Amy Proal, PhD
@microbeminded2
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Microbiologist at PolyBio Research Foundation: helping research teams collaborate on infection-associated chronic disease #me #longcovid #lyme #eds @polybioRF
Joined September 2017
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Pinned Tweet
@Caroline_Bartma
Check out our paper on how pathogens hijack the
#metabolism
of the cells they infect, with
#mitochondria
functioning as part of the innate immune response to counter such activity. With implications for conditions like cancer, atherosclerosis + ME/CFS:
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I am excited to share our new position paper on
#SARS
-CoV-2 reservoir (viral persistence) in Long COVID or post-acute sequelae of COVID (PASC):
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So I have decided to make my situation public. I am not in critical condition and am stable, but since about Feb. 23rd have been very sick with the symptoms of
#COVID19
minus a high fever. My boyfriend first got sick with these symptoms on Feb. 21st and we are both still ill
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So it turns out we did find “something in the blood” of
#ME
/CFS patients: fibrinaloid microclots + hyperactivated platelets (that you can see with your own eyes). Thank you so much to
@polybioRF
donors who helped support part of the study:
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It’s official: A new Lancet Infectious Disease paper solidifies evidence of long-term viral persistence after
#COVID
-19.
Up to a quarter of people in the study harbored viral proteins indicative of persistent virus for up to 14 months after infection:
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Tell
@ChrisCuomo
that 33 scientists from 14 institutions joined forces to write this paper documenting evidence for
#SARS
-CoV-2 persistence as a potential driver of
#LongCOVID
. We call for more clinical trials of drugs capable of clearing persistent virus:
I’m slated to appear on the Cuomo show this Friday (8pm ET on News Nation), to talk about my book The Long Haul, and what we need to do to truly address Long Covid.
As I’m prepping, I’d love to hear what’s on your my mind! What’s most important in new research/policy/moonshots?
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Amazing to have
@resiapretorius
visit Harvard to teach an incredible team of scientists working on
#LongCovid
,
#ME
/CFS, pediatric LongCovid and
#MIS
-C to identify microclots and hyperactivated platelets in samples
@MBVanElzakker
@LaelYonker
@D__Irimia
@bpboribong
@HannahFBues
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For more context: The team found
#SARS
-CoV-2 proteins indicative of viral persistence in 25% of people up to 14 months after
#COVID
. They controlled for vaccination + reinfection. There were very few false positives in the pre-pandemic samples, confirming accuracy of the methods
It’s official: A new Lancet Infectious Disease paper solidifies evidence of long-term viral persistence after
#COVID
-19.
Up to a quarter of people in the study harbored viral proteins indicative of persistent virus for up to 14 months after infection:
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3K
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Instead of going directly home, they gave him a script for an inhaler and told him to go to CVS. The situation is ridiculous. Why did his internist’s office have someone with COVID19 symptoms come in, not test him, and then send him to a crowded pharmacy? I am very angry
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@Caroline_Bartma
Check out our paper on how pathogens hijack the
#metabolism
of the cells they infect, with
#mitochondria
functioning as part of the innate immune response to counter such activity. With implications for conditions like cancer, atherosclerosis + ME/CFS:
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295
925
Important case history of a vaccinated patient who developed
#LongCovid
/PASC and then experienced rapid symptom resolution following administration of antiviral
#Paxlovid
(nirmatrelvir-ritonavir):
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Incredible new paper demonstrating
#SARS
-CoV-2 persistence + associated immune modulation in macaque monkeys. The team found replication competent SARS-CoV-2 virus in macaque lung alveolar
#macrophages
beyond 6 months postinfection:
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2/ We review evidence showing that some Long COVID patients may not fully clear the SARS-CoV-2
#virus
after acute infection. Instead, replicating virus and/or viral RNA - potentially capable of being translated to produce viral proteins - persist in tissue as a "reservoir"
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New preprint: The team did autopsies on 44 patients w/
#COVID
-19 to map + quantify SARS-CoV-2 distribution, replication and cell-type specificity across the human body (including brain) from acute infection through over 7 months following symptom onset:
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Great summary of core
#LongCovid
findings which “collectively suggest that the persistence of
#viral
components may result in chronically elevated IFNs and cytokines. Moreover, certain autoAbs may provide permissive conditions for such viral persistence.”
