Cecropin P1 inhibits porcine reproductive and respiratory syndrome virus by blocking attachment

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• 作者：Chunhe Guo (1)
  Yumao Huang (2)
  Peiqing Cong (1)
  Xiaohong Liu (1)
  Yaosheng Chen (1)
  Zuyong He (1)
  
  1. State Key Laboratory of Biocontrol ; School of Life Sciences ; Sun Yat-sen University ; North Third road ; Guangzhou Higher Education Mega Center ; Guangzhou ; Guangdong ; 510006 ; PR China
  2. College of Veterinary Medicine ; South China Agricultural University ; Guangzhou ; Guangdong ; 510642 ; PR China
  
• 关键词：Cecropin P1 ; PRRSV ; Antiviral activity ; Antimicrobial peptide
• 刊名：BMC Microbiology
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：14
• 期：1
• 全文大小：1,769 KB
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• 刊物主题：Microbiology; Biological Microscopy; Fungus Genetics; Parasitology; Virology; Life Sciences, general;
• 出版者：BioMed Central
• ISSN：1471-2180

文摘

Background Porcine reproductive and respiratory syndrome virus (PRRSV) is a continuous threat to the pig industry, causing high economic losses worldwide. Current vaccines have specific limitations in terms of their safety and efficacy, so the development of novel antiviral drugs is urgently required. The aim of this study was to evaluate the inhibitory effects and underlying molecular mechanisms of the antimicrobial peptide cecropin P1 (CP1) against PRRSV infection in vitro. Results CP1 not only displayed extracellular virucidal activity against PRRSV, but also exerted a potent inhibitory effect when added either before, simultaneously with, or after viral inoculation. The inhibitory effect of CP1 occurred during viral attachment, but not at viral entry into Marc-145 cells. CP1 also inhibited viral particle release and attenuated virus-induced apoptosis during the late phase of infection. CP1 exerted similar inhibitory effects against PRRSV infection in porcine alveolar macrophages, the cells targeted by the virus in vivo during its infection of pigs. The expression of interleukin 6 was elevated by CP1 in porcine alveolar macrophages, which might contribute to its inhibition of PRRSV infection. Conclusions Collectively, our findings provide a new direction for the development of potential therapeutic drugs against PRRSV infection.