Science in Action.

We are a 501(c)3 transforming how complex chronic inflammatory conditions are studied, diagnosed and treated.


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Who we are

About us

Complex chronic inflammatory diseases are not mysterious or hopeless. The opposite is true: we can use new tools to study pathogen activity, environmental exposures, microbiome imbalances, neuroinflammation, gene changes, and other issues in patients with such conditions. PolyBio brings together some of the brightest minds in science to research these topics in a proactive and open-minded fashion.

Our Mission

Our vision

  • To take current research, identify important existing trends, and translate the data into information that doctors can use in the clinic to help their patients. This includes the development of new advanced testing methods that can reliably characterise a growing number of disease-related abnormalities.   

  • To take current research, identify gaps where data is lacking, and use such knowledge to support and collaborate with research teams whose existing tools can tackle the problem and develop new solutions.

Our Values

  • Quality

    We don’t cut corners. One high-quality study to identify and solve a problem is better than 100 studies that use sub-par technologies.

  • Urgency

    We are living in the midst of an epidemic in which the incidence of nearly every of chronic disease is on the rise. We act accordingly.

  • Innovation

    We use novel approaches and new applications of innovative technologies to build on cross-discipline expertise.

  • Compassion

    We know the tremendous suffering experienced by patients with complex chronic disease. Alleviating this suffering is our primary motivation.

  • Transparency

    We are determined to improve patient health but don’t guarantee a magic pill. We are realistic about the complexity of human biology and won’t overpromise.


Areas of study


















Gut-brain axis


Areas of study

  • Genes
  • Microbiome
  • Pathogens
  • Inflammation
  • Brain
  • Immunity
  • Metabolism
  • Hormones
  • Gut-brain axis

Our Core Team

Harvard Medical School/Massachusetts General Hospital neuroscientist with encyclopedic knowledge of brain circuits, brain signaling and the technologies needed to study them.

Microbiologist with expertise on the molecular mechanisms by which pathogens modulate human gene expression, metabolism and immunity. Also serves as PolyBio’s Research Team Coordinator.

Human genome biohacker with major experience in data/computer science. Programmer, innovator and builder of fully integrated personalized medicine platforms.

Scientific Advisory Board

CRISPR-Cas system discovery specialist at Mammoth Biosciences with a passion for developing & using technologies to identify novel genes from big data. Co-founder & Head of Bioinformatics at Ancilia Therapeutics focused on bacteriophage genomics and microbiome. Also an affiliate at the Lawrence Berkeley National Lab, Joint Genome Institute.

Scientist at the Max-Planck-Institute for Biology of Ageing working to understand how cellular organelles sense and respond to intracellular pathogens. Expert in mitochondrial dynamics, parasite biology, and immunometabolism.

Instructor in the Neurology Department of Massachusetts General Hospital & Harvard Medical School. Innovator of experimental models for the study of amyloid biology and infection in neurodegenerative disease.

Clinician-scientist determined to map inflammatory signatures specific to the microbiome in a creative fashion. Also an oral surgeon, Professor of Genomic Medicine, and member of the J. Craig Venter Institute infectious disease department. Life prior to disease is his mantra! 

Physician at Spaulding Rehabilitation Hospital/Dean Center for Tickborne Illness and Pediatric Infectious Disease/Massachusetts General Hospital. Passionate about translating research on Borrelia burgdorferi and related tick-borne pathogens into cutting-edge clinical care.

Board of Directors

Head of Business Development at Bloom Farms, a top-selling cannabis CPG company headquartered in California. Previously he spent eight years at the proprietary trading firm DRW, where he was in charge of the firm’s natural gas volatility portfolio. As an active angel investor, Dane seeks out companies in the Consumer Packaged Goods space in emerging categories focused on ancestral health. Dane holds a BA in Economics from Tufts University.

2x Olympic Gold Medalist and Captain of the USA Women’s Water Polo team. She is a dedicated leader not only to her team, but also to the sport of water polo and the growth of women in sport. This passion for growth is complimented by her entrepreneurial route with her company, 6-8 Sports, which she co-founded with fellow Olympian, Tony Azevedo. At 6-8 Sports, she focuses on business development & strategy and raising funds for the company to fulfill its mission. Maggie holds a Bachelor in Science in Science, Technology, and Society as well as a Master in Science in Management & Engineering from Stanford University.

Over 15 years of experience in the private equity and investment banking industries. He is currently a Partner at Newlight Partners, where he focuses on investments in power and infrastructure. Prior to joining Newlight he worked as Managing Director to its predecessor, the Strategic Investments Group of Soros Fund Management, as an Investment Banking Analyst for Bear Stearns, and as an Analyst for the Royal Bank of Scotland. Mark holds a Bachelor in Science and Foreign Service in International Economics from Georgetown University.

