What started as a “Shelter in Place” check-in with friends Barbara and Daniel Melvin, grew into this article about a family with extreme losses to COVID-19. Barb first told me they had lost 12 family members and friends from COVID-19 in mid-April. By the end of April, the number had grown to 33. The current count is 40 family and friends lost to COVID-19 as of May 18, 2020.
Daniel and Barbara lived in Detroit before relocating to Naples, Florida, in 2001. Barbara has worked in banking for 30 years and is currently a Vice President at First Florida Integrity Bank. Dan is a multi-talented singer, radio personality, and entrepreneur. They are two of the happiest, kindest, giving, and loving people you could be lucky enough to know.
Together, they have worked to give back to their community through philanthropic endeavors, as well as volunteering on numerous nonprofit boards. They celebrate their mutual birthdays, Sept 6 & 10 by holding an annual event called “Party Hearty for Charity,” formerly known as “Party with a Purpose,” their nonprofit organization., They have raised over $90K in the past six years to help support several nonprofit organizations in SouthWest FL.
Barb says, “The coronavirus is real. I first heard about it in March, but like everyone else, we didn’t understand it, and at that time, we didn’t personally know anyone that was sick from it. Then, as time went on, we started to hear about people that we knew who were dying. My husband and I hated to wake up and look at Facebook because it seemed every time we checked someone close to us or someone we knew had died.”
Barbara tells us, some of the churches in Detroit continued to hold services, after the recommendation not to gather in large numbers. The members met to seek comfort in the face of the pandemic. Barbara believes that was crucial for most of the people she knows who were infected and died.
How could one couple know so many people who have passed from COVID-19? They are an extensive close-knit family, descendants of Tom and Etta Rhoades, born slaves. Tom and Etta’s dreams were to keep their descendants together spiritually, in harmony, and in brotherly love. They have honored their ancestors by gathering each year, for 46 years, for a three-day family reunion. Friday is meet and greet (you would need it with over 200 attending). Saturday is picnic time, complete with a softball game between the North and the South. Sunday, everyone goes to a local church, followed by a family dinner. With all those family members together, not an argument or fight ever. Until 2020, when the pandemic hit the family, and they canceled the family reunion.
Barbara shares with us information on a few of those they have lost. “My aunt, Mary Rhoades, died on April 22, 2020, she was 97 years old. She was in good health, and we were praying she made it to 100.” Several of her siblings had achieved that milestone, and she was reasonably healthy for 97 years of age so that expectation was a real one. “Aunt Mary became infected in early April; two weeks later, she was gone. She went to the hospital in Philadelphia for minor surgery, and we believe she was infected there. What hurts the most is she died alone; no family or friends could visit her.”
“Jason Hargrove was a close friend of ours. He was the bus driver who went on Facebook Live to talk about a woman coughing on his bus without covering her mouth. Two weeks later, he was diagnosed with the coronavirus, and he died shortly thereafter. His death was not in vain as the Detroit Department of Transportation made many changes to enhance the safety of their drivers. Jason was a Deacon at my church.”
Barbara continues, “Another close friend of ours was Larry Griffin. He died on April 16. He sang in my husband’s band called “In Full Effect” when they were performing in Detroit. He continued to sing in a new band called “Serieux,” who performed mostly in Detroit but also in Las Vegas. He had a beautiful voice and some great dance moves. He was so healthy until he caught the virus, and, in weeks, he was gone.”
“It spread so much faster in the churches. Many Pastors we knew caught the virus and were gone. They were older and many had health issues, when the virus attacked them they could not fight it off. These 4 Pastors were all a part of the Church of God In Christ (COGIC). Many had large congregations and were still holding services after the call for social distancing. These great men are a true loss for the COGIC community.”
“On April 23, we lost a very dear friend of mine, Lynn Raimey. I called her my sister as her father was the Pastor of my church in Detroit. Her family took me in and treated me like family when I first moved to Detroit and didn’t know anyone. She had many health issues, so when she was infected by the virus, it killed her very quickly.”