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7/ Lastly I should clarify this is not the fault of infectious disease MDs or others at MGH (several of whom I work with directly on research projects and are amazing!) It is because MGH doesn't have the testing capacity they need yet thanks to the federal government.
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2/ The team concludes that “the findings suggest in utero transmission of SARS-CoV-2 and possible persistent intestinal
#viral
reservoirs in the newborns”
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In this new paper
@DrMaureenHanson
argues that persistent enterovirus infection in tissue (enterovirus reservoir) may play a central role in the
#ME
/CFS disease process. I agree.
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Hi
#LongCovid
+
#ME
/CFS patients: my amazing colleague
@MBVanElzakker
is running a study on neuroinflammation in LongCovid + ME/CFS and is looking for new patients to participate. You must be in the Boston area to join the study. If interested please email DSaadi
@mgh
.harvard.edu
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8/ I want to clarify that my boyfriend’s internist is NOT at MGH (it’s a separate practice). My tweets are also not meant to criticize MGH - only to raise awareness of how difficult the general testing situation is in Boston for COVID19
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The gut appears to be a primary site of
#SARS
-CoV-2 reservoirs in at least a subset of long COVID patients. Persistence of the
#virus
in the gut is one of the biggest leads in the space,” said Sara Cherry, PhD 👇
The Perelman School of Medicine has received a $2.1M grant from
@polybioRF
to expand
#longCOVID
research. The funding will support studies focusing on SARS-CoV-2 persistence in the gut, in addition to work defining long COVID immune responses.
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I’m excited to annouce that we’ve started “The PolyBio Podcast.” I will interview scientists whose work is advancing the field of infection-associated chronic disease (
#ME
/CFS,
#LongCovid
, Post Treatment/Chronic Lyme etc)
@polybioRF
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4/ The team writes that “Increased induction of these cytokines in the
#neonatal
intestine by viral RNAs may impact the immune cell development and immune landscape in the neonatal intestine and may potentially affect disease susceptibility in later life.”
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I am incredibly motivated to serve as Scientific Director of this new clinic. Our research program will maximize collaboration with
@polybioRF
’s extensive network of collaborative teams to identify & treat root cause drivers of patient symptoms, including pathogen persistence
I am humbled to announce that thanks to a generous grant from
@cohengive
our
#LongCOVID
center (opening early 2024) will work to understand the differences and similarities between LC and
#Lyme
,
#MECFS
and other infection-associated chronic illnesses. 1/
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More evidence SARS-CoV-2 appears capable of persistence 👉 This team identified
#SARS
-CoV-2 nucleocapsid protein in colon, appendix, ileum, haemorrhoid, liver, gallbladder + lymph nodes tissue from 5 patients 9-180 days after testing negative for the virus:
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Direct infection of platelets in
#LongCovid
is a very important area of ongoing research
@laurenancona
Actually, the Bomsel lab in Paris found direct evidence of infectious SARSCoV2 in
#LongCovid
patients' blood, inside their platelets (poster at Madrid conference) =the real smoking gun
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An incredible thank you to
@cohengive
for this $1M grant to UCSD. The grant was facilitated by
@polybioRF
’s core team and will support a study to characterize the microbial, immune & genetic landscape of ME/CFS, LongCovid, LongLyme and EDS tissue samples:
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“...the long COVID patients had abnormal hyperpolarised xenon MRI scans, indicating ‘significantly impaired gas transfer’ from the lungs to the bloodstream. However their CT scans showed normal results.”:
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5/ And also that “The presence of SARS-CoV-2 RNAs and Spike protein in the intestines of newborns may potentially impact the development of the gut
#microbiome
and the immune system”
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Will more
#COVID
-19 lead to more neurodegenerative disease? I don’t see how not if this research holds. This Harvard team found that amyloid beta (the
#Alzheimer
’s “plaque”) may be an antimicrobial peptide that can form in response to viral infection:
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3/ It is important to note that all newborns that harbored SARS-CoV-2 in stool were negative for the
#virus
via nasal PCR. The team also found that stool homogenates from all 14 newborns in the study elicited elevated inflammatory IL-6 + IFN-γ from macrophages
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In a meeting I watched today, microglia priming was mentioned in
#LongCovid
and
#ME
/CFS. It’s important to clarify what “microglia priming” means. Microglial priming does not mean that after a trigger has “cleared” microglia remain perpetually activated
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2/ We are in Boston, near Massachusetts General Hospital (MGH). We have not been able to get tested for COVID19 at MGH unless we are apparently in critical condition (ICU). Also I have a history of responding poorly to viral infections which is not making the situation easier.
