Archive for the ‘research’ Category

Small Fiber Neuropathy in Lyme Disease & COVID

https://danielcameronmd.com/neuropathy-in-lyme-disease-covid-19/

Small fiber neuropathy in Lyme disease and COVID-19

person with neuropathy due to lyme disease rubbing their foot

Small fiber neuropathy (SFN) is a disorder that affects the small sensory cutaneous nerves, resulting in unusual sensations such as tingling, pins-and-needles and numbness. Some patients may experience burning pain or coldness and electric shock-like brief painful sensations. In most patients, these symptoms start in the feet and progress upwards.¹

By

Small fiber neuropathy with autonomic and sensory dysfunction has been described in Lyme disease patients. In fact, a small study suggests that SFN may be a viable biomarker of post-treatment Lyme disease syndrome, particularly for patients whose main symptoms involve sensory issues.²

In their article, “Resolution of Pain in the Absence of Nerve Regeneration in Small Fiber Neuropathy Following Treatment of Lyme Disease,” the authors describe the case of an 83-year-old woman with a 4-year history of diffuse burning pain in her face, arms, and legs, and muscle spasms in the legs.³

Lyme disease causes small fiber neuropathy in an elderly woman. Complete resolution of symptoms after antibiotic treatment.

Lyme disease testing was positive. “She was then treated with a 40-day course of oral antibiotics for Lyme disease with complete resolution of her neuropathic symptoms.”

“Painful small fiber neuropathy may be a manifestation of Lyme disease,” the authors suggest. “Antibiotic treatment of Lyme disease can result in resolution of the neuropathic pain symptoms.”

Small fiber neuropathy and COVID-19

Now, small fiber neuropathy is being recognized in patients with COVID-19.

Investigators describe the clinical presentation of SFN associated with COVID-19 in two patients.4

Patient 1

A 52-year-old man, who contracted SARS-CoV-2, developed moderate respiratory problems (shortness of breath and productive cough).

“About 3 weeks later, he began to experience burning pain in the feet that spread up to the knees that was associated with imbalance and falls,” the authors explain.

“The pain would wake him at night, impacted his functional capacity, and was associated with allodynia.” (Note: Allodynia is the experience of pain from stimuli that typically is not painful, for example, light touch.)

He was diagnosed with small fiber neuropathy based on symptoms and test results.

The patient’s symptoms were “most compatible with a small fiber-predominant sensory neuropathy unmasked by COVID-19 infection.”

His neuropathic symptoms improved with gabapentin, and a topical lidocaine cream improved his neuropathic symptoms.

Patient 2

A 67-year-old woman with a 10-year history of mild acral tingling and burning pain had been diagnosed with small fiber neuropathy associated with psoriatic arthritis, based upon biopsy results.

Her symptoms had been stable for 10 years until she contracted SARS-CoV-2 and developed severe burning pain in her hands and feet.

“She presented 6 months later with persistent symptoms and occasional orthostasis.”

Her examination and test results supported a diagnosis of small fiber neuropathy.

“This is an example of a chronic pre-morbid sensory and small fiber-predominant autonomic neuropathy exacerbated by COVID-19 infection,” the authors write.

This study was observational and “cannot draw reliable conclusions regarding causative relationships or underlying mechanisms.”

Related Articles:

Autonomic dysfunction, small fiber neuropathy and Lyme disease

Femoral neuropathy and Lyme disease

Chronic inflammatory demyelinating polyneuropathy resolved with antibiotics

References:
  1. Johns Hopkins Medicine. Neurology and Neurosurgery. https://www.hopkinsmedicine.org/neurology_neurosurgery/
  2. Novak P, Felsenstein D, Mao C, Octavien NR, Zubcevik N. Association of small fiber neuropathy and post treatment Lyme disease syndrome. PLoS One. 2019;14(2):e0212222. doi:10.1371/journal.pone.0212222
  3. Resolution of Pain in the Absence of Nerve Regeneration in Small Fiber Neuropathy Following Treatment of Lyme Disease (P06.228) Naomi Feuer, Armin Alaedini Neurology Feb 2013, 80 (7 Supplement) P06.228;
  4. Shouman K, Vanichkachorn G, Cheshire WP, et al. Autonomic dysfunction following COVID-19 infection: an early experience. Clin Auton Res. Apr 16 2021;doi:10.1007/s10286-021-00803-8

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**Comment**

For pain we have also found gabapentin to be extremely helpful as well as LDN, CBD, and MSM.  I’ve also used lidocaine patches with good success as well as a pain cream you can make yourself either with or without DMSO, which is a very powerful pain killer but please read and learn about it before using. You can also purchase ready-made DMSO creams but realize they are often stored in plastic and have other ingredients that are potentially harmful. The plastic issue is important because DMSO is a carrier/penetrating agent which will absorb/penetrate anything in or around it.

