YES, SARS-CoV-2 persistence is real and is implicated in Long Covid

I’ve already written about SARS-CoV-2 persistence, how this might be documented by biomarkers, and how this should not surprise, as may happen also with other viruses.

Now, I think these observations are becoming stronger and stronger, and one clinical study can have practical implications and easy translation in daily practice.

From a biological perspective, a new study further demonstrated that SARS-CoV-2 can spread everywhere in the body. The presence and variability of SARS-CoV-2 were assessed among 71 tissue samples obtained from multiple organs including lung, intestine, heart, kidney, and liver from 15 autopsies with positive swabs and no records of immunocompromise. The virus was detected in most organs in the majority of autopsies. All organs presented intra-host single nucleotide variants (iSNVs) with low, moderate, and high abundances. The iSNV abundances observed within different organs indicate that the virus can mutate at one host site and subsequently spread to other parts of the body. These results indicate that SARS-CoV-2 can replicate, and evolve in a compartmentalized manner, in different body sites, which agrees with the “viral reservoir” theory.

From a clinical perspective, this other study tells us something similar and may help stratify an early risk factor for developing long covid. 4054 people in Hong Kong tested positive for COVID-19 and were admitted to a public health care facility, of whom 167 (4.1%) were admitted to ICU. During a median follow-up time of 251 (interquartile range 240–279) days, 408 (11.9%) were hospitalized for any reason and 16 (0.5%) patients died. After discharge, patients were most often readmitted for respiratory reasons, followed by gastro-intestinal reasons. A higher viral load (lower RT-PCR Ct values) was associated with a higher likelihood of death (Hazard ratio [HR] 5.86, 95% Confidence interval [CI] 2.57–13.33), hospitalization (HR 1.22, 95%CI 1.08–1.39) or hospitalization for cardiovascular disease (HR 12.78, 95%CI 3.67–44.48). Patients with higher viral loads more likely started ACE-inhibitors (HR 1.37, 95%CI 1.12–1.68) and non-opioid analgesics (HR 1.01, 95%CI 1.01–1.23). In a relatively mild COVID-19 population from Hong Kong, the post-acute risk of complications was substantial. These results highlight that higher viral load predict post-acute complications in patients with relatively mild disease.

So, yes, SARS-CoV-2 can spread everywhere in the body, can persist, and the more you have at the beginning of the infection, the higher can be the risk of long term sequelae. This means that, in my opinion, I was right when I speculated that the historical approach of non treating viral infections because they self heal can be on the biggest mistake of historical medicine and this may need to be completely reconsidered!