So, after a pool on Twitter, the vast majority of voters chose yes… so here we are. This is marginally connected to the Reverse AIDS hypothesis, but it bears 100x more pertinence to our current situation.
As with PAID, this wouldn’t be possible without the collaboration of the other person, this one even more than the other parts. Credit where credit is due. First, I need to explain, what are biofilms.
Biofilms are a collective of one or more types of microorganisms that can grow on many surfaces.
One common example of a biofilm dental plaque, is a slimy buildup of bacteria that forms on the surfaces of teeth. Pond scum is another example. Biofilms have been found growing on minerals and metals. They have been found underwater, underground, and above the ground. They can grow on plant tissues and animal tissues, and on implanted medical devices such as catheters and pacemakers.
Surface colonization and subsequent formation of biofilms are best studied in bacteria , although fungi, algae, protozoa, and viruses are also isolated from biofilms in industrial and medical environments. The structure of biofilm communities can protect the bacteria within them from attack by antimicrobials, shear forces, and the immune system.
Furthermore, to achieve cell-cell communication, microorganisms secrete quorum-sensing molecules that control their biological activities and behaviors and play a role in fungal resistance and pathogenicity.
Now we start getting into the complexity of biofilms. Into the chasm of molecular structures and their physiological effects.
Biofilm research is extensive, there are tons of literature on it, they can modulate your immune system, they cause chronic diseases, disrupt the entire physiology, the list goes on, and the biggest of all, they are perfect immune evasive “little houses”. Now to the entire point of this post.
Biofilms and Coronavirus Reservoirs: a Perspective Review
Previous studies have shown that viruses can secondarily colonize preexisting biofilms, and viral biofilms have also been described. In this review, we raise the perspective that CoVs can persistently infect bats due to their association with biofilm structures. This phenomenon potentially provides an optimal environment for nonpathogenic and well-adapted viruses to interact with the host, as well as for viral recombination. Biofilms can also enhance virion viability in extracellular environments.
It has been established that the majority of microorganisms on earth live in biofilms (45, 46). Viruses play an extensive ecological role and have been reported to exist in diverse microbial communities as biofilms. They are involved in several dynamics, such as microbial diversity and biogeochemical cycles, due to their prevalence and variation across diverse ecosystems (47).
The next paragraph is something else.
Viruses, as well as other microorganisms, may come into contact with preexisting biofilms and accidentally adhere and become a part of them, thus constituting secondary colonizers. A study from 2002 supports that biofilms may encompass a set of nonenveloped enteric viruses, including caliciviruses, Rotavirus spp., Astrovirus spp., and hepatitis A virus, among other microorganisms such as Gram-negative bacteria and filamentous fungi (55). Some authors indicate that the human oral cavity may be an active site of infection and reservoir for SARS-CoV-2, assuming its interaction with the host oral microbiota (59), which is mostly in the form of biofilm. Importantly, both virions and virus-infected eukaryotic cells embedded in biofilms have been reported to retain their infectivity. A study investigated the enveloped virus herpes simplex virus 1 (HSV-1) and the nonenveloped virus coxsackievirus type B5 (CVB5) within the fungal Candida albicans biofilms (60). The authors recovered high virus titers from in vitro cultures of the virus-exposed biofilms after extensive washes, indicating that virions and viruses are deeply dispersed into the fungi-produced biofilm matrix, and thus protected. The authors related that biofilm reduced virus sensitivity to chemical inactivation and they discussed some mechanisms that may lead to virion inclusion into the fungal biofilm; for example, by sorption sites from the extracellular matrix, by the natural colloidal characteristic of viruses, or by biomolecules present on biological fluids. Since these viruses encompassed on biofilm kept their viability and infectivity, it indicates that biofilm lifestyle does not limit viral dissemination (60) and even can improve it. Therefore, viruses stored in biofilms may be regarded as temporary or long-term reservoirs in the environment (61).
Since viruses are strict intracellular parasites, we hypothesize that they will be unable to proliferate in biofilms, but they would persist as infectious agents in a reservoir host due to the advantages conferred by the biofilm structure. Furthermore, the maintenance of viral particles inside biofilms facilitates the coinfection process due to physical proximity.
(iii) Genomic recombination events have been shown for several viruses, including CoVs, that are harbored by bats (23). Compared to other RNA viruses, the expanded genome size of CoVs facilitates the acquisition of genes encoding accessory proteins that are beneficial for CoV adaptation to a specific host and, as a result, genome changes caused by recombination, gene interchange, and insertion or deletion are common among CoVs (27). This genetic plasticity is important to interspecies persistence and survival mechanisms (84).