For more on small fiber neuropathy and Lyme/MSIDS:

Category:

Lyme, Pain Management, research, Treatment, Viruses

An Appeal For An Objective, Open, And Transparent Scientific Debate About the Origin of SARS-CoV-2

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)02019-5/fulltext

An appeal for an objective, open, and transparent scientific debate about the origin of SARS-CoV-2

Published:September 17, 2021DOI:https://doi.org/10.1016/S0140-6736(21)02019-5
On July 5, 2021, a Correspondence was published in The Lancet called “Science, not speculation, is essential to determine how SARS-CoV-2 reached humans”.
The letter recapitulates the arguments of an earlier letter (published in February, 2020) by the same authors,which claimed overwhelming support for the hypothesis that the novel coronavirus causing the COVID-19 pandemic originated in wildlife. The authors associated any alternative view with conspiracy theories by stating: “We stand together to strongly condemn conspiracy theories suggesting that COVID-19 does not have a natural origin”. The statement has imparted a silencing effect on the wider scientific debate, including among science journalists.
The 2021 letter did not repeat the proposition that scientists open to alternative hypotheses were conspiracy theorists, but did state: “We believe the strongest clue from new, credible, and peer-reviewed evidence in the scientific literature is that the virus evolved in nature, while suggestions of a laboratory leak source of the pandemic remain without scientifically validated evidence that directly supports it in peer-reviewed scientific journals”. In fact, this argument could literally be reversed. As will be shown below, there is no direct support for the natural origin of SARS-CoV-2, and a laboratory-related accident is plausible.
There is so far no scientifically validated evidence that directly supports a natural origin. Among the references cited in the two letters by Calisher and colleagues,, all but one simply show that SARS-CoV-2 is phylogenetically related to other betacoronaviruses. The fact that the causative agent of COVID-19 descends from a natural virus is widely accepted, but this does not explain how it came to infect humans. The question of the proximal origin of SARS-CoV-2—ie, the final virus and host before passage to humans—was expressly addressed in only one highly cited opinion piece, which supports the natural origin hypothesis, but suffers from a logical fallacy:it opposes two hypotheses—laboratory engineering versus zoonosis—wrongly implying that there are no other possible scenarios. The article then provides arguments against the laboratory engineering hypothesis, which are not conclusive for the following reasons. First, it assumes that the optimisation of the receptor binding domain for human ACE2 requires prior knowledge of the adaptive mutations, whereas selection in cell culture or animal models would lead to the same effect. Second, the absence of traces of reverse-engineering systems does not preclude genome editing, which is performed with so-called seamless techniques.,
Finally, the absence of a previously known backbone is not a proof, since researchers can work for several years on viruses before publishing their full genome (this was the case for RaTG13, the closest known virus, which was collected in 2013 and published in 2020).
Based on these indirect and questionable arguments, the authors conclude in favour of a natural proximal origin. In the last part of the article, they briefly evoke selection during passage (ie, experiments aiming to test the capacity of a virus to infect cell cultures or model animals) and acknowledge the documented cases of laboratory escapes of SARS-CoV, but they dismiss this scenario, based on the argument that the strong similarity between receptor binding domains of SARS-CoV-2 and pangolins provides a more parsimonious explanation of the specific mutations. However, the pangolin hypothesis has since been abandoned,, , , so the whole reasoning should be re-evaluated.
Although considerable evidence supports the natural origins of other outbreaks (eg, Nipah, MERS, and the 2002–04 SARS outbreak) direct evidence for a natural origin for SARS-CoV-2 is missing. After 19 months of investigations, the proximal progenitor of SARS-CoV-2 is still lacking. Neither the host pathway from bats to humans, nor the geographical route from Yunnan (where the viruses most closely related to SARS-CoV-2 have been sampled) to Wuhan (where the pandemic emerged) have been identified. More than 80,000 samples collected from Chinese wildlife sites and animal farms all proved negative.
In addition, the international research community has no access to the sites, samples, or raw data. Although the Joint WHO-China Study concluded that the laboratory origin was “extremely unlikely”,WHO Director-General Tedros Adhanom Ghebreyesus declared that all hypotheses remained on the table including that of a laboratory leak.
A research-related origin is plausible. Two questions need to be addressed: virus evolution and introduction into the human population. Since July, 2020, several peer-reviewed scientific papers have discussed the likelihood of a research-related origin of the virus. Some unusual features of the SARS-CoV-2 genome sequence suggest that they may have resulted from genetic engineering,, an approach widely used in some virology labs.