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People are asking me: what if we did a similar autopsy study to look for
#viruses
in ME/CFS? Well, several teams that performed single autopsy studies on
#ME
/CFS patients found evidence of persistent enterovirus infection in subject brain/body tissue
New preprint: The team did autopsies on 44 patients w/
#COVID
-19 to map + quantify SARS-CoV-2 distribution, replication and cell-type specificity across the human body (including brain) from acute infection through over 7 months following symptom onset:
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6/ Again I should clarify that we don't know if we have COVID19. But it's not knowing that is starting to drive me a bit crazy. It's hard to read about the virus/deaths etc and not have info on my own case. It's also hard to know what measures of precaution to take around others
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5/ We delineate mechanisms by which a SARS-CoV-2 reservoir may contribute to immune,
#coagulation
, and
#neuroimmune
abnormalities,
#microbiome
imbalances, autoimmunity, and latent
#pathogen
reactivation in Long COVID patients
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10/ However many aspects of SARS-CoV-2 reservoir in Long COVID require further study. For example, we need to better understand factors that differentiate SARS-CoV-2 persistence in Long COVID from persistence in asymptomatic individuals. Key areas of investigation are listed here
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“Do we really have to see millions more people join them before we act to reduce transmission by implementing clean air policies and normalizing the use of N95 respirators in society?” 👇
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8/ Treatment of a SARS-CoV-2 reservoir in Long COVID may require combination therapies in which different antivirals or immunomodulators are used synergistically and/or for longer dosing periods to achieve maximum efficacy
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@EJohnWherry
@MBVanElzakker
@MichaelPelusoMD
@VirusesImmunity
@PutrinoLab
@marcus_buggert
@drmfreire
@LaelYonker
@WesElyMD
@resiapretorius
@RudyTanzi
@bpboribong
12/ Thank you
@VitalikButerin
for supporting much of the research on SARS-CoV-2 reservoir outlined in the paper to move forward via the
@polybioRF
#LongCovid
Research Consortium:
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Take down this article. It promotes debunked theories that post-viral sequelae are due to emotional trauma or illness seeking behaviors. This psychologizing of organic disease has ruined the lives of many
#MECFS
patients...and we cannot allow the same happen with
#LongCovid
.
I have written about Long Covid in today’s
@ObsMagazine
, inc. my own and others’ experiences; the evolving theories about what’s causing it; the psychological toll and what validation may look like for different people (feat. v old pic of me)
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Check out this talk I gave at a recent NIH workshop on
#LongCovid
biology. I review our recent Consortium position paper on
#SARS
-CoV-2 reservoir as a driver of LongCovid, and delineate mechanisms by which viral persistence in tissue may drive disease:
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4/ They gave him a mask and after long periods sitting in the waiting room w/ other patients coughing who also think they have COVID19 he was finally told he can’t be tested because he has not been in direct contact with someone who has COVID19.
