Since the discovery of the new coronavirus that causes COVID-19, scientists have been scrambling to understand the different features of the virus. While a lot more is now known about SARS-CoV-2, several key questions have proved more difficult to answer. For example, it remained unclear where the virus travels to in the body and causes the most harm.

To help answer this question, Deinhardt-Emmer, Wittschieber et al. performed postmortem examinations on 11 patients who had recently died of COVID-19. After sampling 61 different organs and tissues from each patient, several tests were used to detect traces of SARS-CoV-2. The experiments showed that the largest pool of SARS-CoV-2 was present in the lungs, where it had caused severe damage to the alveolae, the delicate air sacs at the end of the lungs’ main air tubes.

Small amounts of the virus were also detected in other organs and tissues, but no severe tissue damage was seen. In addition, Deinhardt-Emmer, Wittschieber et al. found that each patient had increased levels of some of the proteins involved in inflammation and blood clotting circulating their bloodstream. This suggests that the inflammation caused by SARS-CoV-2 leads to an excessive immune reaction throughout the entire body.

This research provides important new insights into which areas of the body are most impacted by SARS-CoV-2. These findings may help to design more effective drug treatments that target the places SARS-CoV-2 is most likely to accumulate and help patients fight off the infection at these regions.

In December 2019, several cases of pneumonia caused by a novel Betacoronavirus called SARS-CoV-2 were first described in the city of Wuhan in China (Zhu et al., 2020); the disease was thereafter named ‘coronavirus disease 2019’ (COVID-19) (Lu et al., 2020). Within a few months, the initially localized outbreak spread to countries all over the globe and was declared a pandemic (El Zowalaty and Järhult, 2020). At present, more than 121 million SARS-CoV-2 infections have been reported (Dong et al., 2020). The number of deaths attributed to COVID-19 has exceeded 2.6 million worldwide (Dong et al., 2020).

COVID-19 occurs with varying degrees of severity. While approximately 81% of COVID-19 patients experience mild symptoms, 14% suffer from respiratory distress, and 5% have to be hospitalized (Wu and McGoogan, 2020; Wiersinga et al., 2020). Of these, 20% enter a critical condition with respiratory failure, endovascular complications, or multiple organ dysfunction. Gastroenterological and neurological symptoms have been reported in 36.4% and 18.6% of COVID-19 patients, respectively, in case studies (Wiersinga et al., 2020; Pan et al., 2020; Mao et al., 2020). The clinical observations suggest that COVID-19 is a systemic disease.

While little information has been available to date about the molecular regulation of SARS-CoV-2 infections, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2), two membrane-bound proteins, have been shown to be crucial for the entry of the virus into cells (Wang et al., 2020; Hoffmann et al., 2020). ACE2 is expressed not only in the epithelia of the lung but also in several other epithelial, endothelial, heart, and renal tissues (Hamming et al., 2004). SARS-CoV-2 viral replication and pathogenesis in organisms are currently not well understood due to the lack of appropriate models (Bar-On et al., 2020). One crucial step to elucidate viral pathogenesis is the investigation of the distribution of the virus within the entire body.

In the present study, we (1) included full autopsies, (2) performed autopsies in the early postmortem interval (1.5–15 hr, mean: 5.6 hr), (3) dissected organs and tissues without prior fixation in formalin, (4) measured SARS-CoV-2 RNA in a high number of samples, (5) correlated the viral load with tissue damage using comprehensive histopathological investigations, (6) visualized virus particles in pulmonal tissue samples by means of transmission electron microscopy (TEM), and (7) determined the postmortem serum levels of inflammatory cytokines and prothrombotic factors. Sampling was performed in the very early postmortem interval to provide reliable viral RNA (vRNA) measurements and enabled us to obtain blood serum and well-preserved tissue samples for ultrastructural analysis.

In clinical practice, many critically ill COVID-19 patients show multiple organ involvement in addition to lung failure, in particular vascular dysfunction, including thrombosis and/or impaired microcirculation (Ji et al., 2020). A dysregulated immune response was observed, starting with a phase of immunosuppression followed by a proinflammatory phase and then a cytokine storm (Li et al., 2020). The cytokine storm may play an important role in COVID-19, which supports the hypothesis that COVID-19 could have a strong immunopathological component.

