Zika virus, a mosquito-borne virus, is associated with congenital birth defects and neurological complications. However, despite its significant public health threat, no approved vaccines or antiviral treatments are currently available. Therefore, this study aims to identify kinesin family member 20A as a key host factor promoting Zika virus life cycle. The elevated expression of kinesin family member 20A following Zika virus infection suggests its role in the viral life cycle. Suppressing its expression through gene silencing or inhibiting its function with a small-molecule inhibitor significantly reduced viral infectivity in host cells. Furthermore, kinesin family member 20A is essential for facilitating viral internalization, a key step in the entry step. These findings suggest its significance in the Zika virus life cycle and highlight its potential as a novel therapeutic target for the Zika virus.
Heme oxygenase-1 (HO-1) has antioxidant, anti-apoptotic, and anti-inflammatory properties. Emerging evidence shows that HO-1 also exhibits antiviral activity against severe acute respiratory syndrome coronavirus 2, human immunodeficiency virus, hepatitis B virus, and Ebola virus. Its antiviral effects are mediated not only by its enzymatic function but also through the modulation of interferon-related pathways, thereby inhibiting viral replication. In this study, we investigated the antiviral effects of HO-1 on canine coronavirus (CCoV) and canine influenza virus (CIV) H3N2 using cell-based assays. To determine whether HO-1 suppresses CCoV and CIV, cells were treated with hemin to induce HO-1 expression. Hemin treatment successfully induced HO-1 expression in A72 and Madin-Darby canine kidney cells, resulting in the suppression of CCoV and CIV replication. The canine HO-1 gene was cloned into an expression vector and transfected into cells to achieve transient overexpression. Recombinant canine HO-1 protein was expressed in Escherichia coli and purified using an expression vector. HO-1 overexpression suppressed CCoV and CIV replication in cells. Following viral infection, treatment with purified HO-1 protein led to a reduction in viral protein levels. Therefore, both HO-1 expression and exogenous protein treatment effectively inhibited CCoV and CIV replication. Elevated HO-1 protein levels consistently reduced viral RNA and protein expression in vitro. These findings suggest that HO-1 could serve as a potential therapeutic agent for managing viral infections in dogs.
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