“Although we have lost many family, friends, and associates, we know God is good, and he continues to show us favor even through the midst of this storm. Even though we know of many deaths, we also know of many survivors and to that we are grateful. These people are given a second chance so their test can become their testimony. I know of an entire household, The Washington family of Detroit, who are survivors. Pastor Jamonty, his wife Tamela and their daughter Ariel Washington all recovered and are doing well.”
Barb specifically finds strength in the Beatitudes; “Jesus said in Matthew 5:4, Blessed are they that mourn, for they shall be comforted. It is during these tough times of losing loveda ones that I can refer to scripture to give me the comfort I and my family needs. The question is have you ever suffered? Please know that we all have. But I have come to know through leaning on God and his word, he meets me at my very point of need. As believers, the Bible speaks about plagues and famine and death, and its teachings prepare us for what life has to offer. Oftentimes we don’t understand the current situations, but when we look back, we realize this had to happen.”
As of May 5, 2020, there have been over 72,000 deaths in the United States, and over 257,000 deaths Worldwide. It is critical to find strength either within or in a higher power, focus on the positive, and stay connected.
It is GRAM’s honor to recognize this incredible family.
Blessed are they that mourn, for they shall be comforted.
Family & Friends Lost to Covid-19 (35 as of 5/5/20)
Mary R. – PA
Jason H. – MI
Rachelle Lynn R. – MI
Rev. O’Neil S. – MI
Gerald H. – MI
Curtis H. – MI
Larry G. – MI
Rosalind C. – MI
Rev. Gerald G. – VA
Skylar H. – MI
Rev. David F. – MI
Laneeka B. – MI
Ejuan W. – MI
Darnielita B. – MI
Bishop Phillip B. – MI
Bishop Robert S. – MI
Bishop Robert H. – MI
Tatia W. – MI
Rev. Lonie J. – MI
Carrie W. – MI
Helena J. – VA
James J. – VA
Robert J. – VA
Annette W. – NY
Helen L. – MD
Walter H. – DC
Carol T. – DE
Benjamin T. – DC
William B. – KY
Daniel R. – TX
Karen S. – NC
Denise B. – NC
Doris M. – OH
Trina D. – MI
Earl T. – VA
Nathaniel S. – MI
Lonnie L. – MI
Nathaniel S. Sr. – MI
Nathaniel S. Jr. – MI
Angel R. – IL
Americans for Safe Access + Covid
Americans for Safe Access (ASA) is a 501(c)(3) nonprofit with the mission of ensuring safe and legal access to cannabis for therapeutic use and research. The organization began in 2002 and has been helping educate people, change laws, and get more research out there about the therapeutic benefits of medical cannabis. “We also care about safety, and we want to make sure patients are using cannabis safely and legally throughout the United States,” explains Debbie Churgai, Interim Director for ASA.
GRAM sat down with Churgai to discuss how they are handling COVID-19 for patients throughout the U.S. She tells us, “When it first started, patients were really concerned about there being a lack of access to their medicine. So, one of the first things we did was host a stakeholders call. We contacted a bunch of people: patients, industry professionals, medical professionals, legal professionals, and within two hours, 15-20 people were on the phone strategizing. From that phone call, we then created a letter that we sent to Governors, medical cannabis commissions, and health departments urging them to keep medical cannabis businesses as essential, not just the dispensary but also cultivation and manufacturers so that there was no stop in production or supply chain.”
“It also meant, we needed to make sure patients were receiving safe products, that employees were also being kept safe. Then we started thinking about delivery for states that did not have that yet, and the states that did not yet offer telehealth – we wanted to encourage the changing of regulations at least temporarily to help accommodate the patients. As well as things like tax relief and adding additional caregivers, it wasn’t just about keeping businesses open, it was about making sure that patients were being protected and that products and employees were safe.”
In Colorado, we have seen dispensaries adapt to this crisis by adding hand sanitizer at checkout counters, wearing gloves and masks and only allowing one person in the purchasing area at a time. 33 states now have some sort of medical cannabis program.
According to news around the U.S., cannabis is now considered essential. But it wasn’t that way at first. According to Churgai, “Some states seemed to hold back on making any temporary changes in regulations. Within two weeks though, all the other states began implementing the suggestions we recommended.”
We needed to make sure patients were receiving safe products, that employees were also being kept safe.
