Last updated by The POOG on October 10, 2021.

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 infections

Bonow 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)

Lei et al (2021)[26] show that COVID-19 is primarily a vascular disease.:

we show that S protein alone can damage vascular endothelial cells (ECs) by downregulating ACE2 and consequently inhibiting mitochondrial function.

Lei et al (2021)[26]


Myocarditis is one of the hihg-profile adverse effecrs of the vaccine. Dr. Paul Cottrell explains the phenomenon:

Gastrointestinal System

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 subjects

Zha 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.

Hepatic System

Liver damage has been noted by Wang et al (2020)[22] but I found no other studies specifically dealing with the liver.

Immune System

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 [1] 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.

[1]] 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.

Neurological System

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 symptoms

Vindegaard and Benros (2020)

Renal System

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 care

Ronco, Reis, and Husain-Syed (2020)

Respiratory System

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-19

Li 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.

Brosnahan et al (2020)[25] approach some of what is known about COVID-19 from the viewpoint of a respiratory disease. Lei et al (2021)[26] go further in showing how the S protein creates the underlying respiratory effects.

Reproductive System

Male Fertility

I’m adding this section a year and a half after that I wrote most of this article which is now out of date. Here’s a detailed explanation by Dr. Paul Cottrell of the male reproductive system and how SARS-CoV-2 damages it.

Cottrell shows how vascular leakage caused by the virus and/or the S protein allows IgG and IgM to attack the production of sperm as well as other effects.

Issues Around Pregnancy

Not a lot of work has been done on this issue but one study by Jering et al (2021)[24] identified issues from COVID-19.

Long-Term Effects

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’.

Huang et al (2021)[23] found after 6-months:

At 6 months after acute infection, COVID-19 survivors were mainly troubled with fatigue or muscle weakness, sleep difficulties, and anxiety or depression. Patients who were more severely ill during their hospital stay had more severe impaired pulmonary diffusion capacities and abnormal chest imaging manifestations, and are the main target population for intervention of long-term recovery.

Huang et al (2021)[23]


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.


  1. CD147, a New Target of SARS-CoV-2 Invasion. CUSABIO.


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