Some aspects of the viral pathogenesis and the toxicity of the novel virus SARS-CoV-2 are known based on previous studies of SARS-CoV (Qian et al., 2013). The virus can infect nasal mucous cells, pneumocytes and alveolar macrophages. ACE2 is the main receptor for the cellular binding process (Bar-On et al., 2020). Since the ACE2 receptor is expressed in cells in addition to those in the respiratory system (Jia et al., 2005), it is reasonable to assume that other organ systems can also be targeted by SARS-CoV-2.

Quite a few morphological studies have been published so far. Some are single case reports based on necropsies of the lung, liver and heart (Xu et al., 2020), partial autopsies of the thoracic cavity (Karami, 2020) or full autopsies (Aguiar et al., 2020). Some involve small (n = 2–3) case series based on surgical lung resectates (Tian et al., 2020a) or on full autopsies (Ding et al., 2003; Sekulic et al., 2020; Barton et al., 2020; Varga et al., 2020). Larger case studies (n = 4-28) have focused on single organs such as the lungs (Ackermann et al., 2020), spleen (Xu, 2020), or kidney (Puelles et al., 2020) or on the heart and lungs (Buja et al., 2020; Fox et al., 2020) or liver, heart and lungs (Tian et al., 2020b); others have reported comprehensive organ findings obtained by minimally invasive sampling (Duarte-Neto et al., 2020) or full autopsies (Menter et al., 2020; Schaller et al., 2020; Wichmann et al., 2020; Edler et al., 2020; Bösmüller et al., 2020; Bradley et al., 2020; Remmelink et al., 2020; Skok et al., 2020; Hanley et al., 2020). Several of the aforementioned autopsy studies reported viral loads in selected organs and tissues (Sekulic et al., 2020; Puelles et al., 2020; Tian et al., 2020b; Menter et al., 2020; Wichmann et al., 2020; Bösmüller et al., 2020; Bradley et al., 2020; Remmelink et al., 2020; Hanley et al., 2020). The postmortem interval between death and autopsy was either not reported (Tian et al., 2020b; Bradley et al., 2020; Skok et al., 2020) or was > 48 hr (Lax et al., 2020), 11–84.5 hr (Menter et al., 2020), 72–96 hr (Remmelink et al., 2020), 1–5 days (Wichmann et al., 2020), 4 days (on average with a maximum of 12 days) (Edler et al., 2020), or 6 days (Hanley et al., 2020). The small number of patients in these studies is consistent with the sample size of many other studies but is nevertheless a limitation. However, we analyzed a considerably larger number of organs and tissues than the other groups. To our knowledge, the present study is the only one to date that has measured viral loads in a wide variety of organs and tissues by obtaining and processing 61 samples per patient. The present study is the only study so far that has focused on keeping the postmortem interval as short as possible to avoid bias due to the degradation of SARS-CoV-2 virus particles, SARS-CoV-2 RNA and tissue ultrastructure. Regarding vRNA degradation, the values reported by Puelles et al., 2020 show comparatively low viral loads among their cases, even in the lungs, which is the primary target of SARS-CoV-2. Wichmann et al., 2020 reported the highest values in the lungs of 1.2 x 10⁴to 9 x 10⁹ copies/ml, while the highest values in our study were ~10⁷ vRNA copies/ml. From Table 2 it becomes clear that the duration of post-mortem intervals in our study did not substantially influence the vRNA copy numbers. The importance of obtaining multiple samples from within one organ is emphasized by the results of patient 10 (Figure 1—figure supplement 1), in which only two of seven samples from the heart were positive. If only one sample had been obtained, the result of viral detection could have been a false negative. Based on the mapping of SARS-CoV-2 RNA throughout the whole human body, we were able to correlate the viral loads in many organs and tissues with the macro- and micromorphology. TEM investigations of the lung samples revealed the presence of morphologically intact virus particles in the tissue, which was in line with the vRNA mapping, which showed the highest viral loads in the lungs. The morphologically intact virus particles were located in lung fibrocytes. In agreement with data published by Varga et al., 2020, viral inclusion bodies were detectable using TEM. In lung tissues, the morphology of the viral particles was clearly observed (Figure 2), whereas in other tissues such as liver, heart, and intestine, viral inclusions were not visible by TEM. The loss of structural hallmarks could be due to postmortem cell and tissue turnover and the reduced integrity of virus particles during TEM-related preparations. It has to be stressed that the molecular detection of the virus does not depend on the presence of morphologically intact virus particles.

