Funding Opportunity Number: PAR-25-116
Deadlines: February 5, 2024, March 5, 2024
Background
It has long been known that, in a subset of individuals acutely infected with certain pathogens, chronic sequelae can continue to persist (or develop de novo) long after the acute symptoms have resolved. Commonly referred to as infection-associated chronic illnesses, these conditions are often characterized by a failure to recover following an initial infection even though the original pathogen is no longer detectable using common analytic methods. Several prevalent chronic illnesses – including but not limited to ME/CFS, POTS/dysautonomia, post-treatment Lyme Disease (PTLD), fibromyalgia, mast cell activation syndrome (MCAS), and Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infection (PANDAS), among others – have long been suspected to have an infectious trigger in a certain subset of individuals. Importantly, such conditions tend to involve a core group of symptoms, many of which are neurological and/or mental health-related (for example, extreme levels of fatigue, post-exertional malaise, neurocognitive impairment/brain fog, mood and anxiety disorders, orthostatic intolerance, unrefreshing sleep, headaches, and myalgia/arthralgia, among other symptoms).
While many infectious agents have been linked to the occurrence of infection-associated chronic illnesses, the COVID-19 pandemic has resulted in widespread interest in these phenomena. Recent epidemiological studies indicate that nearly one in five people infected with SARS-CoV-2 (the virus responsible for COVID-19) continue to experience a spectrum of symptoms beyond the acute phase, a condition now referred to as “Post-Acute Sequelae of COVID-19” (PASC) or “Long COVID”. Strikingly, there is a good deal of overlap between the neurological and mental health-related symptoms of PASC (Neuro-PASC) and other suspected infection-associated chronic illnesses such as ME/CFS and POTS, suggesting that these conditions might share an underlying pathophysiology. To date, ongoing work in the field has identified multiple mechanisms of interest that may be therapeutically targetable, including an ongoing exacerbated inflammatory response, microvascular and/or thromboembolic dysfunction, pathogen-induced autoimmunity, bioenergetic failure with metabolic and mitochondrial derangements, gut dysbiosis, and the reactivation of latent pathogens. A deeper understanding of how such mechanisms drive the neuropathophysiology of infection-associated chronic illnesses would greatly enhance ongoing efforts for therapeutic development.
For more detailed information, please see the opportunity webpage.