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Post-COVID-19 immune dysfunction is supported by epidemiological, clinical, and laboratory evidence. Attributing, with little to no evidence, that masking and lack of exposure is the primary driver of increases in bacterial and viral infections discourages critical interventions needed to stop the spread of disease.
The United States and much of the world were caught off guard by the rapid rise in RSV infections. In an almost knee-jerk explanation, many attributed this to the lack of respiratory syncytial virus (RSV) cases and immunological exposure during the preceding year. In a news release, the United States CDC even stated: “… we’re seeing more RSV because, in the past two years, we’ve not seen infections in children as we have. And so these children, if you will, need to become infected [with RSV] to move forward because it’s a disease prevalent in children.” In many circles, this was interpreted as masks, and avoiding crowded settings was harmful since it hurt natural immunity. The concept of “immune debt” entered mainstream medicine.
However, when this statement was made in early November 2022, the total number of RSV cases in the preceding year approximated those in the United States (See Figure IA), even though pediatric hospitals were at critical levels with RSV patients. In addition, according to the National Center for Educational Statistics (NCES), there were few school closures in the United States during the 2021 to 2022 school year, with over 98% of school districts reporting in-person learning, with the remainder reporting hybrid or remote.
Another plausible explanation was the “immune theft,” or immunodeficiency, caused by previous SARS-CoV-2 infection. As of February 2022, the United States CDC estimated that over 75% of children aged 0 to 11 years in the United States had been infected with SARS-CoV-2. Immunocompromise has been found with other viral infections such as measles which can cause decreased antibody function, and seasonal flu, which can cause lymphopenia.
Other countries have also had similar epidemiological experiences with RSV. In Denmark, a prominent peak in RSV cases can be seen in the Fall of 2021 and Fall of 2022. If lack of exposure to RSV were a cause, one would not expect an even more significant number of cases in the 2022-23 RSV season (see Figure IB).
This RSV case pattern was also seen in Sweden. As discussed in Bergmann S. and Lindström M.’s 2022 book Sweden’s Pandemic Experiment, there was almost a total lack of public masking in Sweden, and nationwide closure of kindergartens and primary schools never occurred. Thus, there was little opportunity for “immune debt” to occur, yet RSV cases surged during the ensuing year of the pandemic (see Figure IC).
Finally, in China, where there is very little available data, a huge RSV surge in hospital admissions was not seen at a pediatric hospital in Shanghai, China, when communities reopened in August 2020. China had one of the most stringent lockdowns, and the 2020 to 2021 RSV season and exposure to COVID-19 were limited, with relatively few cases. Despite the lack of exposure to RSV, a large was of RSV hospitalizations did not occur (Figure ID).
In a non-peer-reviewed preprint by Wang L et al children were reported to be almost twice as likely to develop an RSV infection if they had a prior documented COVID-19 infection. Other diseases, such as streptococcal tonsillitis, may also be impacted, which has been observed to have a 34% increase in post-COVID-19 patients. Thus, a post-COVID-19 immune deficiency might also explain the surge of scarlet fever observed in the United Kingdom.
Anthony Leonardi and Rui Proenca first described immunodysfunction and lymphopenia in an article published in Frontiers of Immunology. Phetsouphanh C et al later verified the finding and found that dysfunction may persist for 8 months (the longest time studied) in long COVID patients. This dysfunction was characterized as having “highly activated innate immune cells and a lack of naive T and B cells.” A recent report by Shen XR et al of utmost concern identified SARS-CoV-2 RNA or antigen in T-Cells. They postulated a direct infection through an independent, non-ACE-2 receptor, which caused pronounced cellular apoptosis.
No one knows how severe or long-lasting post-COVID-19 immunodeficiency will be. Of concern is that reinfections can commonly occur in adults and maybe even more frequently in children. Laboratory evidence indicates that, unlike adults, immunologically SARS-CoV-2 naive young children do not develop “robust memory B cell responses.” Thus, reinfections can be expected to occur in children, possibly at a greater frequency than in adults, and carry a significant and additive risk of long COVID, multisystem inflammatory syndrome, and immunosuppression.
These findings also support the contention that infections can cause stealth hospitalizations and deaths from COVID-19; and underscores the inappropriateness of protocols, such as those used by the State of Massachusetts, of only counting hospitalizations caused by COVID-19 in patients who have a positive test and receive corticosteroids. These protocols can underestimate COVID-19 hospitalizations by a factor of 3 and ignore the plethora of long COVID complications affecting many organ systems. After the acute phase of the infection, long COVID can almost double the total number of COVID-19 deaths.
Most importantly, with little to no evidence, the attribution that masking and lack of exposure is the primary driver of the surge in bacterial and viral infections feeds into the narrative of anti-public health conspiracy theorists and discourages critical interventions from mitigating these infections.