Abstract
Human Parainfluenza Virus Type 3 (HPIV3) is one of the main pathogens that cause acute lower respiratory tract infections in infants and young children. However, there are currently no effective antiviral drugs and vaccines. Herein, we found that a natural compound, curcumin, inhibits HPIV3 infection and has antiviral effects on entry and replication of the virus life cycle. Immunofluorescence and western blotting experiments revealed that curcumin disrupts F-actin and inhibits viral inclusion body (IB) formation, thus inhibiting virus replication. Curcumin can also downregulate cellular PI4KB and interrupt its colocalization in viral IBs. This study verified the antiviral ability of curcumin on HPIV3 infection and preliminarily elucidated its influence on viral replication, providing a theoretical basis for antiviral drug development of HPIV3 and other parainfluenza viruses.
Highlights
HPIVs are the second leading cause of acute lower respiratory tract disease in infants, following respiratory syncytial virus (RSV)
0.0 DMSO Curcumin (c) expression in cells, resulting in a decrease of phosphatidylinositol 4-kinase beta (PI4KB) recruited into inclusion body (IB), and on the other hand, it severely interferes with the colocalization of PI4KB and viral IBs, thereby affecting viral replication
Curcumin has been incubated with cells before virus infection in pretreatment, while hemagglutinin-neuraminidase protein (HN) expression of pretreatment is comparable to that of the DMSO group, indicating that curcumin incubating with cells in advance cannot prevent HPIV3 infection
Summary
HPIVs are the second leading cause of acute lower respiratory tract disease in infants, following respiratory syncytial virus (RSV). HPIV3 causes acute lower respiratory tract infection and induces bronchiolitis, pneumonia, etc. Factin and its regulatory factor cofilin played a crucial role in forming HPIV3 IBs and synthesizing viral RNA [11]. In HPIV3- or HRSV-infected host cells, P protein of HPIV3 or N protein of HRSV can both recruit PI4KB to viral IBs, creating a PI4P-enriched microenvironment that reinforces IB structures and facilitates virus replication [13]. Curcumin can interfere with binding of Zika and Chikungunya viruses to host cells to inhibit viral infection [20]. Curcumin can downregulate endogenous PI4KB level in cells, interfering with colocalization of PI4KB and IBs to affect IB formation, thereby inhibiting viral replication. The results of this study theoretically guide the development of new drugs against HPIV3 infection
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