Last updated by The POOG on September 30, 2020.
As more experience with the disease is had and more research is done, the extent of the damage to diverse parts of the body is being documented. In many cases, it is not known to what degree the damage is short-term or long-term. We collect below, damage analyses by major body system.
Although we are aware that the SARS-CoV-2 can attach to at least three different cellular receptors causing infection and damage in most bodily systems, the data in many cases is sparse. As such we will fill in the sections as research becomes available. In the references cited, we may add emphasis in quoted material to highlight key points.
Cardiovascular (CV) System
A literature review found that reporting is sparse but noted that:
Acute cardiac injury, defined as significant elevation of cardiac troponins, is the most commonly reported cardiac abnormality in COVID-19. It occurs in approximately 8–12% of all patients. Direct myocardial injury due to viral involvement of cardiomyocytes and the effect of systemic inflammation appear to be the most common mechanisms responsible for cardiac injury.Bansal (2020)
Another study found a considerably higher level of impact:
In this global survey, cardiac abnormalities were observed in half of all COVID-19 patients undergoing echocardiography. Abnormalities were often unheralded or severe, and imaging changed management in one-third of patients.Dweck et al. (2020)
This is more consistent with a study by Puntmann and Carerj (2020) that found post recovery damage at higher levels:
100 patients recently recovered from COVID-19 identified from a COVID-19 test center, cardiac magnetic resonance imaging revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), which was independent of preexisting conditions, severity and overall course of the acute illness, and the time from the original diagnosis.Puntmann and Carerj (2020)
It is widely known that patients with underlying cardiac comorbidity stand the risk of heightened CV damage and death:
Patients with long-term coronary artery disease and those with risk factors for atherosclerotic cardiovascular disease have a heightened risk of developing an acute coronary syndrome during acute infectionsBonow et al. (2020)
Further, Bonow et al. (2020) report elevated levels of mortality among patients in critical care with CV comorbidity in the 50-60% range against comparable patients without the comorbidity, in the 5-10% range.
Finally, unusually high levels of thrombosis (clotting) are found throughout the major organs and particularly the lungs. Many studies have reported thrombosis. In this article, quoting a US doctor,
I have witnessed many thrombotic events in these patients, and their rates are above and beyond anything that I, for one, have ever seen before … “For sure, there is something going on there …McKeown (2020)
This system of the body has received more minor attention by researchers and the data is sparse. Ng and Tilg (2020) reviewed papers that dealt specifically with gastrointestinal (GI) symptoms such as diarrhea. Presence of the virus is determined from feces analysis.
One study of 74 patients found that:
Up to 28% of those with GI symptoms did not have respiratory symptoms. Here, they showed that this patient group compared with patients without GI symptoms (n=577) had overall more severe/critical disease …Zha and Tilg (2020)
From an examination of two studies these authors found:
in biopsies taken during endoscopy. In two severely diseased patients, the virus could be detected in oesophagus, stomach, duodenum and rectum proving that this virus is present throughout the GI tract … evidence is accumulating that GI symptoms are common and SARS-CoV-2 can be detected in faeces in about 50% of infected subjectsZha and Tilg (2020)
Ng and Tilg (2020) came to similar conclusions. They also noted that the ACE2 receptor on cells seems to be the entry point of the virus in all systems.
Liver damage has been noted by Wang et al (2020) but I found no other studies specifically dealing with the liver.
Emerging research is discovering how the SARS-CoV-2 virus attacks the immune system. While attacks on the other body systems are performed through the ACE2 receptor on organ surfaces, another receptor called CD147 is now know to be an entry point into cells. As Ganier et al. (2020) note:
CD147 (BSG) but not ACE2 is detectable in vascular endothelial cells … from multiple tissues in healthy individuals. This implies that either ACE2 is not expressed in healthy tissue but is instead induced in response to SARS-Cov2 or that SARS-Cov2 enters endothelial cells via an alternative receptor such as CD147.Ganier et al. (2020)
Reference  gives an overview of the function of the CD147 receptor. Reviewing research the article notes:
This study demonstrated that SARS-CoV-2 can infect T cells via its spike protein-mediated membrane fusion, resulting in lymphocytopenia.] CD147, a New Target of SARS-CoV-2 Invasion.
Next we cite three papers, Pushkarsky et al. (2007), Pushkarsky et al. (2001) and Hu et al. (2010), that demonstrate the role of CD147 in the HIV1 infection process. This is the process that down-regulates or destroys immune system T cells.
An early paper by Indian scientists that identified genetic insertions in the SARS-CoV-2 genome as homologous to HIV sequences was retracted. The CD147 entry mechanism, whatever the source may induce an AIDS-like pathology in the way the immune system is affected.
Research into neurological impacts is scarce but is emerging. As with other systems, impairment and damage to the neurological system is high – 45% in one study – with severe COVID-19 infections and with patients with significant comorbidity.
