would
require a substantially larger study than this to detect it.
The rise in the number of circulating monocytes in the three
active treatment groups contrasted with a fall in the placebo
group. Althoughonlythe comparisonbetweenibuprofen and
placeboon day 14reachedstatisticalsignificance, the higher
levelsof circulatingmonocytes were significantly related to
suppressed antibody response andthe absenceofcervicalade-
nitis. Thesedata suggest thattheeffects oftheover-the-counter
drugs on immune functionmightbe mediatedby an effect on
peripheralmonocytes. Thismightoccur bypreventing migra-
tionof circulatingmononuclear leukocytes to infected tissues
and therefore limiting their differentiation to mononuclear
phagocytes. Mononuclear phagocytes (e.g., macrophages) ap-
pear to playa role in initiatingthe immune responseto some
respiratory viruses and may help restrict viral replication
[25-27]. Macrophageshelp initiate antibody production by
processing andpresenting viralantigens, complexed withclass
II majorhistocompatibility complex antigens, to T helperlym-
phocytes, which in turn (via lymphokine and direct contact
pathways) stimulateBlymphocyte differentiation and specific
antibody productjon [28, 29].