On my walk home from Kathy’s office this morning, I ran into 3 old girlfriends from work standing in front of the bus stop across from the hospital. They weren’t waiting for a bus. None had a job you could do from home (medical assistant X 2, check-in clerk) and yes plenty of patients were still showing up to see their doctors, although efforts were underway to convert many to “virtual” visits. Talk naturally turned to Mr. coronavirus and I directed them to my blog. I may have bragged too much about the sufficiencies on Harbal, but none of them followed me through the woods when I finally left and headed home. We talked about the positive aspects of their current activity. The lowly smoker is a pariah in the eyes of the U. Indeed, smoking is illegal everywhere on campus. Maybe bus stops are havens for which the Ann Arbor city government is responsible and hence provide sanctuary. But look what these girls gain by their activity: a clean break from work with no screens in sight or job duties creeping in, fresh air, sunshine, social interaction, even laughter. No wonder the smoker comes back into work with a smile on his/her face. I wondered aloud whether flooding one’s lungs periodically might even keep Mr. corona from settling there, and vowed I’d check into it once I got home.
Despite my lighthearted comments above, smoking is never a good idea. With the major morbitity and mortality from COVID-19 being pulmonary, it stands to reason that those who enter into a relationship with the virus will do worse if they’re already starting out with damaged lungs. But there is surprisingly little addressing this issue in the scientific literature.
Smoking was a risk factor for development of MERS in Saudis during their 2014 epidemic (as was direct exposure to dromedary camels)(1). The receptor for the MERS coronavirus was denser in the lungs of smokers than non-smokers, increasing chances the virus would set up shop there (2). HIV-1 infected smokers have twice the mortality rate as non-smokers, with HIV-1 replication directly promoted by tobacco components (3). Realize HIV is a much different virus than corona. So is herpes simplex. But tobacco seems to inhibit its replication (4).
Big tobacco is in the corona game using the well studied tobacco mosaic virus as a means to grow in tobacco plants large amounts of certain coronavirus proteins that could serve as a vaccine https://www.politico.com/news/2020/02/15/could-tobacco-cure-coronavirus-115329. So maybe tobacco will save us after all. But those cancer sticks aren’t going to do it and now there’s yet another reason to put them away, especially if it’s a Camel. Sorry, Holly.
But to my friends the smokers, I’ll have to admit they’re drinking up some pretty therapeutic stuff at that bus stop https://email@example.com/coronavirus-and-the-sun-a-lesson-from-the-1918-influenza-pandemic-509151dc8065
1. Alraddadi BM, Watson JT, Almarashi A, Abedi GR, Turkistani A, Sadran M, Housa A, Almazroa MA, Alraihan N, Banjar A, Albalawi E, Alhindi H, Choudhry AJ, Meiman JG, Paczkowski M, Curns A, Mounts A, Feikin DR, Marano N, Swerdlow DL, Gerber SI, Hajjeh R, Madani TA. Risk Factors for Primary Middle East Respiratory Syndrome Coronavirus Illness in Humans, Saudi Arabia, 2014. Emerg Infect Dis. 2016 Jan;22(1):49-55. doi: 10.3201/eid2201.151340.
2. Seys LJM, Widagdo W, Verhamme FM, Kleinjan A, Janssens W, Joos GF, Bracke KR, Haagmans BL, Brusselle GG. DPP4, the Middle East Respiratory Syndrome Coronavirus Receptor, is Upregulated in Lungs of Smokers and Chronic Obstructive Pulmonary Disease Patients. Clin Infect Dis. 2018 Jan 6;66(1):45-53. doi: 10.1093/cid/cix741
3. Ande A, McArthur C, Kumar A, Kumar S. Tobacco smoking effect on HIV-1 pathogenesis: role of cytochrome P450 isozymes. Expert Opin Drug Metab Toxicol. 2013 Nov;9(11):1453-64. doi: 10.1517/17425255.2013.816285.
4. Larsson PA1, Hirsch JM, Gronowitz JS, Vahlne A. Inhibition of herpes simplex virus replication and protein synthesis by non-smoked tobacco, tobacco alkaloids and nitrosamines. Arch Oral Biol. 1992 Nov;37(11):969-78.