Coronavirus disease 2019 (Covid-19), caused by severe acute respiratory syndrome coronavirus (SARS-CoV)-2, exerts far-reaching effects on public health and socio-economic welfare. The majority of infected individuals have mild to moderate symptoms, but a significant proportion develops respiratory failure due to pneumonia. Thrombosis is another frequent manifestation of Covid-19 that contributes to poor outcomes. Vitamin K plays a crucial role in the activation of both pro- and anticlotting factors in the liver and the activation of extrahepatically synthesised protein S which seems to be important in local thrombosis prevention. However, the role of vitamin K extends beyond coagulation. Matrix Gla protein (MGP) is a vitamin K-dependent inhibitor of soft tissue calcification and elastic fibre degradation. Severe extrahepatic vitamin K insufficiency was recently demonstrated in Covid-19 patients, with high inactive MGP levels correlating with elastic fibre degradation rates. This suggests that insufficient vitamin K-dependent MGP activation leaves elastic fibres unprotected against SARS-CoV-2-induced proteolysis. In contrast to MGP, Covid-19 patients have normal levels of activated factor II, in line with previous observations that vitamin K is preferentially transported to the liver for activation of procoagulant factors. We therefore expect that vitamin K-dependent endothelial protein S activation is also compromised, which would be compatible with enhanced thrombogenicity. Taking these data together, we propose a mechanism of pneumonia-induced vitamin K depletion, leading to a decrease in activated MGP and protein S, aggravating pulmonary damage and coagulopathy, respectively. Intervention trials should be conducted to assess whether vitamin K administration plays a role in the prevention and treatment of severe Covid-19.

The recent COVID-19 pandemic has altered the face of biology, social interaction and public health worldwide. It has had a destructive effect upon millions of people and is approaching a devastating one million fatalities. Emerging evidence has suggested a link between the infection and gut microbiome status. This is one of the several factors that may contribute towards severity of infection. Given the fact that the gut is heavily linked to immunity, inflammatory status and the ability to challenge pathogens, it is worthwhile to consider dietary intervention of the gut microbiota as means of potentially challenging the viral outcome. In this context, probiotics and prebiotics have been used to mitigate similar respiratory infections. Here, we summarise links between the gut microbiome and COVID-19 infection, as well as propose mechanisms whereby probiotic and prebiotic interventions may act.

Pandemics and subsequent lifestyle restrictions such as ‘lockdowns’ may have unintended consequences, including alterations in body weight. This systematic review assesses the impact of pandemic confinement on body weight and identifies contributory factors. A comprehensive literature search was performed in seven electronic databases and in grey sources from their inception until 1 July 2020 with an update in PubMed and Scopus on 1 February 2021. In total, 2361 unique records were retrieved, of which forty-one studies were identified eligible: one case–control study, fourteen cohort and twenty-six cross-sectional studies (469, 362 total participants). The participants ranged in age from 6 to 86 years. The proportion of female participants ranged from 37 % to 100 %. Pandemic confinements were associated with weight gain in 7·2–72·4 % of participants and weight loss in 11·1–32·0 % of participants. Weight gain ranged from 0·6 (sd 1·3) to 3·0 (sd 2·4) kg, and weight loss ranged from 2·0 (sd 1·4) to 2·9 (sd 1·5) kg. Weight gain occurred predominantly in participants who were already overweight or obese. Associated factors included increased consumption of unhealthy food with changes in physical activity and altered sleep patterns. Weight loss during the pandemic was observed in individuals with previous low weight, and those who ate less and were more physically active before lockdown. Maintaining a stable weight was more difficult in populations with reduced income, particularly in individuals with lower educational attainment. The findings of this systematic review highlight the short-term effects of pandemic confinements.

Although increased weight, and particularly obesity, has been associated with a more severe clinical course of COVID-19 and risk of fatality, the course of the illness can lead to prolonged length of stay. Changes in nutritional status and weight loss during hospitalisation are largely reported in some populations, but still not explored in COVID-19 patients. Considering that patients with COVID-19 show an increased inflammatory response, other signs and symptoms, which can lead to weight and muscle loss, should be monitored. The aim of this article was to establish possible connections between COVID-19, prolonged hospitalisation and muscle wasting, as well as to propose nutritional recommendations for the prevention and treatment of cachexia, through a narrative review. Identification of risk and presence of malnutrition should be an early step in general assessment of all patients, with regard to more at-risk categories including older adults and individuals suffering from chronic and acute disease conditions, such as COVID-19. The deterioration of nutritional status, and consequently cachexia, increases the risk of mortality and needs to be treated with attention as other complications. There is, however, little hard evidence of nutritional approaches in assisting COVID-19 treatment or its management including cachexia.

