Acta Scientific Microbiology (ASMI) (ISSN: 2581-3226)

Review Article Volume 3 Issue 7

Salivary Testing as a Potential and Convenient Tool for Diagnosis of COVID 19

Bramhadev Pattnaik1*, Pinaki Panigrahi2 and Mahendra P Yadav3

1One Health Center for Surveillance and Disease Dynamics, AIPH University, Bhubaneswar, Odisha and Former Director, ICAR-Directorate of Foot and Mouth Disease, Mukteshwar, India
2Department of Pediatrics, Division of Neonatal-Perinatal Medicine, Georgetown University Medical Center, Washington, DC, USA
3Former Vice-Chancellor, SVP University of Agriculture and Technology, Meerut, India

*Corresponding Author: Bramhadev Pattnaik, One Health Center for Surveillance and Disease Dynamics, AIPH University, Bhubaneswar, Odisha and Former Director, ICAR-Directorate of Foot and Mouth Disease, Mukteshwar, India.

Received: May 22, 2020; Published: June 29, 2020



  The novel coronavirus SARS-CoV-2 responsible for Coronavirus infectious disease of 2019 (COVID-19) in human, now a Global pandemic affecting 212 countries in all the five Continents, damages the cells that have ACE2 receptor expression on their surface. Hoffman., et al. (2020) observed that in addition to ACE2 receptor required for cellular attachment of the virion, cellular entry mechanism of the virus requires a cellular serine protease, TMPRSS2 and because alveolar type 2 cells express higher levels of both ACE2 and TMPRSS2 receptors, these cells might be the primary entry point for the virus in the lung. Intestine and kidney also have high expression of ACE2. The virus along with the ACE2 receptor enters the cells by endocytosis that results in reduction of ACE2 on cells, and as a consequence serum level of angiotensin II increases. Angiotensin II acts both as a vasoconstrictor and pro-inflammatory cytokine. Exposure to the virus does not necessarily cause infection, and not all people infected develop ARDS (acute respiratory distress syndrome) or succumb to the disease. Though people of all age group and sex are susceptible, the disease could be more fatal in elderly persons > 60 years of age. Extensive lung damage due to elicitation of Cytokine Storm (cytokine release syndrome; CRS) has been described by Hirano and Murakami (2020) and Shi., et al (2020). Role of specific HLA loci and alleles (class I or II) in developing protective immunity to this virus infection remains to be elucidated. It has been reported by Iwasaki and Yang (2020) that antibodies to SARS-CoV-2 at low concentrations as well as low affinity antibodies in the body can result in antibody-dependent enhancement (ADE) by utilizing Fc receptors on immune cells including macrophages, monocytes and B lymphocytes. ADE has detrimental effect in some patients with virus specific antibodies. High WBC count with associated lymphocytopenia is common in the COVID-19 patients. Ganji., et al. (2020) have reported significant reduction in the numbers of circulating lymphocytes and platelets, CD4+: CD8+ ratio of 2:1, and higher expression of CD8+ and hyperactivation of CTLs and no significant change in the expression level of CD4+ compared to healthy individuals. Anti-viral immune response to SARS-CoV-2 infection was due to over expression of CD8 and hyper activation of CTLs. Pathophysiology and pathology of the disease has been elaborated by Yuki., et al. (2020) and Sahu., et al (2020). The present review compiles the aspects of pathogenesis and involvement of the host immune system in aggravating the disease through the process of immune response.

Keywords: Coronavirus; COVID-19; Immunopathology; Immune Response; Pandemic; SARS



