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GUEST EDITORIAL  
Year : 2020  |  Volume : 63  |  Issue : 2  |  Page : 171-172
COVID-19 and lung pathology


Department of Microbiology, King George's Medical University, Lucknow, Uttar Pradesh, India

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Date of Web Publication18-Apr-2020
 

How to cite this article:
Jain A. COVID-19 and lung pathology. Indian J Pathol Microbiol 2020;63:171-2

How to cite this URL:
Jain A. COVID-19 and lung pathology. Indian J Pathol Microbiol [serial online] 2020 [cited 2020 May 26];63:171-2. Available from: http://www.ijpmonline.org/text.asp?2020/63/2/171/282688




On December 31, 2019, a cluster of cases of pneumonia in people who were later linked to Huanan Seafood Market in Wuhan, Hubei, China, were reported.[1] Just a week later, Chinese health authorities confirmed that these cases were caused by a novel coronavirus, later named as SARS-CoV2.[1]

Coronaviruses are enveloped, RNA viruses, circulating among humans and animals including mammals and birds. They mainly cause respiratory symptoms, but occasionally enteric, hepatic, and neurologic symptoms are also seen.[2] Till date, six coronavirus species are known to cause human diseases.[2] Four of the already-known coronavirus species, i.e., 229E, OC43, NL63, and HKU1, are commonly circulating viruses in human population and cause mild common cold-like symptoms.[2] Two of the already-known strains of coronavirus, severe acute respiratory syndrome-coronavirus (SARS-CoV) and Middle East respiratory syndrome-CoV (MERS-CoV) and now the recently pandemic-causing SARS-CoV2, are zoonotic in origin and cause serious illnesses which can be fatal.[3] SARS-CoV caused the SARS outbreaks in China (2002 and 2003)[3] and MERS-CoV caused the severe respiratory disease outbreaks in the Middle East (in 2012).[4] Now, this recent pandemic due to SARS-CoV2 started in China and has spread to most of the parts of the world causing severe morbidity, fear, and panic.

Coronaviruses are highly prevalent and widely distributed. Their genome is large and undergoes frequent recombination, causing the emergence of novel coronaviruses periodically. Due to frequent cross-species infections and occasional spill-over events, human infections are going to occur.[2]

Coronaviruses such as SARS-CoV2, MERS-CoV, and SARS-CoV can cause significant morbidity and mortality in infected persons. Lung is the most common site of infection for all the three of these viruses, which may manifest as acute respiratory distress syndrome and mortality. Pulmonary involvement is also responsible for the high viral transmission.

Interstitial inflammation, diffuse alveolar damage, and necrotizing bronchitis/bronchiolitis are general histopathological findings of lung in respiratory viral infections.[5],[6] Diffuse alveolar damage is the most commonly observed finding with respiratory virus infections both in acute and late (organizing) stages. The characteristic features of acute diffuse alveolar damage are intra-alveolar edema. Fibrin deposition and formation of hyaline membranes lining the alveolar walls follow. Late diffuse alveolar damage stages are Type II pneumocyte proliferation, granulation tissue formation, followed by collagen deposition. Some of the viral infections (influenza virus, parainfluenza virus, human metapneumovirus, and respiratory syncytial virus [RSV]) produce cytolysis and lead to the formation of multinucleated giant cells. Inclusion bodies may also be associated with interstitial pneumonia (leukocytic infiltration of the alveolar septa), while others (Cytomegalovirus, herpes simplex virus, varicella zoster virus, and adenovirus) are associated with necrotizing bronchiolitis. Viruses such as RSV, Parainfluenza, Human Metapneumovirus, and Measles produce cytolysis and lead to the formation of multinucleated giant cells. Inclusion bodies are also seen in some of the viral infections, especially Herpes group of viruses.[7]

The pathogenesis of SARS CoV begins with virus interaction with host cells through the binding of its envelope protein (spike; S) to angiotensin-converting enzyme 2 (ACE-2), the corresponding receptor. ACE-2 is abundantly expressed on the surface of lung and intestinal epithelial cells, hence making these cells susceptible to SARS-CoV.[8] Several recent case reports have mentioned that chest imaging and histopathological findings of lung caused by SARS-COV2 appear to be similar to those seen in SARS-CoV- and MERS-CoV-infected patients. One study from Italy[9] and other from China[10] described significant pathological lesions in lungs due to novel coronavirus pneumonia. Although the number of studied cases, as expected, was too low, and may be new data will be added soon, it is interesting to see that findings were not much different as seen in viral lung pathology. Common reported findings as reported [Table 1] are listed below.[9],[10]
Table 1: Major histopathological findings of lung in severe acute respiratory syndrome-coronavirus 2 infections

