Understanding the immunology behind COVID-19

3 minute read


People with severe disease have a markedly greater immune response than those with milder COVID-19


The following are excerpts from Dr Harry Nespolon’s interview with Professor Andrew Lloyd, Infectious Diseases Physician at Prince of Wales Hospital, Sydney and Head of the Viral Immunology Systems Program, Kirby Institute.

This interview first appeared on the HealthEd Podcast, “Going Viral”, which can be found at www.healthed.com.au

COVID-19 is an RNA virus from the coronavirus family and a relative to a number of viruses that cause cold-like symptoms as well as the viruses the caused SARS and MERS. In structure it is 80% identical to the virus that caused SARS.

To understand the morbidity related to COVID-19 one has to understand the host response to the viral infection which involves two key elements – the innate response which is the body’s first response on recognising it has been infected by a pathogen, any pathogen, and then there is the development of adaptive immunity, which is the body’s attempt to combat infection by this specific pathogen and commonly involves a humoral response, where the B cells produce antibodies which can recognise this infecting virus and inhibit it from entering cells or replicating once inside the cell, as well as T cell immunity, where circulating lymphocytes are mobilised to either kill or protect against the virus.

The innate response involves the mobilisation of anti-viral immune proteins and key components of the inflammatory process.

The immunological response to COVID-19 is the key explanation as to what happens when some patients develop severe disease. It is has been found that people with severe disease have a markedly greater immune response than those with milder COVID-19.

The immune response is a fine balance between the inflammatory response and the development of more sustained, ongoing, adaptive response. The fact that older people are more likely to develop severe disease is believed to relate to their propensity to have a less well-controlled inflammatory response – to be less efficient in balancing the different aspects of the immune response.

In COVID-19, the most common manifestation of severe disease is the progression of the inflammation of the upper respiratory tract to affect the lower respiratory tract, a pneumonitis.

The inflammation of the lower respiratory tract not only sees fluid leak from the vascular compartment in the lungs into the alveolar space, but also sees the activation of coagulation factors which explains the findings of microemboli in the pulmonary vasculature. In rare cases this activation of clotting factors has extended to other areas in the body, causing problems such as DVTs and strokes.

As yet, it is still not known whether the immune response to COVID-19 will result in long-lasting immunity to re-infection. What is known is that it is unlikely that neutralising antibodies will be the sole determinant of that immunity. It is likely that other factors, such as T cells, will play a part in ongoing protection against this particular coronavirus.

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