ABSTRACT
The coronavirus disease 2019 (Covid-19) pandemic intensified the already catastrophic drug overdose and substance use disorder (SUD) epidemic, signaling a syndemic as social isolation, economic and mental health distress, and disrupted treatment services disproportionally impacted this vulnerable population. Along with these social and societal factors, biological factors triggered by intense stress intertwined with incumbent overactivity of the immune system and the resulting inflammatory outcomes may impact the functional status of the central nervous system (CNS). We review the literature concerning SARS-CoV2 infiltration and infection in the CNS and the prospects of synergy between stress, inflammation, and kynurenine pathway function during illness and recovery from Covid-19. Taken together, inflammation and neuroimmune signaling, a consequence of Covid-19 infection, may dysregulate critical pathways and underlie maladaptive changes in the CNS, to exacerbate the development of neuropsychiatric symptoms and in the vulnerability to develop SUD. This article is part of the special Issue on 'Vulnerabilities to Substance Abuse'.
Subject(s)
COVID-19/epidemiology , Drug Misuse/statistics & numerical data , SARS-CoV-2 , Substance-Related Disorders/epidemiology , Adaptation, Psychological , Angiotensin-Converting Enzyme 2/physiology , Animals , Axons/virology , COVID-19/immunology , COVID-19/physiopathology , COVID-19/psychology , Comorbidity , Disease Susceptibility , Endothelial Cells/virology , Humans , Immunity, Innate , Inflammation/etiology , Kynurenine/metabolism , Neurons/virology , Neurotransmitter Agents/metabolism , Olfactory Mucosa/virology , Pandemics , SARS-CoV-2/physiology , Social Isolation , Stress, Psychological , Substance-Related Disorders/etiology , Substance-Related Disorders/physiopathology , Tryptophan/metabolism , Viral TropismSubject(s)
Betacoronavirus/isolation & purification , Coronavirus Infections/epidemiology , Neurosecretory Systems/physiopathology , Neurotransmitter Agents/metabolism , Pneumonia, Viral/epidemiology , Psychological Distance , Social Isolation/psychology , Stress, Psychological , COVID-19 , Coronavirus Infections/psychology , Coronavirus Infections/virology , Humans , Pandemics , Pneumonia, Viral/psychology , Pneumonia, Viral/virology , SARS-CoV-2ABSTRACT
An increasing body of evidence suggests a protective effect of some psychoactive substances against SARS-CoV-2 (Severe Acute Respiratory Syndrome coronavirus type 2). Recent findings suggest that patients with psychiatric disorders are less affected by SARS-CoV-2 than their caregivers, which may seem surprising given some of the frequent risk factors for an unfavorable course of the disease (e.g., obesity, diabetes, cardiovascular and pulmonary diseases). We propose here a mixed pharmacoepidemiological and pharmacochemical hypothesis to explain these findings. A number of psychotropic drugs exhibit activities against coronaviruses (Middle East Respiratory Syndrome coronavirus (MERS-CoV), the Severe Acute Respiratory Syndrome coronavirus (SARS-CoV-1) and the Infectious Bronchitis Virus (IBV)) and have been put forward as potentially anti-SARS-CoV-2. These treatments include numerous mee-too drugs (chemically and pharmacologically linked to those which have demonstrated anti-SARS-CoV-2 efficacy) which are frequently prescribed in psychiatric settings. Taken alone or in polypharmacy, these drugs could have a prophylactic anti-SARS-CoV-2 effect, explaining the unexpectedly low proportion of patients with psychiatric disorders and COVID-19. Associated factors such as nicotine can also be considered in the context of a broad chemoprophylactic hypothesis in patients with psychiatric disorders taking different psychoactive substances.