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3/ Evidence for SARS-CoV-2 reservoir in Long COVID includes studies that have found SARS-CoV-2 RNA or protein in Long COVID tissue samples collected months after acute
#COVID
-19. Immune responses indicative of a SARS-CoV-2 reservoir have also been documented in
#LongCovid
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9/ Overall, the study of SARS-CoV-2 reservoir in Long COVID may inform the identification of disease mechanisms, biomarkers & therapeutics for other chronic conditions tied to persistent infection including
#ME
/CFS,
#Alzheimer
's, and
#MultipleSclerosis
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6/ Last, one newborn died from gestational autoimmune liver disease (GALD) and another developed necrotizing enterocolitis (NEC). While there is not enough evidence link the conditions directly to the SARS-CoV-2/spike persistence…
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7/ …both NEC and GALD have been previously linked to intestinal inflammation and
#infection
-associated autoantibody responses (respectively)
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Team identifies
#SARS
-CoV-2 NP protein/RNA in appendix + breast tissue of 2 patients who exhibited
#LongCovid
symptoms 175-462 days after initial infection. RNAScope detection of negative-sense viral RNA might indicate ongoing viral replication:
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7/ Our general goal in highlighting SARS-CoV-2 reservoir in Long COVID is to better understand mechanisms underlying viral persistence, to accelerate clinical trials of
#antivirals
or other
#therapeutics
with potential to clear a SARS-CoV-2 reservoir
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4/ Multiple teams have found SARS-CoV-2 proteins - including
#spike
- in Long COVID blood. This protein is likely derived from Long COVID tissue
#reservoir
sites but may "leak" into blood via exosome transport
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Hey! Join me at this webinar where I will attempt to connect
#SARS
-CoV-2 reservoir, herpesvirus reactivation,
#microbiome
dysbiosis, autoantibody production, microclots, vasculature issues, neuroinflammation, vagus nerve signaling + small fiber neuropathy in one
#LongCovid
talk!
Join Solve and
@Interdependence
Thursday, Jan. 6 for a presentation by Dr. Amy Proal (
@microbeminded2
) — the first in a webinar series exploring the pandemic's long-term healthcare, policy, & economic impact. Register:
#Covid19
#LongCovid
#SolveLongCovid
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Not surprising that
#SARS
-CoV-2 can “kick up” previously asymptomatic Bartonella infection.
Bartonella infects vascular endothelial cells. SARS-CoV-2 can also directly infect/inflame the vasculature. It’s a potential double hit to the blood vessels
.
New | Unmasking
#Bartonella
henselae infection in the shadows of
#longCOVID
thanks to clinical metagenomics | European Journal of Clinical Microbiology & Infectious Diseases
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10/ If these findings hold during the peer review process they strongly suggest that SARS-CoV-2 “viral reservoir” in both body/brain should be a central area of
#LongCovid
research
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6/ We identify research priorities and methods to guide continued study of SARS-CoV-2 reservoir in Long COVID. These include autopsy, imaging, & tissue
#biopsy
studies, ultrasensitive assays to identify viral proteins, & use of immune cells as biosensors of SARS-CoV-2 persistence
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I study the illness
#ME
/CFS - a neuroinflammatory condition that usually begins w/ a
#viral
infection (sometimes a
#respiratory
infection!). I have argued for years that infecting
#pathogens
tied to the illness might persist in the central nervous system (CNS) of such patients
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SARS-CoV-2 reservoir also links the factors below.
Persistent RNA/protein will perpetually stimulate mast cells. Spike and other viral proteins in the CNS and/or blood may drive an elevation in clotting & vascular factors that can contribute to neuroinflammation
No better phenomenon for linking together neuroinflammation and vascular dysfunction in
#LongCovid
patients than chronic mast cell over-activation.
