Immunological Response of SARS-CoV-2 Infection

Dr Kelvin Kai-wang TO

Specialist in Clinical Microbiology and Infection
Clinical Associate Professor, the University of Hong Kong



Coronavirus Disease 2019 (COVID-19) pandemic has devastated the world in 2020.  The number of COVID-19 cases has surpassed 62 millions, with over 1.4 million deaths as of 30th November, 2020.  COVID-19 has also led to severe disruption in the socioeconomic activity.  The World Bank has forecasted a 5.2% reduction in global GDP in 20201. 

COVID-19 is caused by a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which was first identified during a pneumonia outbreak in Wuhan in December 2019.  Epidemiological studies showed that SARS-CoV-2 infection has a lower case-fatality rate than that of 2003 SARS-CoV, but can transmit much more efficiently between humans2.  Seroprevalence studies showed that neutralising antibody against SARS-CoV-2 are not found in blood specimens collected before 2020 in Hong Kong3.

Understanding the immune response for COVID-19 is important for clinical practice. First, the correct interpretation of serology results requires a good understanding of the antibody kinetics during infection.  Second, although SARS-CoV-2 can infect different organs and can directly cause tissue damage, many complications of COVID-19 are related to the dysregulated inflammatory response or immune-mediated damage.  Third, understanding the immune correlates of protection is critical for risk assessment and for determining the immunogenicity of vaccines.



Similar to other infections, SARS-CoV-2 infection is accompanied by elevated levels of cytokine and chemokines.  Studies have shown that the cytokine/chemokine pattern in patients with critical illness is distinct from those with moderate disease severity [4].  Critically ill patients (those who died, required mechanical ventilation or ICU admission) had increased levels of all types of cytokines, including those from type 1 (against virus or intracellular bacteria, such as IFN-γ), type 2 (allergic or anti-helminth immunity, such as IL-5) and type 3 (against fungi or extracellular bacteria, such as IL-17) immunity.  Critically ill patients also demonstrated persistently elevated levels of cytokines, while those with less severe disease demonstrated a progressive reduction in cytokine levels after day ten post-symptom onset. Although the cytokine and chemokine levels are elevated among COVID-19 patients, the level is much lower than in other inflammatory conditions.  A meta-analysis showed that the level of IL-6 is much lower among COVID-19 patients than patients with cytokine release syndrome, sepsis or acute respiratory syndrome unrelated to COVID-195.  This observation is important and suggests that the use of different cytokine inhibitors should be carefully evaluated.


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