HAL DRAKESMITH (OXFORD)
IRON AND VIRAL INFECTION
Innate immune responses to infection include an increase in hepcidin levels, which causes
hypoferraemia. In the case of siderophilic pathogens this is a protective response that slows
growth of invading microorganisms by withholding iron. However, the occurrence and effects
of hypoferraemia in the context of viral infection are less clear. Here I will show that
hypoferraemia, if severe and long-lasting enough, powerfully disables adaptive immune
responses to viral vaccine vectors and to influenza virus infection. I will also describe emerging
data that profound hypoferraemia occurs in SARS-CoV-2 infection and associates with poor
patient outcome, in contrast to non-COVID-19 ICU patients where high serum iron and high
transferrin saturation predict mortality. I will discuss the potential implications of these
observations for understanding the pathogenesis of COVID-19.
References:
1) Systemic hypoferremia and severity of hypoxemic respiratory failure in COVID-19. Shah A, et al. Crit
Care. 2020 Jun 9;24(1):320
https://doi.org/10.1186/s13054-020-03051-w
2) Hepcidin-mediated hypoferremia disrupts immune responses to vaccination and infection. Frost JN,
et al. Med. 2, 164-174
https://doi.org/10.1016/j.medj.2020.10.004