We detected the highest viral loads and the most severe tissue damage in the lungs. The lung samples of all patients showed large cells, sometimes multinucleated giant cells, that were similar to the giant cells described in cases of respiratory syncytial virus (RSV) infection. The preliminary immunostaining pattern of the enlarged cells indicated that they represented affected pneumocytes. Squamous (metaplastic) large cells and clusters of giant cells have been reported by most morphological studies, with one exception (Ackermann et al., 2020). The remaining findings from the lung samples agree very well with the findings of other groups, especially the data of Duarte-Neto et al., 2020. The strict topological correlation of viral loads and histopathological damage is emphasized by the results in patient 2. The samples from the upper lung lobes showed normal, unremarkable tissue (Figure 6a) corresponding to a negative viral test result, while the samples from the lower lung lobes revealed severe tissue damage corresponding to high and moderate viral loads (Figure 6b).

All patients who died due to COVID-19 (patients 1–10) had viral RNA in at least some samples of the lymphatic tissue. Lymphatic tissue with a topological relationship with the respiratory tract (e.g. tonsils, cervical lymph nodes, and hilar lymph nodes) was more likely to be positive overall than lymphatic tissue without such a topological relationship (e.g. mesenteric lymph nodes, spleen, and appendix). One remarkable finding in the lymph node samples of all patients was the loss of the follicular structure (Figure 7a). Atrophy of lymphatic tissue has been described in association with SARS-CoV infection by Gu et al., 2005 and discussed as a crucial determinant of disease outcome by Perlman and Dandekar, 2005. Lymphocyte depletion has also been reported by Hanley et al., 2020. The spleen was positive in patients 1, 3, 4, 5, and 9, who presented with the micromorphology of early lung damage, and negative in patients 6, 7, 8, and 10, who presented with the micromorphology of later lung damage or who did not die of COVID-19 pneumonia (patient 2). Further interpretation of the viral loads in the appendix is futile since the appendix showed age-related and chronic pathologic changes accompanied by the loss of lymphatic tissue.

Viral loads in the cardiac tissue were moderate to very low and systematically (in all samples) detected in the patients with early lung damage, while patients with later lung damage displayed high viral loads only sporadically or not at all. The cardiac histology of the left ventricle, anterior wall, and basal portion in patient one with a moderate viral load is presented in Figure 7c,d. Except for the activation of mesenchymal cells, which requires further investigation, the histology was unremarkable. In accordance with Buja et al., 2020, in patient 1, we also observed pericarditis and multifocal acute injury of cardiomyocytes, for example, myocardial contraction band necrosis, which is frequently observed in critically ill patients under catecholamine therapy.

The viral loads in the samples from the vascular tissue (aorta and pulmonary artery) followed a similar distribution pattern depending on the stage of lung damage but were higher compared to those in the cardiac tissue. The unremarkable histology of the thoracic aorta of patient 5 with a high viral load is presented in Figure 7e,f. The conclusion by Varga et al., 2020 that SARS-CoV-2 induces endothelitis cannot be comprehended.

Interestingly, the presence of detectable vRNA in the gastrointestinal tract was variable. The very high viral loads in patient nine throughout the upper gastrointestinal tract as well as in the small and large bowels were noticeable. The histology of the corresponding tissue samples was unremarkable. According to the clinical documentation, patient 9 did not exhibit any gastrointestinal symptoms.

Viral RNA could also be detected in low to very high amounts in the samples from the endocrine organs, urinary tract, nervous system, and reproductive system. Interestingly, the samples of patients 1, 2, 6, and 7, who were treated with lopinavir/ritonavir, tested negative. Our results support the findings of Remmelink et al., 2020. of nonspecific postmortem organ findings despite multiorgan viral spread.

The same distribution pattern among the patients was observed regarding viral RNA in blood. Apart from patients 8–11, who were not subjected to intensive care (patients 8–10) or did not die of COVID-19 (patient 11), it is noticeable that among the patients who received intensive care prior to death (patients 1–7), only patients 3, 4, and 5 tested positive for vRNA in blood, while patients 1, 2, 6, and 7 tested negative. The latter patients were treated with lopinavir/ritonavir, so the effect of antiviral medication on preventing viremia may be indicated. In our study, 4 of 11 patients were treated with an antiviral medication. None of these four patients showed the presence of vRNA in the blood, but one patient showed the presence of vRNA in the bone marrow (patient 1). The application of antiviral drugs is currently being investigated in many studies. However, it has not yet been shown that a significant effect can be achieved by their application (Cao et al., 2020). However, drugs are often used in severe cases in the ICU based on controversial recommendations (Meini et al., 2020). Our data could indicate that lopinavir/ritonavir leads to a reduction in viremia. However, our group size is too small for such a statement, as we could not detect vRNA in the blood, not even in untreated patients in some cases.

