4.6 Article

Meclizine Inhibits Pseudorabies Virus Replication by Interfering With Virus Entry and Release

Journal

FRONTIERS IN MICROBIOLOGY
Volume 12, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fmicb.2021.795593

Keywords

pseudorabies virus; meclizine; antiviral activity; virus entry; virus release

Categories

Funding

  1. National Natural Science Foundation of China [32102637, 32172823]
  2. Yangzhou University Interdisciplinary Research Foundation for Veterinary Medicine Discipline of Targeted Support
  3. Project of the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)

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Pseudorabies virus (PRV) is a significant pathogen in the swine industry, and meclizine has shown notable inhibitory effects against PRV, especially during viral entry and cell-to-cell spreading. The antiviral effect of meclizine was also confirmed in mice experiments, indicating its potential as a therapeutic drug for PRV infection.
Pseudorabies virus (PRV) is a pathogen that causes substantial economic losses to the swine industry. With the emergence and widespread of PRV variants since 2011 in China, current commercial vaccines cannot provide complete protection against PRV infection. Therefore, antiviral drugs may work as an alternative way to control and prevent PRV. In this study, the inhibitory effects and underlying molecular mechanisms of meclizine against PRV were studied. Meclizine displayed a significant inhibitory effect against PRV when it was added before, simultaneously with, or after virus infection. The inhibitory effect of meclizine occurred during viral entry and cell-to-cell spreading but not at viral attachment into PK-15 cells. Meclizine also inhibited viral particle release at the late stage of infection. The antiviral effect of meclizine was tested in mice, and the results showed that meclizine reduced the severity of clinical symptoms and the viral loads in tissues, and delayed the death, after PRV challenge. The above results indicated that meclizine had an inhibitory effect on PRV. Our findings will contribute to the development of potential therapeutic drugs against PRV infection.

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