Our Approach

Innovating neuroscience and NOT psychology. We study the brain itself, with a focus on neuroinflammation, blood vessel issues, cerebrospinal fluid flow, and potential structural problems.

Research on root cause drivers of chronic inflammatory disease. Getting to the “root cause” of illness leads to development of the most effective treatments.

Exploring new frontiers. We prioritize research that moves beyond just blood tests and towards the study of tissue, nerves, cerebrospinal fluid & autopsies.

Our Work

  • Proal AD, VanElzakker MB. Long COVID or Post-acute Sequelae of COVID-19 (PASC): An Overview of Biological Factors That May Contribute to Persistent Symptoms

    The novel virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a pandemic of coronavirus disease 2019 (COVID-19). Across the globe, a subset of patients who sustain an acute SARS-CoV-2 infection are developing a wide range of persistent symptoms that do not resolve over the course of many months. These patients are being given the diagnosis Long COVID or Post-acute sequelae of COVID-19 (PASC). It is likely that individual patients with a PASC diagnosis have different underlying biological factors driving their symptoms, none of which are mutually exclusive. This paper details mechanisms by which RNA viruses beyond just SARS-CoV-2 have be connected to long-term health consequences. It also reviews literature on acute COVID-19 and other virus-initiated chronic syndromes such as post-Ebola syndrome or myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) to discuss different scenarios for PASC symptom development. Potential contributors to PASC symptoms include consequences from acute SARS-CoV-2 injury to one or multiple organs, persistent reservoirs of SARS-CoV-2 in certain tissues, re-activation of neurotrophic pathogens such as herpesviruses under conditions of COVID-19 immune dysregulation, SARS-CoV-2 interactions with host microbiome/virome communities, clotting/coagulation issues, dysfunctional brainstem/vagus nerve signaling, ongoing activity of primed immune cells, and autoimmunity due to molecular mimicry between pathogen and host proteins. The individualized nature of PASC symptoms suggests that different therapeutic approaches may be required to best manage care for specific patients with the diagnosis.

  • Proal AD, VanElzakker MB. Pathogens Hijack Host Cell Metabolism: Intracellular Infection as a Driver of the Warburg Effect in Cancer and Other Chronic Inflammatory Conditions

    The Warburg effect refers to a metabolic state in which cells preferentially use aerobic glycolysis rather than oxidative phosphorylation to generate ATP and macromolecules. A number of chronic inflammatory conditions are characterized by host cells that adopt a sustained, pathological Warburg-like metabolism. In cancer, previously healthy cells shift into a Warburg state centered on rapid energy production and increased cell proliferation that drives tumor formation. Macrophage in atherosclerotic plaque and in sarcoidosis granuloma can also harbor a Warburg-like phenotype that promotes an inflammatory milieu. The question of why host cells in patients with cancer and other chronic inflammatory conditions adapt a pathological Warburg-like metabolism is a matter of debate. This review/hypothesis piece explores how intracellular infection can contribute to this Warburg metabolism or related pathological metabolic states. We detail molecular mechanisms by which viral, bacterial, and protozoan intracellular pathogens can induce, or contribute to, a Warburg-like metabolism in infected host cells in order to meet their own replication and nutritional needs. We also discuss how host defense towards infection may impact cellular metabolic changes. We then provide examples of how many of these same intracellular pathogens have been identified in tumors, atherosclerotic lesions, granuloma, and other tissues containing cells with a Warburg or altered metabolism. Last, we examine further trends associated with infection and host cell metabolism, including how pathogen-driven hijacking of host cell lipid metabolism can support viral, bacterial, and parasite survival and replication.

  • Proal AD, Marshall TG. Myalgic encephalomyelitis/chronic fatigue syndrome in the era of the human microbiome: Persistent pathogens drive chronic symptoms by interfering with host metabolism, gene expression, and immunity

    The illness ME/CFS has been repeatedly tied to infectious agents such as Epstein-Barr virus. Expanding research on the human microbiome now allows ME/CFS-associated pathogens to be studied as interacting members of human microbiome communities. Humans harbor these vast ecosystems of bacteria, viruses and fungi in nearly all tissue and blood. Most well-studied inflammatory conditions are tied to dysbiosis or imbalance of the human microbiome. While gut microbiome dysbiosis has been identified in ME/CFS, microbes and viruses outside the gut can also contribute to the illness. Pathobionts, and their associated proteins/metabolites, often control human metabolism and gene expression in a manner that pushes the body toward a state of illness. Intracellular pathogens, including many associated with ME/CFS, drive microbiome dysbiosis by directly interfering with human transcription, translation, and DNA repair processes. Molecular mimicry between host and pathogen proteins/metabolites further complicates this interference. Other human pathogens disable mitochondria or dysregulate host nervous system signaling. Antibodies and/or clonal T cells identified in patients with ME/CFS are likely activated in response to these persistent microbiome pathogens. Different human pathogens have evolved similar survival mechanisms to disable the host immune response and host metabolic pathways. The metabolic dysfunction driven by these organisms can result in similar clusters of inflammatory symptoms. ME/CFS may be driven by this pathogen-induced dysfunction, with the nature of dysbiosis and symptom presentation varying based on a patient’s unique infectious and environmental history. Under such conditions, patients would benefit from treatments that support the human immune system in an effort to reverse the infectious disease process.