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  1. Alveolar exudative inflammation and interstitial inflammation was the chief finding. Macrophages and monocytes were in abundance in alveoli though few lymphocytes (mainly CD4-positive T cells), eosinophils, and neutrophils were also observed. Multinucleated giant cells were present in moderate number. Focal hemorrhage, occasional organization of exudates in alveolar cavities, and pulmonary interstitial fibrosis were found. Computed tomography (CT) findings showed that there was a moderate-to-severe progression of the lung infiltrates. Percentage of high-density infiltrates increased, and bilateral and multisegmental extension of lung opacities persisted[9]
  2. Serous exudation and fibrin exudation were seen; alveolar septa were edematous and widened. Alveolar septa were also congested, blood vessels were dilated, and monocytic and lymphocytic infiltrates were present
  3. Alveolar epithelium proliferation; proliferation of Type II alveolar epithelia and focal desquamation of alveolar epithelia were significant
  4. Hyaline membrane formation; occasional hyaline thrombi were present in small vessels
  5. Exfoliation of bronchial epithelia was partial
  6. Coronavirus particles were present in bronchial mucosal epithelia and Type II alveolar epithelia were seen under electron microscope
  7. SARS-CoV2 antigen: Presence of the alveolar epithelia and macrophages (immunohistochemistry positive)
  8. Real-time polymerase chain reaction positive for 2019-nCoV nucleic acid.


During the follow-up, pleural effusions, tubular and enlarged appearance of pulmonary vessels, and sudden caliber reduction in the dichotomic tracts were seen. Presence of mediastinal lymphadenopathy with short-axis oval nodes was an uncommon finding.[9] Pulmonary vessel enlargement was seen in areas where new lung infiltrates developed in the follow-up CT scan (an early predictor radiological sign of lung impairment).[10]

Although the number of studied cases was low, lung damage remains the predominant pathology of cases with COVID-19. Understanding the pathogenesis and pathological changes in lung will help in the diagnosis and management of COVID-19.



 
   References Top

1.
World Health Organization. Novel Coronavirus China. World Health Organization; 2020. Available from: https://www.who.int/csr/don/12-january-2020-novel-coronavirus-china/en/.  Back to cited text no. 1
    
2.
Su S, Wong G, Shi W, Liu J, Lai AC, Zhou J, et al. Epidemiology, genetic recombination, and pathogenesis of coronaviruses. Trends Microbiol 2016;24:490-502.  Back to cited text no. 2
    
3.
Zhong NS, Zheng BJ, Li YM, Poon, Xie ZH, Chan KH, et al. Epidemiology and cause of severe acute respiratory syndrome (SARS) in Guangdong, People's Republic of China, in February, 2003. Lancet 2003;362:1353-8.  Back to cited text no. 3
    
4.
Wong G, Liu W, Liu Y, Zhou B, Bi Y, Gao GF. MERS, SARS, and Ebola: The role of super-spreaders in infectious disease. Cell Host Microbe 2015;18:398-401.  Back to cited text no. 4
    
5.
Burke AP, Aubry MC. Viral pneumonias. In: Burke AP, Aubry MC, Maleszewski JJ, Alexiev BA, Tavora FR, editors. Practical Thoracic Pathology. Philadelphia, PA: Wolters Kluwer; 2016. p. 174-80.  Back to cited text no. 5
    
6.
Strano AJ. Light microscopy of selected viral diseases (morphology of viral inclusion bodies). Pathol Annu 1976;11:53-75.  Back to cited text no. 6
    
7.
Pritt BS, Aubry MC. Histopathology of viral infections of the lung. Semin Diagn Pathol 2017;34:510-7.  Back to cited text no. 7
    
8.
Tseng CT, Tseng J, Perrone L, Worthy M, Popov V, Peters CJ. Apical entry and release of severe acute respiratory syndrome-associated coronavirus in polarized calu-3 lung epithelial cells. J Virol 2005;79:9470-9.  Back to cited text no. 8
    
9.
Albarello F, Pianura E, Di Stefano F, Cristofaro M, Petrone A, Marchioni L, et al. COVID 19 INMI Study Group 2019-novel Coronavirus severe adult respiratory distress syndrome in two cases in Italy: An uncommon radiological presentation. Int J Infect Dis 2020;93:192-7.  Back to cited text no. 9
    
10.
Yao XH, Li TY, He ZC, Ping YF, Liu HW, Yu SC, et al. A pathological report of three COVID-19 cases by minimally invasive autopsies. Zhonghua Bing Li Xue Za Zhi 2020;49:E009.  Back to cited text no. 10
    

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Correspondence Address:
Amita Jain
Department of Microbiology, King George's Medical University, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IJPM.IJPM_280_20

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