  1. Hoffmann M., et al. “SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor”. Cell 181 (2020): 271-280.
  2. Hirano T and Murakami M. “COVID-19: A new virus, but a familiar receptor and cytokine release syndrome”. Immunity5 (2020): 731-733.
  3. Shi Y., et al. “COVID-19 infection: the perspectives on immune responses”. Cell Death and Differentiation 27 (2020): 1451-1454.
  4. Iwasaki A and Yang Y. The potential danger of suboptimal antibody response in COVID-19.
  5. Ganji A., et al. “Increased expression of CD8 marker on T-cells in COVID-19 patients”. Blood Cells Molecules and Diseases 83 (2020): 102437.
  6. Yuki K., et al. “COVID-19 pathophysiology: A review”. Clinical Immunology (2019): 108427.
  7. Sahu K K., et al. “COVID-19: update on epidemiology, disease spread and management”. Monaldi Archives Chest Disease1292 (2020): 197-205.
  8. Bar-On YM., et al. “SARS-CoV-2 (COVID-19) by numbers”. eLife (2020): 57309.
  9. Lu R., et al. Genomic characterization and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding”. The Lancet 395 (2020): 565-574.
  10. Wang D., et al. “Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus infected pneumonia in Wuhan, China”. The Journal of the American Medical Association11 (2020): 1061-1069.
  11. Zhou F., et al. “Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study”. Lancet 395(10229):1054-1062.
  12. Gautret P., et al. “Hydroxychloroquine and azithromycin as a treatment of COVID-19: results of an open-label non-randomized clinical trial”. The International Journal of Antimicrobial Agents (2020): 105949.
  13. Rabi F A., et al. “SARS-CoV-2 and Coronavirus Disease 2019: What We Know So Far”. Pathogens3 (2020): 231.
  14. Xiao K., et al. “Isolation of SARS-CoV-2-related coronavirus from Malayan pangolins”. Nature (2020).
  15. Wu F., et al. “A new coronavirus associated with human respiratory disease in China”. Nature7798 (2020): 265-269.
  16. Chen Y., et al. “Structure analysis of the receptor binding of 2019-nCoV”. Biochemical and Biophysical Research Communications 1 (2020): 135-140.
  17. Li W., et al. “Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus”. Nature (2003).
  18. Zhou P., et al. “A pneumonia outbreak associated with a new coronavirus of probable bat origin”. Nature7789 (2020):270-273.
  19. Zhou Y., et al. “Pathogenic T cells and inflammatory monocytes incite inflammatory storm in severe COVID-19 patients”. National Science Review (2020).
  20. Walls A C., et al. “Structure, Function, and Antigenicity of the SARS-CoV-2 Spike Glycoprotein”. Cell2 (2020): 281-292.
  21. Zou X., et al. “Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to 2019-nCoV infection”. Frontiers in Medicine 2 (2020):185-192.
  22. Ou X., et al. “Characterization of spike glycoprotein of SARS-CoV2 on virus entry and its immune cross-reactivity with SARS-CoV”. Nature Communications 1 (2020): 1620.
  23. Belouzard S., et al. “Mechanisms of coronavirus cell entry mediated by the viral spike protein”. Viruses6 (2012): 1011-1033.
  24. Hamming I., et al. “Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis”. The Journal of Pathology 2 (2004): 631-637.
  25. Chen N., et al. “Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study”. Lancet10223 (2020): 507-513.
  26. Wu Z and McGoogan J M. “Characteristics of and important lessons from the Coronavirus Disease 2019 (COVID-19) outbreak in China: Summary of a report of 72314 cases from the chinese center for disease control and prevention”. The Journal of the American Medical Association (2020).
  27. Onder G., et al. “Case-Fatality Rate and Characteristics of Patients Dying in Relation to COVID-19 in Italy”. The Journal of the American Medical Association (2020).
  28. Ferner R E and Aronson J K. “Remdesivir in covid-19”. British Medical Journal 369 (2020): m1610.
  29. Scavone C., et al. “Current pharmacological treatments for COVID-19: what's next?” British Journal of Pharmacology (2020).
  30. Janeway C A Jr., et al. “Immunobiology: The Immune System in Health and Disease”. 5th New York: Garland Science (2001).
  31. Zhu J., et al. “Differentiation of effector CD4 T cell populations”. The Annual Review of Immunology 28 (2009): 445-489.
  32. Mescher M F., et al. “Signals required for programming effector and memory development by CD8+ T cells”. Immunological Reviews 211 (2006): 81-92.
  33. Yoshikawa T., et al. “Severe acute respiratory syndrome (SARS) coronavirus-induced lung epithelial cytokines exacerbate SARS pathogenesis by modulating intrinsic functions of monocyte-derived macrophages and dendritic cells”. Journal of Virology 7 (2009): 3039-3048.
  34. Qin C., et al. “Dysregulation of immune response in patients with COVID-19 in Wuhan, China”. Clinical Infectious Diseases 12 (2020): ciaa248.
  35. Fujimoto I., et al. “Virus clearance through apoptosis dependent phagocytosis of influenza A virus-infected cells by macrophages”. Journal of Virology 7 (2000): 3399-3403.