  • VanElzakker MB, et al. Neuroinflammation and cytokines in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): A critical review of research methods

    Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is the label given to a syndrome that can include long-term flu-like symptoms, profound fatigue, trouble concentrating, and autonomic problems, all of which worsen after exertion. It is unclear how many individuals with this diagnosis are suffering from the same condition or have the same underlying pathophysiology, and the discovery of biomarkers would be clarifying. The name “myalgic encephalomyelitis” essentially means “muscle pain related to central nervous system inflammation” and many efforts to find diagnostic biomarkers have focused on one or more aspects of neuroinflammation, from periphery to brain. As the field uncovers the relationship between the symptoms of this condition and neuroinflammation, attention must be paid to the biological mechanisms of neuroinflammation and issues with its potential measurement. The current review focuses on three methods used to study putative neuroinflammation in ME/CFS: (1) positron emission tomography (PET) neuroimaging using translocator protein (TSPO) binding radioligand (2) magnetic resonance spectroscopy (MRS) neuroimaging and (3) assays of cytokines circulating in blood and cerebrospinal fluid. PET scanning using TSPO-binding radioligand is a promising option for studies of neuroinflammation. However, methodological difficulties that exist both in this particular technique and across the ME/CFS neuroimaging literature must be addressed for any results to be interpretable. We argue that the vast majority of ME/CFS neuroimaging has failed to use optimal techniques for studying brainstem, despite its probable centrality to any neuroinflammatory causes or autonomic effects. MRS is discussed as a less informative but more widely available, less invasive, and less expensive option for imaging neuroinflammation, and existing studies using MRS neuroimaging are reviewed. Studies seeking to find a peripheral circulating cytokine “profile” for ME/CFS are reviewed, with attention paid to the biological and methodological reasons for lack of replication among these studies. We argue that both the biological mechanisms of cytokines and the innumerable sources of potential variance in their measurement make it unlikely that a consistent and replicable diagnostic cytokine profile will ever be discovered.

  • Proal AD, et al. The human microbiome and autoimmunity

    The purpose of this review is to  demonstrate how dysbiosis of the human microbiome can drive autoimmune disease. Humans are superorganisms. The human body harbors an extensive microbiome, which has been shown to differ in patients with autoimmune diagnoses. Intracellular microbes slow innate immune defenses by dysregulating the vitamin D nuclear receptor, allowing pathogens to accumulate in tissue and blood. Molecular mimicry between pathogen and host causes further dysfunction by interfering with human protein interactions. Autoantibodies may well be created in response to pathogens. The catastrophic failure of human metabolism observed in autoimmune disease results from a common underlying pathogenesis – the successive accumulation of pathogens into the microbiome over time, and the ability of such pathogens to dysregulate gene transcription, translation, and human metabolic processes. Autoimmune diseases are more likely passed in families because of the inheritance of a familial microbiome, rather than Mendelian inheritance of genetic abnormalities. We can stimulate innate immune defenses and allow patients to target pathogens, but cell death results in immunopathology.

  • VanElzakker MB. Chronic fatigue syndrome from vagus nerve infection: A psychoneuroimmunological hypothesis

    Chronic fatigue syndrome (CFS) is an often-debilitating condition of unknown origin. There is a general consensus among CFS researchers that the symptoms seem to reflect an ongoing immune response, perhaps due to viral infection. Thus, most CFS research has focused upon trying to uncover that putative immune system dysfunction or specific pathogenic agent. However, no single causative agent has been found. In this speculative article, I describe a new hypothesis for the etiology of CFS: infection of the vagus nerve. When immune cells of otherwise healthy individuals detect any peripheral infection, they release proinflammatory cytokines. Chemoreceptors of the sensory vagus nerve detect these localized proinflammatory cytokines, and send a signal to the brain to initiate sickness behavior. Sickness behavior is an involuntary response that includes fatigue, fever, myalgia, depression, and other symptoms that overlap with CFS. The vagus nerve infection hypothesis of CFS contends that CFS symptoms are a pathologically exaggerated version of normal sickness behavior that can occur when sensory vagal ganglia or paraganglia are themselves infected with any virus or bacteria. Drawing upon relevant findings from the neuropathic pain literature, I explain how pathogen-activated glial cells can bombard the sensory vagus nerve with proinflammatory cytokines and other neuroexcitatory substances, initiating an exaggerated and intractable sickness behavior signal. According to this hypothesis, any pathogenic infection of the vagus nerve can cause CFS, which resolves the ongoing controversy about finding a single pathogen. The vagus nerve infection hypothesis offers testable hypotheses for researchers, animal models, and specific treatment strategies.

