A couple of days ago I read an article in the New York times by noted journalist Gina Kolata. Ms. Kolata is well known as a science writer, first at Science Magazine, then for the last 30 years at the New York Times. She is also an accomplished author, and I have enjoyed several of her books. While she tends to argue for a single point of view in most of her writing, she is usually very effective in communicating complex scientific concepts to non-scientific readers.
This article was quite disturbing because it began by suggesting that new research had identified COVID-19 as causing a syndrome in many severely ill patients that led to immune dysfunction. The exact statement that opened the article reads as follows;
“Now researchers have discovered yet another unpleasant surprise. In many patients hospitalized with the coronavirus, the immune system is threatened by a depletion of certain essential cells, suggesting eerie parallels with H.I.V.”
HIV directly infects the key, controller protein of the immune system, the CD4 T cell, and kills them. It depletes the entire immune system if not treated, and leaves sufferers without any defense to infection. Having taken care of patients with untreated HIV during the early days of that pandemic, I know the devastating effects of that infection. Having a respiratory infection that causes AIDS is an overwhelming concept!
Several things, however, disturbed me about the article.
First, COVID-19 has not been specifically associated with infection of the immune system, and the ACE2 protein the virus targets is not expressed on immune cells. Also, no AIDS-like syndrome has been associated with SARS-CoV-2 infection.
Finally, a major concern with this article was that the cited manuscript was not peer reviewed or published other than being placed on the BioRxiv.org website. Because several manuscripts that had previously received attention on this website proved to be unreliable, I took a more detailed look at the original manuscript.
Remarkable, the manuscript, from researchers at the University of Pennsylvania, presents very interesting data and was much more circumspect with its implications than what was suggested in Ms. Kolata’s article. The authors had extensively evaluated immune function in patients with severe COVID-19. They found a varied number of immune alterations suggesting no single defect or abnormality in these critically infected patients. Interestingly, many of the findings were similar to those seen with overwhelming sepsis or viral infections including Dengue or Ebola virus infections.
There were also several limitations to the studies including small numbers of patients and attempts to correlate extensive immune data with inadequately defined clinical infection subtypes. The researchers also had a common problem in human studies in that due to sampling limitations they could only examine the immune components in blood, which may not represent the infection in the lung or respiratory tract. To their credit, the investigators identified most of these issues.
This suggested the immune changes that are seen during severe coronavirus illness are due to the critical, overwhelming illness of these patients and the flailing attempts of these patients’ immune systems to attempt to control the infection. While some abnormalities may be associated with pre-existing immune problems in these patients (organ transplant patients on immune suppression seem to be uniquely susceptible to COVID-19), the infection itself does not induce immune problems in the way HIV does. This conclusion is supported by almost every piece of information available on SARS-CoV-2 infection.
So in this case, Ms. Kolata overstated the result of an unpublished manuscript and gave conclusions that were not justified by the data. It really just appears to be sensationalized reporting.