Abstract
SARS-CoV-2 is a newly emerging virus that currently lacks curative treatments. Lactoferrin (LF) is a naturally occurring non-toxic glycoprotein with broad-spectrum antiviral, immunomodulatory and anti-inflammatory effects. In this study, we assessed the potential of LF in the prevention of SARS-CoV-2 infection in vitro. Antiviral immune response gene expression was analyzed by qRT-PCR in uninfected Caco-2 intestinal epithelial cells treated with LF. An infection assay for SARS-CoV-2 was performed in Caco-2 cells treated or not with LF. SARS-CoV-2 titer was determined by qRT-PCR, plaque assay and immunostaining. Inflammatory and anti-inflammatory cytokine production was determined by qRT-PCR. LF significantly induced the expression of IFNA1, IFNB1, TLR3, TLR7, IRF3, IRF7 and MAVS genes. Furthermore, LF partially inhibited SARS-CoV-2 infection and replication in Caco-2 intestinal epithelial cells. Our in vitro data support LF as an immune modulator of the antiviral immune response with moderate effects against SARS-CoV-2 infection.
Highlights
A novel coronavirus has generated a pandemic outbreak, designated as COVID-19, that was first reported in Wuhan, China, 2019 and spread rapidly all over the world [1]
LF treatment could induce the mRNA expression of toll-like receptor 3 (TLR3) and 7 (TLR7), which are pattern recognition receptors involved in sensing of RNA viruses (Figure 2B), and of interferon regulatory factor 3 (IRF3) and 7 (IRF7), as well as mitochondrial antiviralsignaling (MAVS), which participate to antiviral innate immunity response signaling pathways (Figure 2C)
LF led to an increase, not significant, in the expression of interferon induced with helicase C domain 1 (IFIH1), which encodes a cytoplasmic receptor critical for sensing of RNA viruses (Figure 2B)
Summary
A novel coronavirus has generated a pandemic outbreak, designated as COVID-19, that was first reported in Wuhan, China, 2019 and spread rapidly all over the world [1]. The 2019 coronavirus is a single-stranded RNA virus, designated as SARS-CoV-2, as it has genetic similarities with SARS-CoV, the virus responsible for the severe acute respiratory syndrome outbreak that occurred in 2002 [2]. SARS-CoV-2 is primarily thought to infect the lungs with transmission through respiratory droplets (aerosols), mainly during close person-to-person contact [6]. The intestine represents another viral target organ supporting SARS-CoV-2 replication [7], with viral shedding into stool occurring in a substantial portion of patients, which makes fecal-oral transmission plausible [8]. Therapeutic interventions against SARS-Cov-2 infection rely on supportive care and respiratory support for severely ill people as well as some antivirals [9,10], and drugs targeted against the abnormal immune-inflammatory response [10,11]
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