Why “Reinfection” Happens with SARS-CoV-2, or Does It? Answer: Yes (in certain cases)

I discussed in earlier posts that immunity can be incomplete, even with recovery; inappropriate, leading to severe disease; long lasting with cellular mediated immunity; or side-stepped or even made to make things worse when infected by a different strain of the same virus. Also, viruses and other microbes can hide in sequestered privileged sites in the body to re-emerge to spread to other sites before the immune system kicks in again or be shed and spread to other susceptible hosts. Herpes viruses such as those that cause cold sores, genital lesions and chicken pox, followed years later by shingles, hide in nerve endings, only to re-emerge when adaptive immunity declines. Bacterial diseases like brucellosis recur producing undulant fever over years by hiding in cells where immunity or antibiotics have a hard time getting. Leptospira hide in the kidneys and shed in the urine to infect humans and other animals, giving them active leptospirosis, after the shedding host has recovered from acute disease and is generally immune but not in the kidneys. Syphilis moves through 4 phases as immunity to this microbe develops: acute genital form; secondary systemic rash form (skin rashes and/or mucous membrane lesions: sores in the mouth, vagina, or anus; symptoms of secondary syphilis may include fever, swollen lymph glands, sore throat, patchy hair loss, headaches, weight loss, muscle aches, and fatigue); latent (hidden) stage of syphilis, a period of time when there are no visible signs or symptoms of syphilis; and the tertiary fatal central nervous system form (can appear 10–30 years after infection was first acquired; affects multiple organ systems, including the brain, nerves, eyes, heart, blood vessels, liver, bones, and joints). Each step it becomes more and more hidden from the immune system or exhausts the immune responses in the final stage. Perhaps, albeit to a much lesser extent, CoV uses some of these strategies to maintain infections in or among individuals. The change in strain internally could also occur if there is sufficient immune selection pressure to accelerate mutation of the virus (see earlier post on monoclonal antibody treatments). No matter which above mechanism has come to play, re-infection with or re-activation of SARS-CoV-2 has occurred https://www.medrxiv.org/content/10.1101/2020.09.22.20192443v1.full.pdf. In Brazil, two cases of “re-infection” has occurred with two different variants, with increased severity, in one case, associated with increased viral load https://www.preprints.org/manuscript/202101.0132/v2. One additional note, as public health fails and more and more virus is present and carelessness allows larger viral doses to be transmitted, these mechanisms, no matter how rare, become more likely to occur and are amplified.