“California has reached out more than any other state, I believe that is due to the fact that every single county there is different, from its tax structure to its implementation of the laws. Massachusetts was high with the questions as well because of them deciding to close down their recreational dispensaries for adult use. Now there is an influx of new patients. Now there are new concerns.”
Each state has a different set of rules and regulations surrounding their medical cannabis programs. “We wanted businesses to all have the same information so we offered a live training on health and safety during COVID-19, that can now be purchased as part of our Patient Focused Certification.1 In the training we provide information such as how to properly put on and take off gloves, how to properly touch things, how to properly sanitize surfaces, and more to make sure that businesses are being as safe as possible during this time.”
“When we realized that we helped assist in making these services essential, we wanted to learn how they actually worked for patients throughout the U.S. We wanted to understand, what do they still need during this time? Are their needs being met as patients? Would they like to see services like telehealth and delivery continue after COVID-19? We realize that we really need to streamline our advocacy efforts at this time, and we felt the survey would be a great way to learn what we can do for patients out there,” Churgai explains.
Help ASA discover what patients need around the United States.
Take the survey here: https://www.safeaccessnow.org/covid-19_survey
COVID-19 Patient Experience Survey asks questions like:
• How do you obtain cannabis?
• Do you feel you are at risk for covid and why?
• Rate your state’s response to the covid crisis.
• How should your state be assisting you more?
Patients are at greater risk for a variety of reasons so ASA is working to ensure that the needs of patients are taken into account. So, in addition to creating this survey, Americans for Safe Access has also created a page on their website dedicated to resources for patients seeking information surrounding COVID-19.2
Churgai says, “Cannabis is real medicine. I have been in this industry for so long, and I am a realist, and I know things will not change overnight. But I do feel the pandemic has highlighted the need for this medicine to be seen as real medicine. At ASA, patients are our priority, we are unbiased, we are not paid to play, and patients will always be our top priority.” You can learn all about Americans for Safe Access by visiting their website: https://www.safeaccessnow.org/
Trends in Endocrinology + Metabolism
The quest for a healthy
Endo-Cannabinoid System (ECS)
Emphasis on immunoregulation
The ECS is a disperse system, extending throughout the body; it is in constant interplay with all other organ systems promoting homeostasis in almost every aspect. Despite that, the ECS is still neglected and not included in the curricula of medical schools. For this reason a few introductory notes are in order (Battista et al, 2012). The ECS is the regulator of cognition, mood, nociception, energy metabolism, oxidation, inflammatory processes and a disease modifier as well (Tantimonaco et al, 2014).
The ECS consists of receptors, ligands to these receptors and enzymes that synthesize and degrade these ligands. The number of known endocannabinoid receptors is still growing to more that 55; the two most outstanding receptors are CB1R, mainly distributed throughout the nervous system and responsible for the psychoactivity of cannabis, and CB2R, mainly distributed on immune cells, even those “disguised” as specialized cells within other organs. Other receptors include TRPVx, GPR55, PPaRs etc; all these receptors form dimers between them as well as heterodimers with other types of receptors, like opioid, dopamine, serotonin, adenosine, catecholamine receptors and many others, thereby promoting a universal regulatory interplay throughout the body. The ligands to these receptors are the endocannabinoids (ECs): lipids of the eicosanoid family, derivatives of arachidonic acid (AA); the latter abounds in cell membranes; five of these are well characterized to date, but two are well studied: Anandamide (AEA) and 2-Arachidonoyl-Glycerole (2AG). ECs in the nervous system act in negative feedback loops, more or less like neurotransmitters, but, unlike them, they are synthesized and degraded on demand, and not stored in micro-vesicles. Several formerly unrelated morbid conditions are now recognized as ECS deficiencies, including, among many, migraine, autism, fibromyalgia, irritable bowel syndrome, etc (Russo, 2016).
The endocannabinoid system is involved in immunoregulation through the CB2 receptor and through receptor independent biochemical pathways. The mechanisms of immunoregulation by ECs include modulation of immune response in different cell types, effect on cytokine network and induction of immunoapoptosis; in brief, ECs down-regulate the innate and adaptive immune response in most, but not all, instances. Manipulation of endocannabinoids in vivo may constitute a novel treatment modality against inflammatory disorders.
