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In any case, it would be reasonable to speculate that such interactions may contribute to the virus-host interplay and hence to the viral pathogenicity.
This will serve as a basis for further investigations on the underlying pathogenesis and the main contributing virus and host factors in ABV infection.
Further analysis of the data sets will contribute to our understanding of virus-host interplay in HCV, and use of the RNA-Seq technology in combination with microarray and proteomics techniques could have a major impact in other infectious diseases.
The nucleoprotein (NP) of IAV is known to contribute to viral pathogenesis, but its role in virus-induced host cell death was hitherto unknown.
Characteristic large structures appear in virus-infected host cells through the life cycle of various viruses.
However, the relative role of transcription and translation inhibition in virus-induced host shutoff is yet elusive.
Nevertheless, the present study contributes towards a better understanding of virus-host interactions leading to the development of GLRD symptoms in red-fruited wine grape cultivars.
These changes reflect that the host miRNAs may have important roles in the virus-host interactions.
The cytoskeletal components underlying plasma membrane including microtubules and actin are involved in virus entry into host cells.
In addition, a large set of host genes was predicted as potential targets for posttranscriptional silencing by TMV-Cg-derived siRNAs, revealing a layer of virus-host interactions that may contribute to viral pathogenicity and host specificity.
The induction of apoptosis and the suppression of antiapoptosis autophagy both regulated by influenza A virus contribute to avoiding host defense, amplify virus replication, and finally trigger the death of host cells with little immunogenicity.
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