In December 2019, in Wuhan, China, the novel coronavirus ‘severe acute respiratory syndrome 2’ (SARS-CoV-2) was discovered as the cause of a pneumonia-like illness and subsequently named coronavirus disease 2019 (COVID-19). COVID-19 spread and is now a global pandemic. With few exceptions, countries in the Northern hemisphere have higher mortality rates from COVID-19. This may be due to an increased prevalence of older people in Northern Europe at higher risk of having cardio-pulmonary and metabolic comorbidities as well as hypovitaminosis D. With increasing age, immunosenescence and ‘inflammaging’ lead to impaired and maladaptive immune responses to SARS-CoV-2 infections, contributing to the enhanced prevalence of severe COVID-19 in older patients. The association of ageing with increased vitamin D deficiency, which is associated with cardiovascular risk factors and disease and worse prognosis in COVID-19 infection, is discussed. Considerable experimental evidence demonstrates the immuno-modulatory properties of vitamin D, in particular, its role in regulating and suppressing the inflammatory cytokine response to viral respiratory infections links the importance of vitamin D sufficiency as a potential protective factor in COVID-19. There is an urgent need for prospective randomised studies to examine whether hypovitaminosis D correlates with severity of COVID-19 disease and the actual benefit of repletion. Moreover, given what has been described as a ‘pandemic of vitamin D deficiency’, especially in Europe, and in the context of the SARS-CoV-2 contagion, the authors support the call for public health doctors and physicians, with support from Governments, to prioritise and strengthen recommendations on vitamin D intake and supplementation.

The hypovitaminosis D kyphotic pig provides a model to study maternal vitamin D (D) carryover on gross and molecular characteristics of bone abnormalities in offspring. Excess maternal D is proposed to protect offspring under nutritional challenges from developing bone abnormalities. Relationships between D sufficiency parameters and bone abnormalities were characterised. Sows (n 37) were fed diets with 0 (−D), 8·125 (+D) or 43·750 (++D) µg D3/kg throughout gestation and lactation. At weaning (3 weeks) pigs were fed diets with 0 (−D) or 7·0 (+D) µg D3/kg, each with 75 and 95 % (LCaP) or 150 and 120 % (HCaP) of the Ca and P requirements. Pigs were euthanised before colostrum consumption at birth (n 27), 3 weeks (n 27) or after the nursery period (7 weeks, n 71) for tissue analysis. At 7 weeks, differences due to maternal D were detected (P≤0·05) in pig growth, serum parameters and mRNA expression regardless of nursery diet. Prevalence of kyphosis in pigs at 13 weeks was affected by maternal D, but not prevented by only HCaP or +D nursery diets. Increased (P≤0·05) serum 25-OH-D3 concentrations in sows fed +D or ++D diets were not reflected by similar magnitudes of 25-OH-D3 in colostrum, 18-d milk, or serum and tissue concentrations in pigs. The mode of action by which maternal dietary D influences development of skeletal abnormalities warrants further investigation.