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A Nicotinic Hypothesis for Covid-19 with Preventive and Therapeutic Implications Volume 343, Issue 1 (2020), P

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A Nicotinic Hypothesis for Covid-19 with Preventive and Therapeutic Implications Volume 343, Issue 1 (2020), P Comptes Rendus Biologies Jean-Pierre Changeux, Zahir Amoura, Felix A. Rey and Makoto Miyara A nicotinic hypothesis for Covid-19 with preventive and therapeutic implications Volume 343, issue 1 (2020), p. 33-39. <https://doi.org/10.5802/crbiol.8> © Académie des sciences, Paris and the authors, 2020. Some rights reserved. This article is licensed under the CREATIVE COMMONS ATTRIBUTION 4.0 INTERNATIONAL LICENSE. http://creativecommons.org/licenses/by/4.0/ Les Comptes Rendus. Biologies sont membres du Centre Mersenne pour l’édition scientifique ouverte www.centre-mersenne.org Comptes Rendus Biologies 2020, 343, nO 1, p. 33-39 https://doi.org/10.5802/crbiol.8 News and events / Actualités A nicotinic hypothesis for Covid-19 with preventive and therapeutic implications Une hypothèse nicotinique pour Covid 19 et ses implications préventives et thérapeutiques , a b, c d b, e Jean-Pierre Changeux ¤ , Zahir Amoura , Felix A. Rey and Makoto Miyara a Institut Pasteur CNRS UMR 3571 Department of Neuroscience and Collège de France, Paris France b Sorbonne Université, Inserm UMRS, Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris) c Assistance Publique-Hôpitaux de Paris, Groupement Hospitalier Pitié-Salpêtrière, Service de Médecine Interne 2, Maladies auto-immune et systémiques Institut E3M d Institut Pasteur, Structural Virology Unit, Department of Virology, CNRS UMR 3569, Institut Pasteur Paris France e Assistance Publique-Hôpitaux de Paris, Groupement Hospitalier Pitié-Salpêtrière, Département d’Immunologie, Paris, France. E-mail: [email protected]. Abstract. SARS-CoV-2 epidemics raises a considerable issue of public health at the planetary scale. There is a pressing urgency to find treatments based upon currently available scientific knowledge. Therefore, we tentatively propose a hypothesis which hopefully might ultimately help save lives. Based on the current scientific literature and on new epidemiological data which reveal that current smoking status appears to be a protective factor against the infection by SARS-CoV-2 [1], we hypothesize that the nicotinic acetylcholine receptor (nAChR) plays a key role in the pathophysiology of Covid-19 infection and might represent a target for the prevention and control of Covid-19 infection. Résumé. L’épidémie de SARS-Cov-2 pose un problème considérable de santé publique à l’échelle planétaire. Il y a urgence extrême de découvrir des traitements qui se fondent sur les connaissances scientifiques disponibles. Nous proposons donc une hypothèse plausible mais provisoire qui puisse le moment venu contribuer à sauver des vies. Elle se fonde sur la littérature scientifique disponible et sur des données épidémiologiques nouvelles qui révèlent que le statut de fumeur parait être un facteur de protection contre l’infection par SARS-Cov-2 [1]. Nous proposons l’hypothèse que le récepteur nicotinique de l’acétylcholine (nAChR) joue un rôle critique dans la pathophysiologie de l’infection Covid-19 et puisse représenter une cible pour la prévention et le contrôle de l’infection. Keywords. Covid-19, smoking, nicotinic receptors, clinical trials of nicotine patches. Mots-clés. Covid-19, fumeurs, récepteurs nicotinique, essais clinique patch nicotine. Manuscript received 16th April 2020, accepted 18th April 2020. ¤ Corresponding author. Jean-Pierre Changeux and Zahir Amoura are equal first authors. ISSN (electronic) : 1768-3238 https://comptes-rendus.academie-sciences.fr/biologies/ 34 Jean-Pierre Changeux et al. Symptomatic Covid-19 disease (as caused by CNS [10]. This propensity has been convincingly doc- SARS-CoV-2 virus) is observed in 2.5 percent of umented for the SARS-CoV-1, MERS-CoV and the infected individuals [2] indicating an individual coronavirus responsible for porcine hemagglutinat- variability in the clinical presentation. Among the ing encephalomyelitis (HEV 67N). In light of the high epidemiological and clinical features of Covid-19, similarity between SARS-CoV-1 and SARS-CoV-2, it is the following features are of special interest for un- quite likely that SARS-CoV-2 also possesses a similar derstanding the patho-physiolology, namely: (1) in potential. Neuroinfection has been proposed to po- outpatients with favorable outcome : neurologi- tentially contribute to the pathophysiology and clin- cal/psychiatric disorders, especially loss of sense of ical manifestations of Covid-19 [10] with the neu- smell which is specific of the disease and (2) in hos- roinvasive potential of SARS-CoV-2 suggested to play pitalized older patients with a poor prognosis : sys- a role in the respiratory failure of Covid-19 patients temic hyperinflammatory syndrome with