Alternatively, adaptation to humans might result from undirected laboratory selection during serial passage in cell cultures or laboratory animals,, , including humanised mice.Mice genetically modified to display the human receptor for entry of SARS-CoV-2 (ACE2) were used in research projects funded before the pandemic, to test the infectivity of different virus strains.
Laboratory research also includes more targeted approaches such as gain-of-function experiments relying on chimeric viruses to test their potential to cross species barriers.,
A research-related contamination could result from contact with a natural virus during field collection, transportation from the field to a laboratory,characterisation of bats and bat viruses in a laboratory, or from a non-natural virus modified in a laboratory. There are well-documented cases of pathogen escapes from laboratories., , ,
Field collection, field survey, and in-laboratory research on potential pandemic pathogens require high-safety protections and a strong and transparent safety culture. However, experiments on SARS-related coronaviruses are routinely performed at biosafety level 2,, which complies with the recommendations for viruses infecting non-human animals, but is inappropriate for experiments that might produce human-adapted viruses by effects of selection or oriented mutations.
Overwhelming evidence for either a zoonotic or research-related origin is lacking: the jury is still out. On the basis of the current scientific literature, complemented by our own analyses of coronavirus genomes and proteins,, , , , , we hold that there is currently no compelling evidence to choose between a natural origin (ie, a virus that has evolved and been transmitted to humans solely via contact with wild or farmed animals) and a research-related origin (which might have occurred at sampling sites, during transportation or within the laboratory, and might have involved natural, selected, or engineered viruses).
An evidence-based, independent, and prejudice-free evaluation will require an international consultation of high-level experts with no conflicts of interest, from various disciplines and countries; the mandate will be to establish the different scenarios, and the associated hypotheses, and then to propose protocols, methods, and required data in order to elucidate the question of SARS-CoV-2’s origin. Beyond this issue, it is important to continue debating about the risk–benefit balance of current practices of field and laboratory research, including gain-of-function experiments, as well as the human activities contributing to zoonotic events.
Scientific journals should open their columns to in-depth analyses of all hypotheses. As scientists, we need to evaluate all hypotheses on a rational basis, and to weigh their likelihood based on facts and evidence, devoid of speculation concerning possible political impacts. Contrary to the first letter published in The Lancet by Calisher and colleagues,we do not think that scientists should promote “unity” (“We support the call from the Director-General of WHO to promote scientific evidence and unity over misinformation and conjecture”).
As shown above, research-related hypotheses are not misinformation and conjecture. More importantly, science embraces alternative hypotheses, contradictory arguments, verification, refutability, and controversy. Departing from this principle risks establishing dogmas, abandoning the essence of science, and, even worse, paving the way for conspiracy theories. Instead, the scientific community should bring this debate to a place where it belongs: the columns of scientific journals.,
JvH, CDB, ED, and JH contributed equally. They wrote the first version of the manuscript, integrated the other authors’ modifications, and managed the interactions with the editors. All the other authors contributed to the writing of the manuscript and acknowledged the latest version. We declare no competing interests.
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**Comment**
All I can say is “AMEN.”
These rational voices are desperately needed as mob mentality is growing – particularly in medicine and science with more & more articles shaming and attacking doctors who depart from the accepted narrative. There are also calls for these doctors to be sanctioned by medical boards. There is a push for “consensus” based medicine which will effectively stop all progressive thought and progress, and will punish those who think for themselves or have an original thought. 
We are living through perilous times where freedom of thought and speech is being threatened daily.
For more:

Nobel Prize Winner Dr Luc Montagnier states:

  • SARS-CoV-2 appears to be a benign bat coronavirus modified to integrate spike proteins that allows the virus to enter human cells by attaching to ACE-2 receptors
  • The virus also appears to have been modified to integrate an envelope protein from HIV called GP141, which tends to impair the immune system. A third modification appears to involve nanotechnology, which allows the virus to remain airborne longer