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New
@polybioRF
podcast: I interviewed Dr. Akiko Iwasaki: Professor of Immunobiology and Molecular, Cellular & Developmental Biology at Yale University. Listen on Spotify () or watch on Youtube ()
@VirusesImmunity
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I want to add that I see
#SARS
-CoV-2 persistence as part of a larger picture in which other latent pathogens and/or
#microbiome
organisms also harbored by a patient play an important role in the ultimate set up symptoms they develop
"For
@microbeminded2
.. persistence may be key to
#LongCovid
. 'I see it as the upstream driver of most of those other things,' she says.. the spike protein has been shown to cause clotting, so if this leaks out of the virus reservoir into the blood, it could explain microclots"
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This is the most straightforward explanation for chronic symptoms in at least a subset of
#LongCovid
patients. Partly b/c if the
#virus
is still present its activity can directly contribute to other phenomena also being documented in LongCovid
Sharing a theory.
There is no long Covid; its just Covid. Long Covid is a chronic infection triggering both autoimmunity and abnormal micro clotting..
@resiapretorius
@microbeminded2
@dbkell
@MBVanElzakker
#TreatLongCovid
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So motivated to move more
#LongCovid
research and clinical trials forward via LCRC! Thank you
@VitalikButerin
and Kanro for the incredible support
We are excited to announce a $15M gift from Kanro: a philanthropic fund to support scientific research established by Vitalik Buterin, co-founder of Ethereum:
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3/ My boyfriend and I have self-quarantined ourselves in our apartment since Feb. 23rd. Today my boyfriend called his internist and said has the COVID19 symptoms. After a phone screen they told him to come in to the office. He went there wearing no mask because we don’t have one.
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11/ Thank you to all the authors who contributed to the paper including
@EJohnWherry
@MBVanElzakker
@MichaelPelusoMD
@VirusesImmunity
@PutrinoLab
@marcus_buggert
@drmfreire
@LaelYonker
@WesElyMD
@resiapretorius
@RudyTanzi
@bpboribong
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“It’s very encouraging to hear that some of the researchers working on these trials were at the forefront of the
#HIV
/AIDS epidemic; the experience they bring to the table is invaluable at a time like this,” said Junior White, a person with
#LongCovid
👇
NEW: This morning,
@polybioRF
announced a new round of funding for
#LongCovid
research, focused on understanding viral persistence and identifying potential treatments. Read more:
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I’ve seen some people tweet that
#coronaviruses
might not be capable of persistence. But over the past decades, coronavirus RNA/protein has been identified in a range of human samples after acute illness, and sometimes connected to chronic disease
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2/ Because the vagus nerve is an essential component of the
#autonomic
nervous system and regulates body functions such as heart rate, digestion, and respiratory rate, direct infection of the nerve by SARS-CoV-2 may contribute to related symptoms
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@VitalikButerin
@ARPAHealth
@DoD_DHA
17/ If we don’t implement these solutions it is our
#children
who will suffer most. How many
#SARS
-CoV-2 infections can our children sustain with a virus capable of persistence before their health inevitably declines? We must act now.
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It’s important to acknowledge that vaccinated people can acquire/transmit the Delta variant. While vaccinated individuals should experience less severe acute
#COVID
-19, they may still be at risk for LongCovid/PASC (which has been shown to develop after asymptomatic/mild COVID-19)
Now that's what you call a superspreader event (black circle = index case, green = vaccinated)
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This important study found a significantly elevated frequency of
#SARS
-CoV-2-specific TNF-α-producing CD8+ T cells in patients with pulmonary
#LongCovid
(PASC). PASC subjects experienced an average symptom duration of over 6 months:
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Interesting case history: The team found
#SARS
-CoV-2 RNA in the cerebrospinal fluid of a woman (via RT-PCR) who was hospitalized w/ headache, dizziness, anxiety, palpitations, diarrhea + panic attacks 114 days after an initial asymptomatic case of COVID-19:
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4/
@MBVanElzakker
has long-hypothesized that direct infection of the vagus nerve by herpesviruses or enteroviruses could occur in
#ME
/CFS, contributing to autonomic dysfunction in patients with the condition:
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Yes! This article lays out excellent research goals for the study of
#LongCovid
and
#ME
/CFS. With a focus on viral persistence (especially in the central nervous system), autopsy studies, analysis of tissue biopsies + intelligently designed mouse models 🙌
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This new preprint found that exposure + antibody responses to previous Coronaviruses may modulate the NeuroPASC (
#LongCovid
) immune response in a manner that could make such patients less likely to clear the SARS-CoV-2 virus:
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@MBVanElzakker
8/ Overall direct infection of the vagus nerve and/or brainstem by different persistent viral (or even bacterial) pathogens could underly common symptom development in
#LongCovid
and
#ME
/CFS
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@cstroeckw
Yes!