In a case series of 214 patients with coronavirus disease 2019, neurologic symptoms were seen in 36.4% of patients and were more common in patients with severe infection (45.5%) according to their respiratory status, which included acute cerebrovascular events, impaired consciousness, and muscle injury.Mao et al. (2020)
Apart from physiological implication and damage, psychological and psychiatric symptoms are emerging. A review study that only found two papers dealing with COVID-19 infection directly, noted:
investigating COVID-19 patients found a high level of post-traumatic stress symptoms (PTSS) (96.2%) and significantly higher level of depressive symptomsVindegaard and Benros (2020)
Kidney damage is also being observed. In some cases kidney failure requiring replacement therapy has occurred.
Kidney involvement is frequent in COVID-19; >40% of cases have abnormal proteinuria at hospital admission. Acute kidney injury (AKI) is common among critically ill patients with COVID-19, affecting approximately 20–40% of patients admitted to intensive careRonco, Reis, and Husain-Syed (2020)
The high homology or similarity between the original SARS-CoV virus and the current SARS-CoV-2 virus (79%) with similar ARDS pathology suggests results from earlier studies of the SARS epidemic will apply to the current disease.
To this end, a study done on 24 patients in 2003, 36 days after hospital admission, found:
Parenchymal abnormality was found in 96% (23 of 24) of patients and ranged from residual ground-glass opacification and interstitial thickening in group 2 (nine of 24, 38%) to fibrosis in group 1 (15 of 24, 62%).Antonio et al. (2003)
That is, all but one of the patients recorded damage that lasted after release.
Li and Zia (2020) made similar observations:
Ground-glass opacities (GGOs) and consolidation with or without vascular enlargement, interlobular septal thickening, and air bronchogram sign are common CT features of COVID-19Li and Zia (2020)
Reviews of several papers by McGonagle et al. (2020) and LevI et al. (2020) found that the common respiratory infection caused in COVID-19 is a pulmonary thrombosis caused by the unusual immune response induced by the virus. This leads to extensive inflammation and thrombosis or blood clotting in lung tissue.
The authors have described the COVID-19 pneumonia and its pathology, linked to death when associated with underlying comorbidity, and to long lasting lung damage in other cohorts.
A major problem with assessing long-term effects is that the disease is too recent to allow good studies to be done. Zhaet al. (2020), followed two patients one month after discharge from critical care. One showed no effects while the other showed fibrosis, a common effect of the disease. All one may conclude from this is that longer-term effects will exist but severity, duration and prevalence cannot at this time be assessed.
Although it is early to assess long-term effects, some indications are emerging. A survey by Lambert (2020) from the Indiana University School of Medicine lists 98 effects associate with COVID-19 infection experienced months after ‘recovery’.
The evidence is that SARS-CoV-2 can infect all major bodily systems but may not necessarily do so. For example in one study28% of candidates exhibited signs of GI infection but not respiratory infection.
One general observation is that patients with acute infection and underlying comorbidity experience heightened damage in any system and a notably higher incidence of mortality. One study found a 50-60% mortality among acute care patients with comorbidity versus 5-10% without.
High levels of detectable damage or impairment was observed in 96% of all patients in neurological and respiratory studies.
In one study ~10% of all patients exhibited cardiac abnormalities. In a global survey half of those tested were found to have cardiac abnormalities.
Returning to acute care patients, a study found that 20-40% of patients experienced renal problems and kidney failure
While the studies found significant short-term damage, medium-term damage of up to 3 months has been observed. Long-term damage cannot be assessed at this point although studies of the effect of the related ARDS-causing corona viruses SARS-CoV and MERS-CoV suggest that we will see long-term lung damage due to fibrotic scarring.
The ability of the virus to attack multiple organs and systems appears to be unique and is worrisome, particularly if the virus experiences a gain-of-function mutation. The D614G mutation observed in the southern US is such an example, Zha et al (2020).
The question as to whether asymptomatic persons experience damage is an open one. This is not a virus that you really want to catch, especially in the form of an acute infection.
- Antonio, G.E., Wong, K.T., Hui, D.S.C., et al. Thin-Section CT in Patients with Severe Acute Respiratory Syndrome Following Hospital Discharge: Preliminary Experience. Radiology Vol. 228, No. 3, Sep 1, 2003; doi.org/10.1148/radiol.2283030726.
- Bansal, M. Cardiovascular disease and COVID-19. 2020 Diabetes India, May–June 2020; doi: https://doi.org/10.1016/j.dsx.2020.03.013.
- Bonow, R.O., Fonarow, G.C., O’Gara, P.T., et al. Association of Coronavirus Disease 2019 (COVID-19) With Myocardial Injury and Mortality. JAMA Cardiol. 2020;5(7):751-753. doi:10.1001/jamacardio.2020.1105.
- Dweck, M.R., Bularga, A., Hahn, R.T., et al., Global evaluation of echocardiography in patients with COVID-19, European Heart Journal – Cardiovascular Imaging, 2020, jeaa178, https://doi.org/10.1093/ehjci/jeaa178.