Cellular and molecular microbiologist, Dr. Judy Mikoviz also believes COVID-19 is a product of human manipulation:  https://madisonarealymesupportgroup.com/2020/05/04/retroviral-lyme-msids-role-in-covid-19-facemasks-are-immunosuppressive/

She states:

  • COVID-19 — the disease — is not caused by SARS-CoV-2 alone, but rather that it’s the result of a combination of SARS-CoV-2 and XMRVs (human gammaretroviruses)

  • SARS-CoV-2 also appears to have been manipulated to include components of HIV that destroys immune function along with XMRVs

Category:

research, Viruses

Can Lyme Disease Cause Bone Loss?

https://danielcameronmd.com/lyme-disease-bone-loss/

Can Lyme disease cause bone loss?

man with lyme disease having leg bone examined by doctor

Arthritis is a well-known manifestation of Lyme disease. And although studies have detected Borrelia burgdorferi (Bb) by culture and PCR in bone and marrow of humans and dogs,¹ little is known about the effects of Bb infection on bone tissue, outside articular surfaces.

By

In a 2003 case report, “Bone marrow manifestation of Lyme disease (Lyme Borreliosis),” Kvasnicka et al.² describe a 35-year-old man, who presented with fever, night sweats, inguinal lymph node enlargement and splenomegaly. He also exhibited neurologic symptoms including hyperkinesis and ataxia.

Based on results from a lumbar puncture, doctors initially suspected the patient had infectious meningoencephalitis. However, a bone marrow trephine biopsy was also performed and revealed several small- to intermediate-sized epithelioid granulomas, according to the authors.

“Bone marrow abnormalities have rarely been reported in Lyme borreliosis. In this patient the bone marrow lesions had a characteristic ring-like appearance” which is occasionally seen with infectious diseases.

Western blot testing showed “an increased IgM antibody titre for Borrelia burgdorferi indicating a recent infection,” writes Kvasnicka et al.

The patient was treated with antibiotics and recovered.

The authors suggest “In patients with neurological symptoms, fever and granulomatous myelitis, an early disseminated infection with Borrelia burgdorferi, should be considered in the differential diagnosis and specific serological tests should be performed.”

Lyme disease induces bone loss in mice

In their article “The Lyme Disease Pathogen Borrelia burgdorferi Infects Murine Bone and Induces Trabecular Bone Loss,” investigators provide the “first evidence that B. burgdorferi infection induces bone loss in mice and suggest that this phenotype results from inhibition of bone building rather than increased bone resorption.”

The authors examined “whether B. burgdorferi infection affects bone health in mice,” and point out that “bone pathologies are observed in diseases associated with other spirochete bacteria, including syphilis and periodontitis.”

“Bone pathologies are observed in diseases associated with other spirochete bacteria, including syphilis and periodontitis.”

Other studies have found that long bones from mice infected with Borrelia burgdorferi tended to be more brittle than bones of mock-infected controls.

The authors found that “B. burgdorferi infection in mice causes a level of osteopenia in the trabecular regions of long bones that would be considered a clinically significant finding in humans.”

However, “structural and biomechanical properties of cortical bone were not affected by infection.”

Related Articles:

TMJ arthritis triggered by Lyme disease

Lyme disease protein tricks immune system, ignites arthritis

Lyme arthritis following an operation: 5 cases

References:
  1. Tang TT, Zhang L, Bansal A, Grynpas M, Moriarty TJ. The Lyme Disease Pathogen Borrelia burgdorferi Infects Murine Bone and Induces Trabecular Bone Loss. Infect Immun. 2017;85(2):e00781-16. Published 2017 Jan 26. doi:10.1128/IAI.00781-16
  2. Kvasnicka HM, Thiele J, Ahmadi T. Bone marrow manifestation of Lyme disease (Lyme Borreliosis). Br J Haematol. 2003 Mar;120(5):723. doi: 10.1046/j.1365-2141.2003.04084.x. PMID: 12614200.

Category:

Lyme, research

Have We Finally Reached a Lyme Research Tipping Point?

https://www.lymedisease.org/lyme-research-tipping-point/

Sept. 16, 2021

If there were such a thing as an Olympic competition for Lyme research, I have a pretty good idea who would be on Team USA.

A recent paper entitled “Recent Progress in Lyme Disease and Remaining Challenges,” co-authored by 31 researchers from 19 separate institutions, reads like an all-star lineup of Lyme disease researchers.