@polybioRF
we are analyzing ME/CFS small fiber neuropathy punch biopsy samples for pathogens/organisms. Skeletal muscle samples next. Our pipeline for tissue analysis can identify RNA viruses in samples, plus DNA viruses, bacteriophage, bacteria, fungi and archea.
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3/ The findings beg the question 👉 Could persistent SARS-CoV-2 infection of the vagus nerve contribute to dysautonomia in
#LongCovid
?
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This preprint identified SARS-CoV-2 RNA in the bone marrow megakaryocytes (MK) of severe COVID-19 patients. Then - in mice - they showed these infected MKs promoted formation of non-neutralizing afucosylated anti-spike IgG antibodies + pulmonary thrombosis:
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Hi - I am working to help
@MBVanElzakker
recruit subjects for an ongoing fMRI
#ME
/CFS imaging study at the Harvard/MIT Martinos Center in Boston. The study is designed to test how function of brain blood vessels may contribute to ME/CFS
#pwme
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2/ We have formed a global
#Consortium
to study SARS-CoV-2 persistence: to determine if reservoirs of the
#virus
in LongCOVID tissue can drive widespread dysfunction including clotting,
#microbiome
, and neuroimmune abnormalities:
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@polybio
@NIHDirector
@ARPA_H
15/ Overall SARS-CoV-2 RNA has been found in the lymph node tissue of
#children
hundreds of days after infection. That is concerning for the health of our next generation. We must take more action now on a global level to study SARS-CoV-2 persistence:
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@fi_lowenstein
@VirusesImmunity
@MEActNet
@patientled
@MarkedByCovid
@itsbodypolitic
@PutrinoLab
@C19LH_Advocacy
@TheCrankyQueer
@ErinSandersNP
@WesElyMD
@DataDrivenMD
@EbonyJHilton_MD
Viruses have a tremendous capacity to drive chronic disease. They hijack the metabolism of the cells they infect. Their proteins directly modulate human gene expression + the activity of the immune system. They can infect nearly every human body site. Do not underestimate this.
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“In conditions without biomarkers of recovery, what the person with the condition tells you IS the biomarker” Yes! 🙏 🙌
FFS. LISTEN to your patients with chronic conditions -
#dysautonomia
,
#LongCovid
,
#EDS
,
#MECFS
. In conditions without biomarkers of recovery, what the person with the condition tells you IS the biomarker. Work in partnership, because that is what good clinicians do.
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@MBVanElzakker
7/ Indeed, ME/CFS autopsy studies have found enterovirus RNA directly in the brainstem:
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The finding below is consistent with this Harvard preprint () that used sensitive Simoa assays on
#LongCovid
blood. They found SARS-CoV-2 spike antigen in a majority of patients up to 12 mo. post-diagnosis (suggesting active
#SARS
-CoV-2 reservoir in tissue)
Not only did LC have higher levels of IgG against Spike, but also had IgG against distinct epitopes within the Spike protein, identified by
@S_Tabachnikova
with
@serimmune
Kathy Kamath. See the distinct peaks in purple vs. controls. (11/)
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@meghanor
Yes! But also logical that the virus might just be “hiding out” in the area of the body where a patient has ongoing symptoms. For example this team found SARS-CoV-2 RNA/protein in olfactory bulb tissue of patients with loss of smell after COVID-19:
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I share this concern👇
#SARS
-CoV-2 persistence in tissue (in patients with
#LongCovid
or otherwise) should be a central research focus in the world right now. Our
@polybioRF
team is working to set up collaborations on the topic, but we need even more scientists to jump in!