It is obvious that the health of the ECS is of great importance in many ways, including the facing of a viral infection like COVID-19. A healthy ECS depends on many factors, most importantly from proper nutrition (McPartland et al, 2014).
Dietary ω3 fatty acids seem to act as homeostatic regulators of the ECS, acting in opposite directions if consumed by obese or non-obese individuals. Little change in EC levels are seen in individuals with normal weight, not fed a high ω6 diet.
Dietary ω6 fatty acids are also essential, but should be in a balance to ω3s; suggested balance is ω3:ω6=1:1 to 1:3 for proper ECS signaling and prevention of peroxidation in general. Arachidonic acid is an essential component of the ω6 fatty acids.
Probiotics and prebiotics play a significant part in ECS health, but, for a bizarre reason, they are generally not mentioned: They up-regulate CB2Rs residing on immune cells of the gut; they also modulate CB1Rs, depending on conditions, for instance, they down-regulate CB1Rs in obese individuals and help them gain less or no fat.
Some flavonoids, like kaempferol, genistein, epigallocatechine gallate, and curcumin enhance the ECS; same happens with some anthocyanidins, like cyanidin and delphinidin, although with a different mechanism.
Phthalates, pesticides, additives to pesticides like piperonyl butoxide act as ECS disruptors, meaning that consuming organic food may be a sound protective measure, along with intake of detoxifiers, in case of health problems consistent with ECS deficiency not otherwise explained.
Chronic stress impairs the ECS by decreasing levels of AEA and 2AG, and possibly through changes in CB1R expression too. Stress management may reverse the effects of chronic stress on ECS signaling. Anecdotal reports and common experience suggest that techniques such as meditation, yoga, deep breathing exercises and practicing of sex as well, exhibit mild cannabimimetic effects, thereby balancing the system.
Exercise is also an ECS regulator: Long-term exercise leads to sustained elevations of ECs, and predictable CB1R down-regulation.
Chronic alcohol consumption and binge drinking likely desensitize or down-regulate CB1R and impair EC signaling. Alcohol is not compatible with a healthy ECS.
Nicotine is an ECS deregulator: It induces EC production in some areas of the brain, while decreasing them in others. It should be avoided too.
Caffeine, acutely administered, potentiates CB1R-mediated effects through antagonizing adenosine at the A1 receptor (AA1R). At the undisturbed state, AA1Rs tonically inhibit CB1R activity; Caffeine antagonism on AA1Rs sets CB1Rs free of inhibition, thereby enhancing ECS function, for example by letting 2AG activate CB1Rs. During chronic administration of caffeine, the effects are blurred by individual differences in adaptation. In general, CB1Rs are down-regulated.
Chocolate: Cocoa contains sm-all amounts of at least three N-acyl-ethanolamines with cannabimimetic activity, expressed either directly by activating cannabinoid receptors, or indirectly, by increasing AEA levels (di Tomaso et al, 1996).
Battista et al, 2012: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303140/
Tantimonacco et al, 2014: https://pubmed.ncbi.nlm.nih.gov/24526057/
(Russo, 2016): https://pubmed.ncbi.nlm.nih.gov/28861491/
(McPartland et al, 2014): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3951193/
(di Tomaso et al, 1996): https://pubmed.ncbi.nlm.nih.gov/8751435/
COVID-19 + Cannabis
Is it ethical not to investigate the use of phytocannabinoids?
I have been very curious to see what experts had to say about cannabis use in the COVID-19 epidemic, and thus have been researching extensively. I have found only broad generalizations, along with the popular refrain “cannabidiol does not cure coronavirus”. I find it to be a very over-simplified statement (who is talking about treatment of the virus itself, anyway?) and so I decided to do my own research.