The patients with vRNA in the blood also showed vRNA in the bone marrow. Patients 1, 8, and 9 were negative for vRNA in the blood but positive in the bone marrow. Patient 9 showed the highest viral loads by far in the bone marrow. The histology of the bone marrow, apart from hypercellularity, a left shift and an increased number of megakaryocytes, showed a significant amount of hemophagocytosis (Figure 6b). Hemophagocytosis was also reported by Hanley et al., 2020 and is a morphological feature of macrophage activation syndrome (MAS) or hemophagocytic lymphohistiocytosis (HLH) (Crayne et al., 2019; Al-Samkari and Berliner, 2018). The clinical characteristics of COVID-19, including very high ferritin levels and very high levels of proinflammatory interleukins, resemble those of MAS and HLH (Colafrancesco et al., 2020) and have already led to several therapeutic attempts (Dimopoulos et al., 2020). Further studies are needed to clarify this aspect.

A positive test result based on qRT-PCR can be determined with the Ct-value. Due to the further spread of the pandemic, clinicians have discussed the release of this value as part of the test result, as the viral load has been identified as an important prognostic indicator (Magleby et al., 2020). The authors suggest using the Ct-value to identify patients with a high risk for severe clinical courses. Further studies also indicate that the viral load may serve as a surrogate marker of infectivity associated with mortality rates (Faico-Filho et al., 2020).

However, the College of American Pathologists reminds us to be cautious in interpreting the results (Rhoads et al., 2020; Jaafar et al., 2020). As a multitude of intra- and interlaboratory factors influence detection, the Ct-value has to be critically evaluated. Due to the relatives' necessary consent before the autopsy, the specimen collection is only possible with a time delay in clinical routine. Our study did this particularly urgently, but there are still differences in the time of sample collection. This is an important limitation of our study and must be noted when considering the results. However, the subsequent processing of the samples was performed identically. We use the same methods for the RNA-extraction as well as the same qRT-PCR method.

Another important reason for the detection of Ct-values is the statement about infectiousness. Jaafar et al. showed that the culture of the virus is successful up to a Ct-value of 25 (70%). At a Ct-value of 30, this value drops to 20%, and values above 35 as associated with only a low likelihood (3%) of the possibility of culture (Jaafar et al., 2020). These values show a correlation to a certain extent, although it should be noted that the culture of viruses from patient material is generally challenging and that no absolute indication can be made based on a Ct-value for this purpose exclusively.

To further elucidate the immunological host response, we measured IL-6 and IL-8 in postmortem serum samples. The serum levels of interleukin six were significantly elevated in all patients, including patient 11, who died of multiple organ failure following ileus. The serum levels of IL-8 were also significantly elevated. In accordance with other autopsy studies (Wichmann et al., 2020; Lax et al., 2020), we observed thromboembolic events in 4 of the 11 patients. Patient 2 died of pulmonary embolism, and patient 4 suffered multiple lung and spleen infarctions due to venous thromboses. Patients 5 and 10 presented with sporadic emboli in the lung histology. In conjunction with the general impairment of the microcirculation, which was histologically visible as homogenous eosinophilic sludge in the small arterioles, capillaries and venules in multiple organ samples from patients 1, 8 and 9, 7 (of 11), several patients suffered hypercoagulation. Some studies hypothesize that SARS-CoV-2 can induce noncoordinated reactions between the coagulation and fibrinolysis systems that result in hypercoagulation and hemorrhage (Ji et al., 2020). The levels of the measured pro-thrombotic factors were almost all significantly elevated in all patients.

In summary, we presented an autopsy series of 11 patients with COVID-19. The autopsies were performed in the early postmortem interval to avoid bias due to the degradation of vRNA, virus particles, and tissue structures. SARS-CoV-2 RNA could be detected in very high to high amounts in the lungs and in very high to very low amounts in the lymphatic tissue. TEM visualized SARS-CoV-2 particles in the lung tissue. Viral loads and histological tissue damage were strongly correlated in the lungs even at the organ level (patient 2). Histological structure changes were also present in the lymph nodes (atrophy and loss of follicles). High viral loads were detected in many other tissue samples from different extrapulmonary organs and tissues without evident tissue damage based on light microscopy.

RNA data generated or analysed during this study are included in the supporting files.