The authors include many names familiar to the Lyme community including: Monica Embers, PhD, John Aucott, MD, Kim Lewis, PhD, Ed Breitschwerdt, DVM, DACVIM, Nicole Baumgarth, DVM, PhD, and Brian Fallon, MD.

The lead author, Jason Bobe MSc, is an associate professor in the genetics and genome science department at the Icahn School of Medicine at Mount Sinai in New York City.

Bobe is part of Mount Sinai’s Resilience Project. It seeks to discover why some people are more able than others to resist or recover from certain illnesses, including Lyme disease.

Recent advancements in Lyme disease

This paper does an excellent job of summarizing the advancements in Lyme and tick-borne diseases over the past five years. It also identifies gaps in knowledge, remaining challenges, the need for additional funding and further research.

The paper paints a comprehensive picture of what causes acute Lyme disease, including immune activation, dissemination, and inflammation.  In addition, it looks at newly discovered biological markers that may aid in the development of improved diagnostics.

Included is a detailed description of several potential causes of symptoms of Lyme disease that persist after standard treatment. The authors propose that the most salient hypotheses are “persistence of infection or antigenic debris, persistence of inappropriate immune activation and inflammation, or some combination of these.”

Topics covered in the publication includes the weakness of current standard Lyme disease diagnostics and a review of several emerging diagnostic assays. Included in the section on treatment is a review of recent drug discoveries and complementary therapies, including natural and botanical medicines.

Direct detection test for Lyme?

Another co-author, Brandon Jutras PhD, is an assistant professor of biochemistry in the Virginia Tech College of Agriculture and Life Sciences. His team is working to develop a new direct diagnostic test for acute Lyme disease.

In 2019, Jutras discovered that Borrelia burgdorferi sheds peptidoglycan, a mesh-like substance that forms the cell wall of the bacteria once it invades the human body. Although all bacteria have peptidoglycan, many do not shed it.

“Current Lyme disease diagnostics are indirect, meaning that the tests are detecting antibodies produced by the human in response to the infection, rather than detecting the bacteria itself,” said Jutras. “This method is prone to error and relies on the individual’s immune system, which can take weeks to make enough antibodies to detect, not to mention that everyone’s immune system is different.”

“We are trying to develop and critically test a procedure whereby we detect peptidoglycan, which is a unique piece of the bacterium that causes Lyme disease,” said Jutras. “The piece is a specific and abundant fragment that may act as a direct biomarker for an active infection and, in theory, be detectable within hours of transmission from an infected tick.”

Other Lyme research

Portions of the paper include research done by the authors. Some highlights include:

  1. Monica Embers showing Lyme persists after a standard course of antibiotics, Lyme spirochetes in multiple organs after antibiotics, and Lyme spirochetes in an autopsied brain (despite treatment).
  2. John Aucott, ongoing research as Director of the Johns Hopkins Lyme Disease Research Center, including examining why brain inflammation persists after Lyme disease treatment.
  3. Kim Lewis’ work on eradicating drug-tolerant infections as well as his new investigation into the gut microbiome as it pertains to persistent Lyme disease.
  4. Brain Fallon’s decades of research on neurological Lyme which will be continuing at Columbia University’s new Cohen Center for Health and Recovery from Tick-Borne Diseases.
  5. Nicole Baumgarth’s research into how Lyme spirochetes evade the immune system.
  6. Ed Breitschwerdt and Richard Maggi’s decades of work on developing treatment for Bartonella and other co-infections.

The authors also encourage collaborative efforts like that being done by co-author Liz Horn, PhD, the principal investigator at the Lyme Disease Biobank (LDB). The LDB was created by the Bay Area Lyme Foundation and has partnered with the National Disease Research Interchange as well as LymeDisease.org’s MyLymeData research project.

Need for federal funding

The authors highlight the urgent need for adequate federal funding to “support advancement in the scientific and clinical understanding of the disease, or to develop and evaluate innovative approaches for prevention, diagnosis, and treatment.”

The paper reads like a summary of all 14 of the previous Tick-borne Disease Working Group (TBDWG) sub-committee reports generated by the 2018 and 2020 working groups. If you’ve read any of the TBDWG sub-committee reports (some of them over 100+ pages long), you know this summary was a heavy lift.

Monica Embers was recently appointed to the 2021-2022 TBDWG. I hope this paper will be required reading for the 13 other members!

“It is very exciting to have the opportunity to shape future funding priorities regarding tick-borne disease research and response,” said Embers. “I’d like to see more of an emphasis on the neurological impacts of Lyme disease and a renewed commitment to improving how we diagnose and treat the disease.”