According to all the studies to date (Nichols & Kaplan, 2020), there is no doubt that CBD is immunomodulatory and anti-inflammatory. By “immunomodulatory” we mean basically immunosuppressive, since it generally suppresses the proliferation and activation of mitogen stimulated T-cells, as well as the production of pro-inflammatory cytokines (Chen et al., 2012); the point that should be made here is that the immuosuppressive action of CBD is in no way related to the immunosuppressive action in drugs such as methotrexate or cyclophosphamide. These drugs alter immunity as suppressors only, while CBD (and THC for that matter) modulates its response either by suppressing or by enhancing it, depending on the level of existing T-cell activation (Chen et al., 2012). These findings apply to HIV infections and it remains to be proven if they apply to other corona viruses as well; nevertheless, some data are available: In SARS-CoV infections (very similar to current SARS-CoV-2), a severe decrease in circulating T-cells was observed in the acute phase (Channappanavar et al, 2014). It is therefore possible and worth investigating whether the same applies to COVID-19, which would mean that the two basic phytocannabinoids, namely CBD and THC, would be indicated for the treatment of the acute phase. We have no definite proof at this point.
There is no doubt that CBD is immunomodulatory and anti-inflammatory.
In the COVID-19 epidemic, people are dying mainly of an inflammatory cytokine storm, leading to non-reversible ARDS (Acute Respiratory Distress Syndrome). Several drugs, new and old are tested in the pursuit of a means to contain the storm reaction of the immune system in a balanced way. Since bibliographical evidence suggests that CBD has multiple modes of anti-inflammatory action, very comparable to colchicine (Drugs.com) save the serious adverse side effects (Leung et al, 2015), it is only reasonable to have it tested in the present contingency. There is also some preclinical evidence that THC is useful in preventing the equivalent of ARDS in mice (Rao et al, 2015). I propose that it should be included in the therapeutic protocols on equal terms as colchicine and chloroquine.
Overall, phytocannabinoids manifest their effect by directly suppressing effector T-cells, and by inhibiting kinase cascades and transcription factors leading to production of pro-inflammatory molecules. One such example is the inhibition of phosphorylated p38, which leads to a decrease in the functionality of the inflammatory transcription factors AP-1 and NF-κB, thereby reducing inflammation. Another interesting aspect is the emergence of pro-inflammatory micro-RNAs (miRNAs) at the onset of ARDS (Umbrello et al, 2016), associated to Toll-like Receptor (TLR) and NF-κB signaling (Juknat et al, 2019). miRNA-induced inflammation is not amenable to corticosteroid treatment, but is responsive to CBD and THC (Umbrello et al, 2017). This is another line of research, very much worth pursuing.
In particular, the aforementioned actions of phytocannabinoids are manifested by the inhibition of the production and/or activity of important inflammatory cytokines such as, IFN-γ, IL-6, IL-1β, IL-2, IL-17A, TNF-α (mediated through enhancement of endogenous adenosine signaling (A2A receptors) (Nichols & Kaplan, 2020, Carrier et al, 2006), and chemokines such as CCL-2, which attracts monocytes, T-cells and dendritic cells to areas of inflammation. CBD, with its inhibitory effect on cryopyrin (NALP3), inhibits macrophage inflammasome activation, and thus the caspase-1 cascade is not activated or, were it activated, it would be controlled (Han & Mallampalli, 2015, Libro et al., 2016). Two pro-inflammatory interleukins, IL-1β and IL-6, are emerging as the decisive factors that dictate whether a COVID-19 case will evolve into ARDS (through the combination of macrophage activation syndrome and immune dysregulation [Hellenic Institute for the Study of Sepsis, 2020]) or will self-cure. IL-1β is responsible for 25% of cases, while IL-6 for 75% (Professor E. Giamarellos, personal communication). Interestingly, they are both mitigated by CBD (Nichols & Kaplan, 2020). There is less evidence for THC (Kozela et al, 2010, Keen et al, 2014). In view of this knowledge, not testing CBD as a preventive of ARDS in the context of COVID-19 might even be considered unethical.
In addition, cannabidiol directly induces inflammatory immunocyte suppression by up-regulating the IκB kinase complex, which inhibits the activity of the NF-κB transcription factor (Nichols & Kaplan, 2020). CBD also plays a regulatory role in inflammation by triggering the production of Treg and MDSC (Myeloid Derived Suppressor Cells) (Dhital et al, 2017), as is the case in simple respiratory viral diseases, especially during the early phase.