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Author details

1. Stefanie Deinhardt-Emmer

   Institute of Medical Microbiology, Jena University Hospital, Jena, Germany

   Contribution

   Conceptualization, Data curation, Software, Formal analysis, Supervision, Funding acquisition, Validation, Investigation, Visualization, Methodology, Writing - original draft, Project administration, Writing - review and editing

   Contributed equally with

   Daniel Wittschieber

   For correspondence

   stefanie.deinhardt-emmer@med.uni-jena.de

   Competing interests

   No competing interests declared

   "This ORCID iD identifies the author of this article:" 0000-0003-4495-4052

2. Daniel Wittschieber

   Institute of Forensic Medicine, Jena University Hospital, Jena, Germany

   Contribution

   Conceptualization, Data curation, Software, Formal analysis, Supervision, Validation, Investigation, Visualization, Methodology, Writing - original draft, Project administration, Writing - review and editing

   Contributed equally with

   Stefanie Deinhardt-Emmer

   Competing interests

   No competing interests declared

3. Juliane Sanft

   Institute of Forensic Medicine, Jena University Hospital, Jena, Germany

   Contribution

   Data curation, Formal analysis, Investigation, Methodology

   Competing interests

   No competing interests declared

4. Sandra Kleemann

   Institute of Forensic Medicine, Jena University Hospital, Jena, Germany

   Contribution

   Investigation, Methodology

   Competing interests

   No competing interests declared

5. Stefan Elschner

   Institute of Forensic Medicine, Jena University Hospital, Jena, Germany

   Contribution

   Investigation, Methodology

   Competing interests

   No competing interests declared

6. Karoline Frieda Haupt

   Institute of Medical Microbiology, Jena University Hospital, Jena, Germany

   Contribution

   Data curation, Formal analysis, Investigation, Methodology

   Competing interests

   No competing interests declared

7. Vanessa Vau

   Institute of Medical Microbiology, Jena University Hospital, Jena, Germany

   Contribution

   Data curation, Formal analysis, Investigation, Methodology

   Competing interests

   No competing interests declared

8. Clio Häring

   Section of Experimental Virology, Institute of Medical Microbiology, Jena University Hospital, Jena, Germany

   Contribution

   Data curation, Formal analysis, Investigation, Methodology

   Competing interests

   No competing interests declared

9. Jürgen Rödel

   Institute of Medical Microbiology, Jena University Hospital, Jena, Germany

   Contribution

   Resources, Writing - review and editing

   Competing interests

   No competing interests declared

10. Andreas Henke

    Section of Experimental Virology, Institute of Medical Microbiology, Jena University Hospital, Jena, Germany

    Contribution

    Investigation, Methodology

    Competing interests

    No competing interests declared

11. Christina Ehrhardt

    Section of Experimental Virology, Institute of Medical Microbiology, Jena University Hospital, Jena, Germany

    Contribution

    Funding acquisition, Writing - review and editing

    Competing interests

    No competing interests declared

12. Michael Bauer

    Department of Anaesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany

    Contribution

    Resources, Data curation

    Competing interests

    No competing interests declared

    "This ORCID iD identifies the author of this article:" 0000-0002-1521-3514

13. Mike Philipp

    Department of Anaesthesiology and Intensive Care Medicine, Greiz General Hospital, Greiz, Germany

    Contribution

    Data curation, Investigation

    Competing interests

    No competing interests declared

14. Nikolaus Gaßler

    Section of Surgical Pathology, Institute of Forensic Medicine, Jena University Hospital, Jena, Germany

    Contribution

    Resources, Supervision, Investigation, Methodology, Writing - review and editing

    Competing interests

    No competing interests declared

15. Sandor Nietzsche

    Department of Electron Microscopy, Jena University Hospital, Jena, Germany

    Contribution

    Investigation, Methodology, Writing - review and editing

    Competing interests

    No competing interests declared

16. Bettina Löffler

    Institute of Medical Microbiology, Jena University Hospital, Jena, Germany

    Contribution

    Conceptualization, Resources, Data curation, Software, Supervision, Validation, Visualization, Writing - original draft, Project administration, Writing - review and editing

    Contributed equally with

    Gita Mall

    Competing interests

    No competing interests declared

17. Gita Mall

    Institute of Forensic Medicine, Jena University Hospital, Jena, Germany

    Contribution

    Conceptualization, Resources, Data curation, Software, Formal analysis, Supervision, Validation, Investigation, Visualization, Methodology, Writing - original draft, Project administration, Writing - review and editing

    Contributed equally with

    Bettina Löffler

    Competing interests

    No competing interests declared

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