Biofilms may contribute to viral recombination events, especially for supporting an environment in which distinct and infectious viruses are physically close and in the presence of extracellular enzymes and genetic fragments. These viruses would be released from the biofilm and would coinfect the same host cell, leading to gene exchanges and recombination. Therefore, the facilitated cell coinfection by diverse viruses allows the evolution and emergence of new viral particles that can undergo spillover events to other animals.
A biosafety level 2 surrogate for studying SARS-CoV-2 survival in food processing environmental biofilms
Biofilm can act as a reservoir in protecting, harboring, and dispersing SARS-CoV-2 from biofilm to the meat processing facility environment. We used Murine Hepatitis Virus (MHV) as a surrogate for SARS-CoV-2 virus and meat processing facility drain samples to develop mixed-species biofilms on commonly found materials in processing facilities (Stainless-Steel (SS), PVC and tiles). The results showed that MHV was able to integrate into the environmental biofilm and survived for a period of 5 days at 7°C. There was no significate difference between the viral-environmental biofilm biovolumes developed on different materials SS, PVC, and tiles. There was a 2-fold increase in the virus-environmental biofilm biovolume when compared to environmental biofilm by itself. These results indicate a complex virus-environmental biofilm interaction which is providing enhanced protection for the survival of viral particles with the environmental biofilm community.
You could also Google SARS-CoV-2 and dental biofilms, there is quite a few number of papers about it, but I don’t base this entire post on merely connecting dots, and circumstantial evidence.
Over the last 6 months I had quite few number of people telling me same. Previously infected with Wuhan or Alpha, recovered , went to a dentist to do something (interestingly enough, 6 of them were for cavity), something burst, they felt a bitter, strong taste in their mouth, gulp the saliva down.
After a few days, they tested positive for Covid, with symptoms. So what is my argument here, this is one “science” that researchers might contest for years to come. SARS-CoV-2 does, in fact, stay hidden inside biofilms in your body, not only in your mouth, but gut, colon, and nerves. Gut and Colon and I know for a fact, from doctors who worked in Covid Critical care and had over 10.000+ each, they are not able to publish their findings.
Right now some doctors and PhDs are arguing that the persistence of the virus in nerves is one of the (many) causes of Long Covid. I would go further, recent studies that I shared show the persistence of the S1 part of the Spike Protein inside monocytes, and the virus itself can infect CD4 lymphocytes.
I personally believe parts of the virus can get inside, stay in, and get released into the body with bacteria and their byproducts after a while, giving rise to very odd, strong, persistent secondary and chronic infections. Everything else I said can and is based on evidence, but this one is barely on anecdote and observation.
That is why I kept mentioning protein interactions and referring to a few SARS-CoV-2 papers.
I raised this question once more. How do you treat a disease with 12 different, simultaneous, immune response ?
Biofilm formation and toxin production provide a fitness advantage in mixed colonies of environmental yeast isolates
Chronic biofilm-based infections: skewing of the immune response
Many of the deadliest bacterial diseases that plague humanity in the modern age are caused by bacterial biofilms that produce chronic infections. However, most of our knowledge of the host immune response comes from the study of planktonic pathogens. While there are similarities in the host response to planktonic and biofilm bacteria, specific immune responses toward biofilms have not been well studied; the only apparent difference is the inability to clear the bacteria allowing the biofilm infection to become chronic. In some cases, the biofilms skew T-cell response toward a balance that allows a stalemate between the host and the pathogen, in which the infection can become persistent. In this minireview, we will summarize well-known examples of this phenomena as well as some emerging studies that may indicate that this situation is much more common than initially thought.
And of course, this would not be one of my posts without a road to Rome.
there was that one paper about SarsCov2 hanging out in gut microflora right?
anecdotally i think probiotocs might help Long covid
Good information and discussion. I used serrapeptase after recovering from main symptoms, to clear/clean biofilm of gut - but I only use it for 7 days at any one time. I've read of some people using it for 12 months + with no problems. But I've read accounts of people have sudden severe reaction after 3 weeks. Used before once - had to stop after 10-14 days because stools became very pale and blood iron levels dropped below normal. I've read it's sometimes used as a chelator to reduce mineral build up. Different people have different tolerances, have to be careful with it. Good observations also about keeping gum/teeth clear. Lemon tea (real lemons) - hydrogen peroxide mouthwash - daily nasal rinse (only the lower cavity) - bio yoghurt on empty gut.