Outline

To summarize the entire paper would be difficult as it is over 80 pages long, with nearly 350 references, and swimming in deep science. If you are interested in a particular topic, I have provided an outline and a link to the paper below.

The topics included in this paper include:

  1. Introduction
  2. Clinical and Translational Medicine
    1. Diagnosis
      1. Exposure to Ticks
      2. Serological Testing
      3. Signs and Symptoms
      4. EM Lesion
      5. Direct Detection of Bb
      6. Emerging Diagnostics
    2. Treatment
      1. Drug Discovery and Preclinical Studies
      2. Complementary Therapies
    3. Well-Defined LD Patient Subgroups With Posttreatment Sequelae
      1. Antibiotic Refractory Lyme Arthritis
      2. PTLD
  3. Fundamental Knowledge
    1. Genomic Insights From Borreliaceae Lineages
    2. Proteomic Insights From Borreliaceae Lineages
    3. Transmission of Bb via Ixodes Spp. Vectors
    4. Pathogenesis
      1. Immune Activation and Inflammation in Untreated LD
      2. Inflammation and Immune Dysregulation Among Patients With Persistent LD
        1. CRP in Patients With Persistent Symptoms Following Treatment
        2. IFN-y and Antibiotic-Refractory Lyme arthritis patients
        3. CCL19 Among PTLD Patients
        4. IL-23 Among European PTLD Patients
        5. Autoantigens and Self-Reactivity In LA
    5. Persistence
      1. Persistent Antigenic Debris
      2. Persistent Infection
  4. Prevention
    1. Ecological Prevention
    2. Human Vaccine
    3. Field Building
      1. Biorepositories and Research Cohorts
        1. Lyme Disease Biobank
        2. Lyme Disease Research
        3. Long Island Outdoor Worker Cohort
      2. Data Repositories
        1. LymeMIND Commons
  5. Discussion
READ THE PAPER

Reference

Bobe JR, Jutras BL, Horn EJ, Embers ME, Bailey A, Moritz RL, Zhang Y, Soloski MJ, Ostfeld RS, Marconi RT, Aucott J, Ma’ayan A, Keesing F, Lewis K, Ben Mamoun C, Rebman AW, McClune ME, Breitschwerdt EB, Reddy PJ, Maggi R, Yang F, Nemser B, Ozcan A, Garner O, Di Carlo D, Ballard Z, Joung H-A, Garcia-Romeu A, Griffiths RR, Baumgarth N and Fallon BA (2021) Recent Progress in Lyme Disease and Remaining Challenges. Front. Med. 8:666554. doi: 10.3389/fmed.2021.666554

LymeSci is written by Lonnie Marcum, a Licensed Physical Therapist and mother of a daughter with Lyme. In 2019-2020, she served on a subcommittee of the federal Tick-Borne Disease Working Group. Follow her on Twitter: @LonnieRhea  Email her at: lmarcum@lymedisease.org.

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**Comment**

I’m an optimistic person by nature; however, I have little hope for true change in Lyme-land.  All we have to do is look around at the continuing censorship, persecution, and real misinformation about COVID to see there are powerful forces at work that just don’t seem to step down despite protests, good scientific information, and facts.

Category:

Lyme, research

Do an Altered Gut Microbiota and an Associated Leaky Gut Affect COVID-19 Severity?

https://journals.asm.org/doi/10.1128/mbio.03022-20?

mBio

Volume 12, Number 1
23 February 2021
 
ABSTRACT
 
Coronavirus disease 2019 (COVID-19), which has been declared a pandemic, has exhibited a wide range of severity worldwide. Although this global variation is largely affected by socio-medical situations in each country, there is also high individual-level variation attributable to elderliness and certain underlying medical conditions, including high blood pressure, diabetes, and obesity. As both elderliness and the aforementioned chronic conditions are often associated with an altered gut microbiota, resulting in disrupted gut barrier integrity, and gut symptoms have consistently been associated with more severe illness in COVID-19 patients, it is possible that dysfunction of the gut as a whole influences COVID-19 severity. This article summarizes the accumulating evidence that supports the hypothesis that an altered gut microbiota and its associated leaky gut may contribute to the onset of gastrointestinal symptoms and occasionally to additional multiorgan complications that may lead to severe illness by allowing leakage of the causative coronavirus into the circulatory system.
 

For more: 

Category:

Gut Health, research, Viruses