Abstract
Rotavirus (RV) is the major causes of severe diarrhea in infants and young children under five years of age. There are no effective drugs for the treatment of rotavirus in addition to preventive live attenuated vaccine. Recent evidence demonstrates that microRNAs (miRNAs) can affect RNA virus replication. However, the antiviral effect of miRNAs during rotavirus replication are largely unknown. Here, we determined that miR-7 is upregulated during RV replication and that it targets the RV NSP5 (Nonstructural protein 5). Results suggested that miR-7 affected viroplasm formation and inhibited RV replication by down-regulating RV NSP5 expression. Up-regulation of miR-7 expression is a common regulation method of different G-type RV-infected host cells. Then, we further revealed the antiviral effect of miR-7 in diarrhea suckling mice model. MiR-7 is able to inhibit rotavirus replication in vitro and in vivo. These data provide that understanding the role of cellular miR-7 during rotaviral replication may help in the identification of novel therapeutic small RNA molecule drug for anti-rotavirus.
Highlights
Rotavirus (RV) is one of the most common causes of severe diarrhea in infants and young children under five years of age
We find that MIR-7 was able to inhibit rotavirus replication both in vitro and in vivo, which was achieved by targeting the rotavirus gene that encodes NSP5 and influencing viroplasm formation and viral genome replication
Total RNA was extracted from MA104 cells infected with ZTR-68 (MOI = 0.1) at 12, 24, 36, and 48 h post-infection(hpi). quantitative real-time polymerase chain reaction (qRT-PCR) results showed that the expression of miR-7 continued to increase until it peaked at 36 hpi (Figure 1A)
Summary
Rotavirus (RV) is one of the most common causes of severe diarrhea in infants and young children under five years of age. Live attenuated vaccines are available to protect against rotavirus infection, there are still approximately 125 million episodes of rotavirus gastroenteritis every year, resulting in approximately 200,000 child fatalities [1]. There are no effective drugs for the treatment of rotavirus in addition to the preventative live vaccine [2]. The mechanisms of rotavirus infection and proliferation, especially the regulatory role of small RNA molecules, remains to be elucidated. It is a non-enveloped virus and possesses icosahedral capsids. The double-stranded RNA genome of rotavirus consists of 11 distinct segments encoding six structural proteins (VP1 to VP4, VP6, and VP7) and six non-structural proteins (NSP1 to NSP6) [3]
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