Can the COVID-19 virus negatively affect the behavior of carriers? | Chroniclers


Mr. Editor,

The current pandemic is causing a dramatic change in our lives, far beyond what we even thought was acceptable until 2020. Such a great sacrifice is said to be necessary to protect our loved ones, the healthcare system and the economy. However, this is not without legitimate concerns and fears.

As public opinion continues to await more data on the real implications of COVID-19 vaccines, the scientific debate has ignited over extremely contradictory conclusions. And the only measures capable of containing the viral spread always seem to be social distancing and personal precautions (wearing appropriate masks, washing hands, monitoring for possible suspicious symptoms, etc.): in other words, adherence. maximum of all to the rules of behavioral prophylaxis. [1].

No wonder, then, that many are beginning to perceive this situation as an endless and frightening tunnel. For this reason, now like never before, we are in desperate need of trust. Trust in institutions, communication, research. And above all, to have confidence in ourselves as citizens.

I would like to say a few words on the last aspect of the question. For the past year and a half, we have been asked to control our decisions in the most responsible and prudent manner. Which essentially means having the best control over our behavior. While this is something we take for granted every day, it can be different today despite our best efforts. Why?

My answer may sound a little odd, or at least unusual when it comes to viruses. But for every deception, there is an unconscious victim of the trick: the more control she thinks she has, the less she actually has. We represent SARS-CoV-2 primarily acting as a passive actor in the so-called “host adaptation process” [2].

This is proven, for example, by the current discussion about how quickly it is evolving into more transmissible and stimulating strains. Nonetheless, what I would like to point out is that we still lack the flip side of the coin: whether this virus might be able to actively adapt the host for its own purposes.

After all, from an evolutionary perspective, this is a much less rare trait than you might think at first glance. Dr Bouayed and Dr Bohn suggested this theoretical approach for SARS-CoV-2 in their work [3]. Several parasites show the ability to manipulate host behavior in order to improve transmission and spread.

Among them, some worth mentioning are Nematomorphs (toward), Ophiocordyceps (mushroom), Plasmodium Malariae and Toxoplasma gondii (protozoa), Wolbachia(bacteria), Rage (virus). The mechanisms behind their strategy are not always known, and most of the time they remain a complete secret to us and their hosts. Fortunately this is no longer the case with rabies, thanks to the invaluable work of Dr Hueffer and his team.

In 2017, they discovered something amazing: a short sequence of amino acids inserted into the viral glycoprotein is able to alter behavior, turning the infected animal into a frenzied and aggressive mood. [4, 5, 6].

This is due to the neurotoxic properties of the twine, which is almost identical to the venom of some snakes. The results of the experiment showed a key role played by this “snake-like toxin” sequence in the disruption of normal nicotinic receptor activity in the central nervous system, highlighting how the rabies-derived peptide (RV- 183A or RV-183P) induces subtle effects but decisive oscillations in cerebral communication [7]. The consequences are better verifiable by looking at the following link:

Regarding our current situation, an important question must be raised. Indeed, the presence of a “snake like toxin” sequence does not seem to be specific to the rabies virus. In May 2020, Dr Changeaux, professor emeritus of neuroscience at the Institut Pasteur, proposed a “nicotine hypothesis” _for COVID-19 [8]. On this occasion, he highlighted how the SARS-CoV-2 spike glycoprotein contains a motif homologous to that of snake neurotoxins and the RABV neurotoxin-like region.

Further away in silico the findings, made by Dr Farsalinos and his team, recognized a superposition between the peptide fragment aa375-390 and a sequence of the homolog of the neurotoxin NL1 [9]. Their work strongly supported the idea that this amino acid sequence interacts with nicotinic acetylcholine receptors and that SARS-CoV-2 itself could be considered a blocker of their function. Something was confirmed later, in early 2021, thanks to molecular modeling and docking experiments conducted by Dr Alexandris and Dr Lagoumintzis [10, 11].