  36. Yang Z Y., et al. “pH-dependent entry of severe acute respiratory syndrome coronavirus is mediated by the spike glycoprotein and enhanced by dendritic cell transfer through DC-SIGN”. Journal of Virology 11 (2004): 5642-5650.
  37. Huang C., et al. “Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China”. Lancet 10223 (2020): 497-506.
  38. Zheng M., et al. “Functional exhaustion of antiviral lymphocytes in COVID-19 patients”. Cellular and Molecular Immunology 5 (2020): 533-535.
  39. Huang H., et al. “High levels of circulating GM-CSF (+) CD4(+) T cells are predictive of poor outcomes in sepsis patients: a prospective cohort study”. Cellular and Molecular Immunology 6 (2019): 602-610.
  40. Xu Z., et al. “Pathological findings of COVID-19 associated with acute respiratory distress syndrome”. The Lancet Respiratory Medicine 4 (2020): 420-422.
  41. Tian S., et al. “Pulmonary Pathology of Early-Phase 2019 Novel Coronavirus (COVID-19) Pneumonia in Two Patients with Lung Cancer”. Journal of Thoracic Oncology 5 (2019): 700-704.
  42. Tian S., et al. “Pathological Study of the 2019 Novel Coronavirus Disease (COVID-19) Through Postmortem Core Biopsies”. Modern Pathology (2020b): 1-8.
  43. Koutsogiannaki S., et al. “The Use of Volatile Anesthetics as Sedatives for Acute Respiratory Distress Syndrome”. Translational Perioperative and Pain Medicine 2 (2019): 27-38.
  44. Fang M., et al. “Perforin-dependent CD4+ T-cell cytotoxicity contributes to control a murine poxvirus infection”. Proceedings of the National Academy of Sciences of the United States of America 25 (2012): 9983-9988.
  45. Lovren F., et al. “Angiotensin converting enzyme-2 confers endothelial protection and attenuates atherosclerosis”. The American Journal of Physiology-Heart and Circulatory Physiology 295 (2008): H1377-H1384.
  46. Zeng H., et al. “Human pulmonary microvascular endothelial cells support productive replication of highly pathogenic avian influenza viruses: possible involvement in the pathogenesis of human H5N1 virus infection”. Journal of Virology 2 (2012): 667-678.
  47. Jia H P., et al. “ACE2 receptor expression and severe acute respiratory syndrome coronavirus infection depend on differentiation of human airway epithelia”. Journal of Virology 23 (2005): 14614-14621.
  48. Patel S K., et al. “Emerging markers in cardiovascular disease: where does angiotensin-converting enzyme 2 fit in?” Clinical and Experimental Pharmacology and Physiology 8 (2013): 551-559.
  49. Wenham C., et al. “COVID-19: the gendered impacts of the outbreak”. Lancet10227 (2020): 846-848.
  50. Jin J., et al. “Gender differences in patients with COVID-19: Focus on severity and mortality”. Frontiers in Public Health 8 (2020): 152.
  51. Saule P., et al. “Accumulation of memory T cells from childhood to old age: central and effector memory cells in CD4(+) versus effector memory and terminally differentiated memory cells in CD8(+) compartment”. Mechanisms of Ageing and Development 3 (2006): 274-281.
  52. Li M., et al. “Age related human T cell subset evolution and senescence”. Immunity and Ageing (2019).
  53. Connors T J., et al. “Airway CD8(+) T Cells Are Associated with Lung Injury during Infant Viral Respiratory Tract Infection”. The American Journal of Respiratory Cell and Molecular Biology 54 (2016): 822-830.
  54. Smits S L., et al. “Exacerbated innate host response to SARS-CoV in aged non-human primates”. PLOS Pathogens 2 (2010): e1000756.
  55. Wong H R., et al. “Leukocyte subset derived genome wide expression profiles in pediatric septic shock”. Pediatric Critical Care Medicine 3 (2010): 349-355.
  56. Nickbakhsh S., et al. “Virus-virus interactions impact the population dynamics of influenza and the common cold”. Proceedings of the National Academy of Sciences of the United States of America 52 (2019): 27142-27150.
  57. Thuen Jan von der and Erden Menno van der. “Histopathology and genetic susceptibility in COVID-19 pneumonia”. European Journal of Clinical Investigation (2020).
  58. Margo C., et al. “Complement Associated Microvascular Injury and Thrombosis in the Pathogenesis of Severe COVID-19 Infection: A Report of Five Cases”. Translational Research S1931-5244.20 (2020): 30070-30070.
  59. Chen W-H., et al. “Potential for developing a SARS-CoV receptor binding domain (RBD) recombinant protein as a heterologous human vaccine against coronavirus infectious disease (COVID)-19”. Human Vaccines and Immunotherapeutics (2020).
  60. Du L., et al. “The spike protein of SARS-CoV- a target for vaccine and therapeutic development”. Nature Reviews Microbiology 7 (2009): 226-236.
  61. Decaro N., et al. “COVID-19 from veterinary medicine and one health perspectives: What animal coronaviruses have taught us”. Research in Veterinary Science 131 (2020): 21-23.


Citation: Bramhadev Pattnaik., et al. “Immunopathology of COVID-19 Caused by SARS-CoV-2: A Brief Review". Acta Scientific Microbiology 3.7 (2020): 79-88.


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