All the above actions of CBD are related to the suppression of innate (primary) immunoreactivity. Innate immunoreactivity is extremely useful at the beginning of viral infections, but harmful when it eventually gets out of control in the course of the disease: In high risk groups, it can lead to ARDS (acute respiratory distress syndrome). This is what patients have been dying from in the ICUs of the world.
Apart from this, CBD exerts an immunoapoptotic activity (ie withdraws inflammatory immune cells by the programmed cell death mechanism that is called “apoptosis”), as well as an apoptotic activity on infected cells; both actions appear to be important in controlling the degree of inflammation and the progression of infection (Nichols & Kaplan, 2020).
In addition to treating uncontrolled inflammation in the context of viral disease in general, cannabinoids cause significant changes in epigenetic mechanisms (D’Addario et al, 2013), including methylation, histone modification, and non-coding RNA. The epigenetic regulation of viral infections through cannabinoids has received considerable attention in the literature, but this line of knowledge is not fully understood yet. With the increased methylation of host DNA under the influence of cannabis and methylating agents, the expression of many genes may be inhibited, and in particular of the genes related to cell-virus interaction, i.e., genes governing the entry of the virus into the cell, its structural integration, its output and subsequent inflammation (Tahamtan et al, 2016).
Based on the above theoretical / bibliographical data, CBD should be well suited for the exacerbation stage of COVID-19 infection, for exactly the same reasons as colchicine, which has already begun to be administered experimentally. The only difference is that CBD is free from important adverse effects. By the same token, its use as a prophylactic should be discouraged; the same applies to the initial phase of the infection: Full capacity of innate immunity is what is required initially. Concerning patients that already use CBD for other conditions; given the fact that immunosuppression is dose dependent, they should probably keep using it during the epidemic, but in small doses, arbitrarily estimated at less than 15mg/day in divided doses. If larger doses are needed, and in order to err on the safe side, then CBD combined with strict social distancing should suffice. Smoking and vaping should be discouraged altogether (Williams, 2020).
CBD should be well suited for the exacerbation stage of COVID-19 infection.
A final word of caution: Neither CBD nor any other cannabinoid and anti-inflammatory terpene have been systematically tested in the clinical setting of the present epidemic, and therefore cannot be formally recommended by clinicians. Cannabinoids can contribute to infectivity and/or pathogenicity in certain viral infections; in others, they can diminish make viruses less infective and/or less pathogenic. In both cases, multiple biochemical routes affect host immunity, cell signaling and effector mechanisms involved in the viral cell cycle. In this respect, the role of vitamin D is extremely important in the enhancement of public health, but beyond the scope of the present discussion. In any case, caution is in order and medical supervision as well (Reiss, 2010).
Note 1: CBG, other cannabinoids and terpenes have not been taken into account in this small review because a) they would greatly confuse understanding of an already complicated matter b) There is little research available in the literature of cannabis to date.
Note 2: In the literature, CBD and THC are considered as isolated substances, thus without the notorious “entourage effect” of preparations from whole plants (Russo, 2018). The main exception is a few studies with AIDS/HIV patients, who were also smoked cannabis users. There is a possibility that the use of whole spectrum oils would have a different effect on the immune response to viruses.
Other supportive measures (like vitamins D and C, glutathione, acetaminophene etc) that could enhance innate immunity are available, but have not been addressed here.
Carrier, E. J., Auchampach, J. A., & Hillard, C. J. (2006). Inhibition of an equilibrative nucleoside transporter by cannabidiol: A mechanism of cannabinoid immunosuppression. Proceedings of the National Academy of Sciences, 103(20), 7895–7900.
Channappanavar, R., Zhao, J., & Perlman, S. (2014). T cell-mediated immune response to respiratory coronaviruses. Immunol Res, 59(1–3), 118–128.
Chen, W., Kaplan, B. L. F., Pike, S. T., Topper, L. A., Lichorobiec, N. R., Simmons, S. O., Ramabhadran, R., et al. (2012a). Magnitude of stimulation dictates the cannabinoid-mediated differential T cell response to HIVgp120. Journal of Leukocyte Biology, 92(5), 1093–1102.
Chen, W., Kaplan, B. L. F., Pike, S. T., Topper, L. A., Lichorobiec, N. R., Simmons, S. O., Ramabhadran, R., et al. (2012b). Magnitude of stimulation dictates the cannabinoid-mediated differential T cell response to HIVgp120. Journal of Leukocyte Biology, 92(5), 1093–1102.