This characteristic should be considered of the utmost importance now, in light of two facts. First: many studies show a surprising ability of SARS-CoV-2 to invade central nervous system tissues, suggesting that the virus can gain access to the brain by first infecting the olfactory bulb and then spreading to the brain [12]. Such remarkable neurotropism raises many concerns, and research around the world is making an extraordinary effort to study its consequences. Second: the cholinergic pathway plays an essential role in the modulation of dopaminergic reward responses as well as locomotor behavior, emotional state, attention, learning and memory. [13, 14].

And the rabies lesson clearly teaches that anything capable of altering its activity could potentially have a chance to control the host’s behavior. What if the virus is currently hijacking the minds of infected people, in order to make them inappropriately hyperactive, anxious, impulsive, sociable? So, in the end, much more transmissive? My reasoning is highly speculative, and the only intention is to show things that I consider of great importance and

deserving of urgency in vivo investigation. If those who should be protecting others (i.e. the paucisymptomatic infected person) are led by the virus not to do so, the only barrier we currently have could inevitably collapse. Conversely, if we change the rules about what controls us, we will change the rules about what we can control. So, a crucial question to ask now is: can we trust ourselves, if we are infected?

Adriano Castagna is an Italian physiotherapist, specializing in the rehabilitation of spinal cord injuries. He had the opportunity to study at the Santa Lucia Foundation of IRCCS (Scientific Institute for Research, Hospitalization and Health) in Rome, where he then worked in the field of neurological rehabilitation.


[1] West R, Michie S, Rubin GJ, Amlôt R. Application of behavior change principles to reduce the transmission of SARS-CoV-2. Nat Hum behaves 4, 451-459 (2020).

[2] Simmonds P, Aiewsakun P, Katzourakis A. Prisoners of war – host adaptation and its constraints on virus evolution. Nat Rev Microbiol. 2019 May; 17 (5): 321-328.

[3] Bouayed J, Bohn T. Behavioral manipulation – key to successful global spread of novel coronavirus SARS-CoV-2? J Med Virol. August 19, 2020: 10.1002 / jmv.26446.




[7] Hueffer K, Khatri S, Rideout S, et al. The rabies virus alters the behavior of the host through a snake toxin-like region of its glycoprotein that inhibits neurotransmitter receptors in the CNS. Scientific representative. October 9, 2017; 7 (1): 2818.

[8] Changeux JP, Amoura Z, Rey FA, ​​Miyara M. A nicotine hypothesis of Covid-19 with preventive and therapeutic implications. CR Biol. 2020 Jun 5; 343 (1): 33-39.

[9] Farsalinos K, Eliopoulos E, Leonidas DD, et al. Nicotinic cholinergic system and COVID-19: in silico identification of an interaction between SARS-CoV-2 and nicotinic receptors with potential implications for therapeutic targeting. Int J Mol Sci. August 13, 2020; 21 (16): 5807.

[10] Alexandris N, Lagoumintzis G, Chasapis CT, et al. Nicotinic cholinergic system and COVID-19: In silico evaluation of nicotinic acetylcholine receptor agonists as potential therapeutic interventions. Toxicol Rep. December 19, 2020; 8: 73-83.

[11] Lagoumintzis G, Chasapis CT, Alexandris N, et al. Nicotinic cholinergic system and COVID-19: in silico identification of interactions between the nicotinic acetylcholine receptor α7 and the cryptic epitopes of the SARS-Co-V and SARS-CoV-2 Spike glycoproteins. Food Chem Toxicol. March 2021; 149: 112009.

[12] Kumari P, Rothan HA, Natekar JP, et al. Neuroinvasion and encephalitis after intranasal inoculation of SARS-CoV-2 in K18-hACE2 mice. Virus. Jan 19, 2021; 13 (1): 132

[13] Granon S, Faure P, Changeux JP. Executive and social behaviors under regulation of nicotinic receptors. Proc Natl Acad Sci United States. August 5, 2003; 100 (16): 9596-601.

[14] Kessler P, Marchot P, Silva M, et al. The three-fingered toxin fold: a multifunctional structural scaffolding capable of modulating cholinergic functions. J Neurochem. 2017 Aug; 142 Suppl 2: 7-18

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