Pooled evidence conveys the association between
polyunsaturated fatty acids and
infectious disease. SARS-CoV-2, an enveloped
mRNA virus, was also reported to interact with
polyunsaturated fatty acids. The present review explores the possible mode of action, immunology, and consequences of these
polyunsaturated fatty acids during the
viral infection.
Polyunsaturated fatty acids control
protein complex formation in
lipid rafts associated with the function of two SARS-CoV-2 entry gateways:
angiotensin-converting enzyme-2 and cellular
protease transmembrane
protease serine-2. Therefore, the viral entry can be mitigated by modulating
polyunsaturated fatty acids contents in the body. α-
Linolenic acid is the precursor of two clinically important
eicosanoids eicosapentaenoic acid and
docosahexaenoic acid, the members of ω-3
fats. Resolvins, protectins, and maresins derived from
docosahexaenoic acid suppress
inflammation and augment phagocytosis that lessens microbial loads.
Prostaglandins of 3 series,
leukotrienes of 5 series, and
thromboxane A3 from
eicosapentaenoic acid exhibit anti-inflammatory, vasodilatory, and platelet anti-aggregatory effects that may also contribute to the control of pre-existing pulmonary and
cardiac diseases. In contrast, ω-6
linoleic acid-derived
arachidonic acid increases the
prostaglandin G2,
lipoxins A4 and B4, and
thromboxane A2. These
cytokines are pro-inflammatory and enhance the immune response but aggravate the
COVID-19 severity. Therefore, the rational intake of ω-3-enriched foods or supplements might lessen the complications in
COVID-19 and might be a preventive measure.
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