Se is a micronutrient essential for human health. Sub-optimal Se status is common, occurring in a significant proportion of the population across the world including parts of Europe and China. Human and animal studies have shown that Se status is a key determinant of the host response to viral infections. In this review, we address the question whether Se intake is a factor in determining the severity of response to coronavirus disease 2019 (COVID-19). Emphasis is placed on epidemiological and animal studies which suggest that Se affects host response to RNA viruses and on the molecular mechanisms by which Se and selenoproteins modulate the inter-linked redox homeostasis, stress response and inflammatory response. Together these studies indicate that Se status is an important factor in determining the host response to viral infections. Therefore, we conclude that Se status is likely to influence human response to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and that Se status is one (of several) risk factors which may impact on the outcome of SARS-CoV-2 infection, particularly in populations where Se intake is sub-optimal or low. We suggest the use of appropriate markers to assess the Se status of COVID-19 patients and possible supplementation may be beneficial in limiting the severity of symptoms, especially in countries where Se status is regarded as sub-optimal.

As COVID-19 continues to spread worldwide, severe disease and mortality have been observed in obese patients. We discuss how obesity and obesity-associated factors such as ‘meta-flammation’, dietary fat intake and paradoxical suppression of the innate immune response within the pulmonary compartment may be crucial determinants in the host response to a novel viral pathogen. Modulation of immune cell bioenergetics and metabolic potential plays a central role in the innate immune response to infection, and as we strive to combat this new global health threat, immunometabolism of the innate immune system warrants attention.

Recent scientific evidence has indicated that the elderly have increased risk of COVID-19 infections, with over 70s and 80s being hardest hit – especially residents of care homes and in clinical settings, ethnic minorities, people who work indoors and those who are overweight and obese. Other potential risk factors include lack of exposure to sunlight, darker skin pigmentation, co-morbidities, poor diet, certain medications, disadvantaged social and economic status, and lifestyle factors such as smoking and excessive consumption of alcohol. A key question is to understand how and why certain groups of people are more susceptible to COVID-19, whether they have weakened immune systems and what the roles of good nutrition and specific micronutrients are in supporting immune functions. A varied and balanced diet with an abundance of fruits and vegetables and the essential nutrients like vitamin D, vitamin A, B vitamins (folate, vitamin B6 and vitamin B12), vitamin C and the minerals, Fe, Cu, Se and Zn are all known to contribute to the normal functions of the immune system. Avoidance of deficiencies and identification of suboptimal intakes of these micronutrients in targeted groups of patients and in distinct and highly sensitive populations could help to strengthen the resilience of people to the COVID-19 pandemic. It is important to highlight evidence-based public health messages, to prevent false and misleading claims about the benefits of foods and food supplements and to communicate clearly that the extent of knowledge between micronutrients and COVID-19 infection is still being explored and that no diet will prevent or cure COVID-19 infection. Frequent handwashing and social distancing will be critical to reduce transmission.

SARS-CoV2 infects respiratory epithelial cells via its cellular receptor angiotensin-converting enzyme 2, causing a viral pneumonia with pronounced inflammation resulting in significant damage to the lungs and other organ systems, including the kidneys, though symptoms and disease severity are quite variable depending on the intensity of exposure and presence of underlying conditions that may affect the immune response. The resulting disease, coronavirus disease 2019 (COVID-19), can cause multi-organ system dysfunction in patients requiring hospitalisation and intensive care treatment. Serious infections like COVID-19 often negatively affect nutritional status, and the resulting nutritional deficiencies may increase disease severity and impair recovery. One example is the viral infection measles, where associated vitamin A (VA) deficiency increases disease severity and appropriately timed supplementation during recovery reduces mortality and hastens recovery. VA may play a similar role in COVID-19. First, VA is important in maintaining innate and adaptive immunity to promote clearance of a primary infection as well as minimise risks from secondary infections. Second, VA plays a unique role in the respiratory tract, minimising damaging inflammation, supporting repair of respiratory epithelium and preventing fibrosis. Third, VA deficiency may develop during COVID-19 due to specific effects on lung and liver stores caused by inflammation and impaired kidney function, suggesting that supplements may be needed to restore adequate status. Fourth, VA supplementation may counteract adverse effects of SARS-CoV2 on the angiotensin system as well as minimises adverse effects of some COVID-19 therapies. Evaluating interactions of SARS-CoV2 infection with VA metabolism may thus provide improved COVID-19 therapy.