D’Addario, C., Di Francesco, A., Pucci, M., Finazzi Agrò, A., & Maccarrone, M. (2013). Epigenetic mechanisms and endocannabinoid signalling. FEBS J, 280(9), 1905–1917.
Dhital, S., Stokes, J. V., Park, N., Seo, K. S., & Kaplan, B. L. F. (2017). Cannabidiol (CBD) induces functional Tregs in response to low-level T cell activation. Cellular Immunology, 312, 25–34.
Han, S., & Mallampalli, R. K. (2015). The Acute Respiratory Distress Syndrome: From Mechanism to Translation. J.I., 194(3), 855–860.
Hellenic Institute for the Study of Sepsis. (2020, April 9). Personalised Immunotherapy For SARS-CoV-2 (COVID-19) Associated With Organ Dysfunction — Full Text View — ClinicalTrials.gov. https://clinicaltrials.gov. Retrieved April 14, 2020, from https://web.archive.org/web/20200414135606/
Juknat, A., Gao, F., Coppola, G., Vogel, Z., & Kozela, E. (2019). miRNA expression profiles and molecular networks in resting and LPS-activated BV-2 microglia — Effect of cannabinoids. PLoS ONE, 14(2), e0212039.
Keen, L., Pereira, D., & Latimer, W. (2014). Self-reported lifetime marijuana use and interleukin-6 levels in middle-aged African Americans. Drug and Alcohol Dependence, 140, 156–160.
Kozela, E., Pietr, M., Juknat, A., Rimmerman, N., Levy, R., & Vogel, Z. (2010). Cannabinoids Δ9-Tetrahydrocannabinol and Cannabidiol Differentially Inhibit the Lipopolysaccharide-activated NF-κB and Interferon-β/STAT Proinflammatory Pathways in BV-2 Microglial Cells. J. Biol. Chem., 285(3), 1616–1626.
Leung, Y. Y., Yao Hui, L. L., & Kraus, V. B. (2015). Colchicine — Update on mechanisms of action and therapeutic uses. Seminars in Arthritis and Rheumatism, 45(3), 341–350.
Libro, R., Scionti, D., Diomede, F., Marchisio, M., Grassi, G., Pollastro, F., Piattelli, A., et al. (2016). Cannabidiol Modulates the Immunophenotype and Inhibits the Activation of the Inflammasome in Human Gingival Mesenchymal Stem Cells. Front. Physiol., 7.
Nichols, J. M., & Kaplan, B. L. F. (2020). Immune Responses Regulated by Cannabidiol. Cannabis and Cannabinoid Research, 5(1), 12–31.
Rao, R., Nagarkatti, P. S., & Nagarkatti, M. (2015). Δ9Tetrahydrocannabinol attenuates Staphylococcal enterotoxin B-induced inflammatory lung injury and prevents mortality in mice by modulation of miR-17–92 cluster and induction of T-regulatory cells. Br J Pharmacol, 172(7), 1792–1806.
Reiss, C. S. (2010). Cannabinoids and Viral Infections. Pharmaceuticals, 3(6), 1873–1886.
Russo, E. B. (2018). The Case for the Entourage Effect and Conventional Breeding of Clinical Cannabis: No “Strain,” No Gain. Front. Plant Sci. , 9.
Tahamtan, A., Tavakoli-Yaraki, M., Rygiel, T. P., Mokhtari-Azad, T., & Salimi, V. (2016). Effects of cannabinoids and their receptors on viral infections. J. Med. Virol., 88(1), 1–12.
Umbrello, M., Formenti, P., Bolgiaghi, L., & Chiumello, D. (2016). Current Concepts of ARDS: A Narrative Review. IJMS, 18(1), 64.
Williams, V. (2020, March 24). What Smokers Should Know About COVID-19. Https://newsnetwork.mayoclinic.org/ . Mayo Clinic News Network. Retrieved April 14, 2020, from
Colchicine Uses, Side Effects & Warnings — Drugs.com. Retrieved from https://www.drugs.com/mtm/colchicine.html, Apr 14, 2020
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