I am concerned about sub-threshold neutralizing antibodies tied to disease enhancing antibodies leading to greater persistence of COVID. Those with long COVID are canaries in the coalmine and we should be directing far more attention to the pathogenesis underlying these cases.
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Heck yeah! Leave it to
@PutrinoLab
to define the problem, devise a creative solution, and move forward rapidly (while sharing the knowledge openly with the world!) We’re working on similar quantification methods for
@polybioRF
funded microclot projects at Harvard + other sites
Them: Microclots and platelet hyperactivation in
#LongCovid
can't be quantified by conventional standards, so we shouldn't use it as a biomarker
Us: Hold our beer(s).
Step 1: Take blood, spin blood, stain blood, look at blood under a microscope and capture an image of it 1/
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7/ This French team presented a poster showing spike in
#LongCovid
blood. They also found SARS-CoV-2 double stranded RNA indicative of viral replication in the platelets of LongCovid patients:
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New
@polybioRF
podcast! I interviewed Dr. Resia Pretorius: Department Head/Research Professor at Stellenbosch University in South Africa. Listen on an App like Spotify () or watch on Youtube ()
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@MBVanElzakker
5/ Signaling from the vagus nerve to the
#brainstem
in the CNS also controls the “sickness response,” where the brain mounts flu-like symptoms, nausea, and pain in response to inflammation:
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Both research & clinical trials on SARS-CoV-2 reservoir in
#LongCovid
are gaining speed! Thanks
@WStoneReports
for including me in this segment highlighting key findings and considerations:
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@VitalikButerin
@ARPAHealth
@DoD_DHA
16/ Both the private and government sectors must invest in infrastructure to clean the
#air
in schools, airports and other buildings to remove
#viruses
. These include germicidal UV light, HEPA filters and technologies that also clear pollutants from the air
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This is an incredibly important preprint to inform
#LongCovid
. Among many analyses, the team recruited 4 patients w/ prolonged + recurrent olfactory function loss after
#COVID
-19 (time from first COVID-19 symptoms to inclusion ranged from 110-196 days):
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It has been a hard week for me watching what I consider to be one of the biggest health scandals of our time occur in relation to two affordable, widely available drugs that may offer potential benefit to patients with
#COVID
-19 (
#hydroxychloroquine
+ ivermectin)
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And the million dollar question is: what were the IgG antibodies in the blood of the
#fibromyalgia
patients created in response to? Certainly a broad range of pathogens/organisms induce IgG antibody production
Research paper: IgG from patients with
#fibromyalgia
induced sensory hypersensitivity in mice; the mice displayed increased sensitivity to noxious mechanical and cold stimulation. IgG depleted serum or serum from healthy controls had no effect.
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Thanks for the shoutout
@PutrinoLab
! I helped coin the term “infection-associated chronic disease” to describe conditions like ME/CFS & LongCovid. It’s an alternative to “post-viral disease” which assumes full pathogen clearance when that should be a hypothesis not an assumption
Ok. Another request, another 🧵. Today, we address the strained relationship between psychology, psychiatry and
#LongCovid
. Much of this may also apply to
#pwME
and other infection-associated chronic illnesses (h/t again
@microbeminded2
) and other “invisible” illnesses (1/n)
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@VitalikButerin
@ARPAHealth
@DoD_DHA
15/ The US government must develop a “warp speed” program focused on the rapid development of novel
#antivirals
or other therapeutics capable of targeting a wide range of chronic viral pathogens. Open source development must be prioritized.
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