4.6 Article

miR-541-3p Promoted Porcine Reproductive and Respiratory Syndrome Virus 2 (PRRSV-2) Replication by Targeting Interferon Regulatory Factor 7

Journal

VIRUSES-BASEL
Volume 14, Issue 1, Pages -

Publisher

MDPI
DOI: 10.3390/v14010126

Keywords

PRRSV; type I interferon; miR-541-3p; IRF7

Categories

Funding

  1. National Foundation of China [41907121]
  2. key scientific research projects of Henan provincial institution of higher education [22A180004]
  3. Special Project of National Natural Science Foundation of China [31941001]
  4. Henan Natural Science Foundation [182300410077]
  5. China Postdoctoral Science Foundation [2021M690926]
  6. Henan Normal University Outstanding Youth Science Fund [20170031]
  7. National Science Foundation of China [31472177]

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PRRSV-2 infection may enhance its replication in host cells by up-regulating miR-541-3p, which can inhibit host immune response. MiR-541-3p negatively regulates the transcription of type I interferon by targeting IRF7, further promoting PRRSV-2 replication.
Porcine reproductive and respiratory syndrome (PRRS) is a disease caused by PRRS virus (PRRSV), which seriously harms the pig industry. Revealing the mechanism by which PRRSV inhibits immune response will help prevent and control PRRS. Here, we found that PRRSV-2 may hijack host miR-541-3p to inhibit host innate immune response. Firstly, this work showed that miR-541-3p mimics could facilitate the replication of PRRSV-2 and the results of the quantitative real time polymerase chain reaction (qRT-PCR) showed that PRRSV-2 could up-regulate the expression of miR-541-3p in MARC-145 cells. Since previous studies have shown that type I interferon could effectively inhibit the replication of PRRSV-2, the present work explored whether miR-541-3p regulated the expression of type I interferon and found that miR-541-3p could negatively regulate the transcription of type I interferon by targeting interferon regulatory factor 7 (IRF7). More importantly, PRRSV-2 infection could down-regulate the expression of IRF7 and over-expression of IRF7 could down-regulate the replication of PRRSV-2 in MARC-145 cells. In conclusion, PRRSV-2 infection up-regulated the expression of miR-541-3p to promote its replication in MARC-145 cells, since miR-541-3p can negatively regulate the transcription of type I interferon by targeting IRF7.

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