increased [11, 12]. Our nicotinic hypothesis proposes that the levels of circulating cytokines and atypical acute res- virus could enter the body through neurons of the piratory distress syndrome with loss of neurological olfactory system and/or through the lung leading to control of lung perfusion regulation and hypoxic diVerent clinical features with diVerent outcome, and vasoconstriction [3]. This raises the issue of the basis contrasts with the currently accepted view that ACE2 of inter-individual variability for the susceptibility to is the principal receptor of SARS-CoV-2 for its entry infection. into cells. The nAChR appears as a hypothetical clue for As mentioned, loss of sense of smell frequently the main clinical manifestations of Covid-19. It is occurs in Covid-19 patients [13]. Furthermore, sev- accepted that the angiotensin converting enzyme 2 eral studies have reported that some patients in- (ACE2), represents the principal receptor molecule fected with SARS-CoV-2 show neurologic signs such for SARS-CoV-2 [4–6]. ACE2 is expressed at the tran- as headache (about 8 %), nausea and vomiting (1 %) scriptomic level in the lung, the small intestine and [11]. More recently, a study of 214 Covid-19 patients colon, in the kidney, in the testis, in the heart mus- [14] further found that about 88 % (78/88) of the se- cle and in the brain, yet the protein is not detected vere patients displayed neurologic manifestations in- in the lung [7]. In the brain, ACE2 is expressed in cluding acute cerebrovascular diseases and impaired both neurons and glia and particularly present in consciousness. Based on an epidemiological survey the brain stem and in the regions responsible for on Covid-19, the median time from the first symp- the regulation of cardiovascular functions, including tom to dyspnea was 5.0 days, to hospital admission the subfornical organ, paraventricular nucleus, nu- was 7.0 days, and to the intensive care was 8.0 days cleus of the tractus solitarius, and rostral ventrolat- [15]. Therefore, the latency period may be adequate eral medulla [8]. Additional receptors or co-receptors for the virus to enter the nervous system, invade the are, however, not excluded. The relationship between brain stem and aVect the medullary neurons of the nicotine and ACE2 has been explored in the frame- respiratory centers. However, variability of the neuro- work of cardiovascular and pulmonary diseases [9]. logical signs was observed with patients having anos- Accordingly, in the ACE/ANG II/AT1R arm, nicotine mia, showing in general a mild evolution without pul- increases the expression and/or activity of renin, ACE monary attack, in contrast with those without anos- and AT1R, whereas in the compensatory ACE2/ANG- mia suggesting a diversity in the mode of prolifera- (1–7)/MasR arm, nicotine down regulates the expres- tion and /or progression of the virus. sion and/or activity of ACE2 and AT2R, thus suggest- More than 20 years ago, Mohammed, Norrby & ing a possible contribution of acetylcholine receptors Kristensson [16], in a pioneering study, showed with in ACE2 regulation. This possibility has not yet been a broad diversity of viruses (Poliovirus, Herpes sim- explored in the framework of viral neuroinfections. plex virus, West Nile virus , Vesicular Stomatitis Virus, There is strong evidence for a neurotropic action influenza H1N1 virus [17]), that viruses enter the ol- of SARS-CoV-2 infection. It has been demonstrated factory epithelium and progress first through the ol- that β-coronaviruses to which the SARS-CoV-2 be- factory pathway in an anterograde direction and then longs, do not limit their presence to the respiratory in a retrograde manner to the reticular neurons pro- tract and have been shown to frequently invade the jecting to the olfactory bulbs, the median raphe neu- C. R. Biologies, 2020, 343, nO 1, 33-39 Jean-Pierre Changeux et al. 35 rons (serotoninergic) and the ventral and horizontal cytokine profile shows striking analogies with the diagonal band (cholinergic) [16,18]. This olfactory in- cytokine storm syndrome, leading to the hyper- fection route scheme [18] has been recently extended inflammatory syndrome described in a subgroup to Covid-19 infection [2, 11]. To further investigate of Covid-19 patients [30]. Systemic coagulopathy the molecular aspects of Covid-19 propagation in with venous and arterial thrombosis is one of the the brain and its pharmacology, we have been aided critical aspects of the morbidity and mortality of by abundant studies on rabies virus (RABV) a nega- Covid-19. In line with our hypothesis, one should tive polarity, single-strand RNA virus that is distinct note that hematopoietic α7-nAChR deYciency in- from the coronaviruses [18–20]. nAChRs were shown creases platelet reactive status, which could explain to be the first receptors for RABV [21]. Structural the thrombogenic presentation of Covid-19 [31]. Al- studies
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