Sir, research indicates that BAME communities are disproportionately adversely impacted by SARS-CoV2 (COVID-19). The HSJ reported the results of an analysis of deaths of NHS staff from COVID-19 based upon media reports up to 22 April 2020.1 Those from BAME communities were found to account for 63% of the deaths, yet the communities only formed 21% of all NHS staff. Among medical staff the comparable figures were even more concerning, 95% and 44% respectively. An ONS analysis found that a proportion of the excess risk of adverse risk COVID-19 presents to BAME groups is accounted for by demographics, socio-economic profiles and some dimensions of health, but the remainder remained unexplained.

Pan et al.2 recently reported the findings of a systematic review to assess whether ethnicity had been reported in research relating to patients with COVID-19 and its relation to clinical outcomes. They concluded that BAME individuals are at raised risk of adverse outcomes including hospitalisation, ITU admission and mortality.

For COVID-19, severe disease is characterised by a proinflammatory hypercytokinemia which damages heart, kidney, liver and lung tissues with the latter leading to acute respiratory distress syndrome.3

The response of different skin types to UV radiation may be estimated using the Fitzpatrick scale comprising six phototypes which are semi-quantitative in that each has an associated minimal erythematous UV dose (MED) range.4 By way of confirming an apparent correlation between phototype MED values and ethnicity related COVID-19 death risk I calculated the r values5 for men (r = 0.81) and women (r = 0.81) using ONS fully adjusted model data6 and author estimated MED values7 for the relevant ethnic groups.

I believe that the strong correlations support the logical hypothesis that ultraviolet radiation (UVR) skin exposure induced immunosuppression reduces the risk of hypercytokinemia development in COVID-19 infected individuals and in turn the following cascade of predictions:

  • UV induced inflammation in the skin induces immunosuppression which is locally protective and also acts systemically

  • Immunoregulatory efficiency as it relates to hypercytokinemia risk, is inversely correlated with increasing Fitzpatrick Skin Type code.

Possible mechanisms for the greater innate immunomodulation efficiency in lower MED range phenotypes groups might include:

  • Differences between skin types are related to phenotypic variations, more probably those in the genes coding for elements of the NF-κB protein complex and/or IL-6-STAT3 signalling pathways

  • Utilisation of vitamin D in the management of an inflammatory response8 in the skin is more efficient/optimised in lower MED range skin phenotypes. However, the effect is systemic so improving immunomodulation efficiency

  • The efficiency with which UVR induced regulatory T cells mediated immunosuppression is induced (whether a continuous or discrete process) is inversely correlated with skin phenotype MED value when corrected for the age of the individual.

UVR induced systemic immunosuppression would effect a reduction in periodontal inflammation and thereby reduce periodontal disease severity. Skin lesions reported in C19 patients are autoimmune reactions caused by COVID-19 induced numerical deficiency or functional defect/s in regulatory T cells.

A more detailed summary of the above may be accessed online.9