- Ganier, C., Du-Harpur, X., Harun, N., et al. CD147 (BSG) but not ACE2 expression is detectable in vascular endothelial cells within single cell RNA sequencing datasets derived from multiple tissues in healthy individuals. bioRXiv, July, 2020; doi: https://doi.org/10.1101/2020.05.29.123513. Involvement of HAb18G/CD147 in T cell activation and immunological synapse formation.
- Hu, J., Dang, N., Yao, H., et al. (2010). Involvement of HAb18G/CD147 in T cell activation and immunological synapse formation. J Cell Mol Med. 2010 Aug; 14(8): 2132–2143. Published online 2010 Jan 15. doi: 10.1111/j.1582-4934.2010.01012.x.
- Lambert, N. J. & Survivor Corps. COVID-19 “Long Hauler” Symptoms Survey Report. Indiana University School of Medicine; 2020; https://dig.abclocal.go.com/wls/documents/2020/072720-wls-covid-symptom-study-doc.pdf.
- Levi, M., Thachil, J., Iba, T., et al. Coagulation abnormalities and thrombosis in patients with COVID-19. Lancet Haem. May 11, 2020DOI:https://doi.org/10.1016/S2352-3026(20)30145-9
- Li, Y. and Xia, L. Coronavirus Disease 2019 (COVID-19): Role of Chest CT in Diagnosis and Management. American Journal of Roentgenology. June, 2020; 214: 1280-1286.
- Mao, L., Jin, H., Wang, M., et al. Neurologic Manifestations of Hospitalized Patients With Coronavirus Disease 2019 in Wuhan, China. JAMA Neurol. 2020;77(6):683-690. April 10, 2020. doi:10.1001/jamaneurol.2020.1127.
- McGonagle, D., O’Donnell, J.S., Sharif, K.,et al. Immune mechanisms of pulmonary intravascular coagulopathy in COVID-19 pneumonia. Lancet Rheu. May 07, 2020; DOI:https://doi.org/10.1016/S2665-9913(20)30121-1.
- McKeown, L.A. German COVID-19 Autopsy Data Show Thromboembolism, ‘Heavy’ Lungs. tctMD, May 11, 2020. https://www.tctmd.com/news/german-covid-19-autopsy-data-show-thromboembolism-heavy-lungs.
- Ng,S.C., and Tilg, H. COVID-19 and the gastrointestinal tract: more than meets the eye. BMJ Gut. 2020; http://dx.doi.org/10.1136/gutjnl-2020-321195.
- Puntmann, V.O. and Carerj, M.L. Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19). JAMA Cardiol. Published online July 27, 2020. doi:10.1001/jamacardio.2020.3557.
- Pushkarsky, T., Yurchenko, V., Laborico, A., and Bukrinsky, M. (2007) CD147 stimulates HIV-1 infection in a signal-independent fashion. BBRC. Volume 363, Issue 3, 23 November 2007, Pages 495-499; https://doi.org/10.1016/j.bbrc.2007.08.192.
- Pushkarsky, T., Zybarth, G., Dubrovsky, L., et al. (2001). CD147 facilitates HIV-1 infection by interacting with virus-associated cyclophilin A. PNAS. May 22, 2001 98 (11) 6360-6365; https://doi.org/10.1073/pnas.111583198
- Ronco, C., Reis, T., and Husain-Syed, F.Management of acute kidney injury in patients with COVID-19. Lancet. Volume 8, ISSUE 7, P738-742, July 01, 2020; DOI:https://doi.org/10.1016/S2213-2600(20)30229-0
- Vindegaard, N. and Benros, M.E. COVID-19 pandemic and mental health consequences: Systematic review of the current evidence. Brain Behav Immun. 2020 May 30 doi: 10.1016/j.bbi.2020.05.048.
- Wang, K. et al. SARS-CoV-2 invades host cells via a novel route: CD147-spike protein. : bioRxiv. (2020); doi: ttps://doi.org/10.1101/2020.03.14.988345.
- Zha, L., Shen, Y., Pan, L., et al. (2020). Follow-up study on pulmonary function and radiological changes in critically ill patients with COVID-19. J Infect. 2020 May 27 doi: 10.1016/j.jinf.2020.05.040.
- Zhang, L., JacksonC.B., Mou, H., et al. The D614G mutation in the SARS-CoV-2 spike protein reduces S1 shedding and increases infectivity. bioRxiv. June 12, 2020; doi: https://doi.org/10.1101/2020.06.12.148726.
- Yijin Wang, Shuhong Liu, Hongyang Liu, et al. SARS-CoV-2 infection of the liver directly contributes to hepatic impairment in patients with COVID-19. Journal of Hepatology, Volume 73, Issue 4, October 2020, Pages 807-816; https://doi.org/10.1016/j.jhep.2020.05.002.