  • Proal AD, et al. Autoimmune disease and the human metagenome

    The prevailing theory of autoimmune disease, that the body creates autoantibodies that attack “self,” was developed during an era when culture-based methods vastly underestimated the number of microbes capable of persisting in and on Homo sapiens. Thanks to the advent of culture-independent tools, the human body is now known to harbor billions of microbes whose collective genomes work in concert with the human genome. Thus, the human genome can no longer be studied in isolation. Some of these microbes persist by slowing the activity of the vitamin D receptor nuclear receptor, affecting the expression of endogenous antimicrobials and other key components of the innate immune system. It seems that bacteria that cause autoimmune disease accumulate over a lifetime, with individuals picking up pathogens with greater ease over time, as the immune response becomes increasingly compromised. Any one autoimmune disease is likely due to many different microbes within the metagenomic microbiota. This helps explain the high levels of comorbidity observed among patients with autoimmune conditions. What are commonly believed to be autoantibodies may instead be created in response to this metagenomic microbiota when the adaptive immune system is forced to deal with disintegration of infected cells. Similarly, haplotypes associated with autoimmune conditions vary widely among individuals and populations. They are more suggestive of a regional infectious model rather than a model in which an illness is caused by inherited variation of HLA haplotypes

  • Proal AD, et al. Microbe-microbe and host-microbe interactions drive microbiome dysbiosis and inflammatory processes

    An extensive microbiome comprised of bacteria, viruses, bacteriophages, and fungi is now understood to persist in nearly every human body site, including tissue and blood. The genomes of these microbes continually interact with the human genome in order to regulate host metabolism. Many components of this microbiome are capable of both commensal and pathogenic activity. They are additionally able to persist in both “acute” and chronic forms. Inflammatory conditions historically studied separately (autoimmune, neurological and malignant) are now repeatedly tied to a common trend: imbalance or dysbiosis of these microbial ecosystems. Population-based studies of the microbiome can shed light on this dysbiosis. However, it is the collective activity of the microbiome that drives inflammatory processes via complex microbe-microbe and host-microbe interactions. Many microbes survive as polymicrobial entities in order to evade the immune response. Pathogens in these communities alter their gene expression in ways that promote community-wide virulence. Other microbes persist inside the cells of the immune system, where they directly interfere with host transcription, translation, and DNA repair mechanisms. The numerous proteins and metabolites expressed by these pathogens further dysregulate human gene expression in a manner that promotes imbalance and immunosuppression. Molecular mimicry, or homology between host and microbial proteins, complicates the nature of this interference. When taken together, these microbe-microbe and host-microbe interactions are capable of driving the large-scale failure of human metabolism characteristic of many different inflammatory conditions.

Amy Proal: Introduction to PolyBio; ME/CFS & Long Covid/PACS research considerations
Michael VanElzakker: Studying the intersection of autonomic, neurovascular, & glymphatic systems
Matthew Anderson: Neuropathology study of immune penetration at the perivascular spaces in autism
Lena Pernas: Toxoplasma - mitochondria interactions, and Toxoplasma activity in COVID-19
Felix Ellet: Microfluidic devices visualizing host-pathogen interactions in Lyme
Resia Pretorius: Consequences of coagulation in COVID-19 and Long Covid
Marcelo Friere: Host-viral inflammatory responses in the saliva of COVID-19 patients
William Eimer: "Rethinking Alzheimer’s: Infection, amyloid, & innate immunity
Clovis Palmer: Targeting cellular metabolism to control viral replication and immunity
David Paez-Espino: Virome discovery and cataloging in chronic disease
Roberta Sclocco: Studying the autonomic nervous system with ultrahigh resolution MRI
Kris Fobes: RCCX in Long Covid and other conditions involving persistent infection
SolveME Webinar: "ME/CFS in the Era of the Human Microbiome" with Amy Proal.
CMRC2020: "ME/CFS History & Cerebrovascular Response" with Mike VanElzakker.
"ICA Conference: "Antibodies and Infection in the Era of the Metagenome" with Amy Proal
Science for ME: Questions & Answers with Dr. Michael VanElzakker
ME/CFS Research with Dr. Michael VanElzakker: Vagus nerve Infection and Triggers."
The Human Virome; What is it and Why Should We Care?, with Amy Proal
OMF: "Neuroinflammation in ME/CFS" with Mike VanElzakker.
The UTI microbiome and Persistent Human Pathogens, with Amy Proal

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