A paper set to appear in the journal, Clinical Infectious Diseases will be the first to explore mortality associated with COVID-19 reinfection.
The research is predicated by the death of an 89-year old Dutch woman previously diagnosed with a rare form of bone marrow cancer.
The authors have theorized that the cell-depleting treatment the patient received prior to testing positively for COVID-19 contributed to severe manifestations of the illness.
“Two days after a new chemotherapy treatment, 59 days after the start of the first COVID-19 episode, the patient developed fever, cough, and dyspnea. At admission, her oxygen saturation was 90% with a respiratory rate of 40/minute,” the authors wrote in the report.
Though rare, academicians have known that COVID-19 reinfection is possible since August.
Researchers from the University of Hong Kong produced preliminary data on a 33-year old resident who contracted the novel coronavirus, completed viral clearance, and then tested positive again 142 days later.
In this instance, the patient did not exhibit instructive symptoms of COVID-19 upon reinfection.
Whatever mechanisms prevented the patient from experiencing another symptomatic case did not appear to prevent SARS-CoV-2 from penetrating host cells. The patient did make a full recovery, however.
“The patient got re-infected 4.5 months after the first infection. Therefore, it shows that for this patient, the immunity induced by the first infection is short-lasting,” the researchers said of their findings. “This case illustrates that re-infection can occur even just after a few months of recovery from the first infection. Our findings suggest that SARS-CoV-2 may persist in humans, as is the case for other common-cold associated human coronaviruses, even if patients have acquired immunity via natural infection.”
Earlier this week, the Lancet reported on the first case of SARS-CoV-2 reinfection in the US after a 25-year-old man tested positive for the virus for a second time at a Nevada health facility.
Following recovery and between April and May, the patient received two negative tests. Not only did COVID-19 inflict him again in June, but it did so more aggressively than it had the first time around. This may be due to the presence of two separate coronavirus strains.
Viral inoculum, which refers to the initial dose one is exposed to and viral load, which independently describes the copies of RNA being replicated in an infected person’s body per mL may additionally play a role. Or perhaps the antibodies prepositioned to fight off SARS-COV-2 facilitated inflammation studied to compound adverse outcomes.
Whatever the reason, the young subject required medical intervention to breathe during the second bout.
Building genome evidence for SARS-CoV-2 reinfection may mean that exposure to it “does not result in a level of immunity that is 100% protective for all individuals,”
This case, as well as the cases indexed above and the two other instances of COVID-19 reinfection recorded globally (Netherlands and Ecuador), introduces a multipronged attack on our projected route to normalcy.
The first regards the herd immunity theory, i.e as the pandemic runs its course the proportion of individuals who develop a natural immunity to COVID-19 will outnumber those who have not. Eventually, these outliers will be protected by a targeted vaccine.
This theory falls apart when we consider COVID-19’s lethality and the yet to be determined number of carriers who remain asymptomatic. More to the point, the immunology is really inconsistent on this front.
It’s fair to characterize reinfection data as thin on the ground because at this point it is. Five global cases in and of themselves are not enough to go back to the drawing board. But no reasoned appreciation can say the same for demographics who continue to defy statistical prognosis. Which brings us to the other concerning element supplied by reinfection cases: COVID-19’s unpredictable pathology.
Young, otherwise healthy COVID-19 patients sometimes develop critical iterations of the respiratory disease. Sometimes symptoms associated with fatal outcomes do not reflect respiratory complications at all. Some recover in 14 days, while others continue to struggle months after being diagnosed.
It may be electorally convenient to chalk these up to aberrations, but it doesn’t reduce COVID-19’s destructive pace.
SARS-CoV-2 is an RNA virus, which means when it replicates it does so uniquely. The more times RNA is copied, the more errors occur.
The more errors that occur the higher the chance that one of those errors will prove to be advantageous to the pathogen’s ultimate survival.
With rising reports of mutated strains, it is not beyond the realm of possibility that SARS-CoV-2 will produce a sequence capable of reinfecting the same host the way coronaviruses responsible for the common cold do.
Thirty-eight million people have been infected with the novel coronavirus as of the time of this writting. Thanks to greed and incompetence the virus has been gifted a wealth of opportunities to perfect its invasion.
“The implications of these data are that SARS-CoV-2 can adapt with enough genetic dexterity to avoid a natural immune response in a manner to re-establish detectable levels of infection in an individual,” the authors concluded in the new Lancet report.