Summary auto-generated
This study examined how influenza A virus (fowl plague strain) controls mRNA splicing differently in permissive and non-permissive cell types. Researchers infected primary chick embryo fibroblasts (CEF), which support productive viral replication, and mouse L cells, which do not. They found that spliced mRNAs from viral RNA segments 7 and 8 accumulated to much higher levels in L cells than in CEF. Using protein synthesis inhibitors, they demonstrated that in CEF, virus-specific protein synthesis is required to promote splicing of both segment 7- and segment 8-encoded mRNAs. However, in L cells, splicing of segment 7 transcripts occurred independently of new protein synthesis, while segment 8 splicing still required virus proteins. The authors propose that this differential control of splicing may explain why L cells cannot support productive FPV infection, particularly through effects on matrix protein expression and viral RNA synthesis.
Key findings
- Spliced viral mRNAs accumulate at much higher proportions in non-permissive L cells compared to permissive CEF cells
- In CEF, virus protein synthesis is required to promote efficient splicing of both vRNA 7 and vRNA 8 transcripts
- In L cells, vRNA 7 splicing occurs efficiently without requiring new virus protein synthesis, unlike vRNA 8 splicing
- The differential control of mRNA splicing between cell types may contribute to the inability of FPV to replicate in L cells
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Abstract
Spliced transcripts of influenza A (fowl plague) virus (FPV) RNA (vRNA) segments 7 and 8 accumulate to a much greater extent during non-productive infection of mouse L cells, than they do during productive infection in primary chick embryo fibroblasts (CEF). Virus-specific protein synthesis, or a consequent event in virus replication appears necessary to promote splicing of vRNA segment 8-encoded mRNAs in both cell types, and of vRNA segment 7-encoded mRNAs in CEF. In L cells, however, splicing of the segment 7-encoded mRNAs seems to be independent of such virus-specific control. This observation is discussed in relation to the defect in expression of vRNA 7 which has been observed previously in FPV-infected L cells, and which is thought to account for the failure of virus replication.