Viruses are obligate intracellular pathogens. They hijack host functions, divert host resources and suppress host defense responses to achieve successful infection . These involve an array of interactions with cellular factors, which, inevitably or coincidentally, often lead to host physiological disorders manifested by a variety of disease symptoms [2, 3]. Understanding molecular details from infection of a virus to symptom development of the host is one major mission of plant virologists. Transcriptome profiling has been used extensively in the past decade to understand mechanisms underlying plant-virus interaction [4, 5]. Transcriptional response of plants to virus infection is shown to vary depending on virus species, virus strains and the genetic backgrounds of host plants [6–8]. However, it shows a tight link with phenotypes and thus is useful to reveal how a virus colonizes a host, how a host mounts a defense response against a virus, and how a compatible virus-host interaction results in disease symptoms [6–8]. Also, these studies find that some genes may be commonly regulated by different viruses in different host plants . For example, a set of ribosomal genes have been shown to be up-regulated in Arabidopsis, Nicotiana benthamiana and rice infected with Turnip mosaic virus (TuMV), Plum pox potyvirus (PPV) and Rice stripe virus (RSV), respectively [10–12].
Rice, one of the main crop plants as well as a model for monocot plant research , is host to many viruses. Among them, Rice dwarf virus (RDV), a member of the genus Phytoreovirus in the family Reoviridae, is one of the most widespread and disastrous rice-infecting viruses causing great yield reduction in south East Asia [14–16]. RDV is transmitted in a propagative and circulative manner by leafhoppers (Nephotettix spp.) . Typical symptoms associated with RDV infection include severe dwarfism, increased tilling and white chlorotic specks on the infected leaves .
RDV are icosahedral double-shelled particles of approximately 70 nm in diameter. The genome of RDV is composed of 12 segments of double stranded RNAs, which are named S1-S12, respectively, according to their migration during sodium dodecyl sulfate–polyacrylamide gel electrophoresis. S1, S2, S3, S5, S7, S8, and S9 encode seven structural proteins, namely, P1, P2, P3, P5, P7, P8, and P9, respectively. P1, a putative RNA polymerase; P5, a putative guanylyltransferase; and P7, a nonspecific nucleic acid binding protein form the core of RDV together with viral dsRNAs . P3 and P8 are major components of the inner and outer protein shells that encapsidate the core, respectively [20, 21]. P2 and P9 are minor components of the outer capsid [22, 23]. The structural features and the process of assembly of RDV virions have been well studied [24, 25]. Besides structural proteins, RDV encodes at least five non-structural proteins, namely Pns4, Pns6, Pns10, Pns11, and Pns12, respectively. Pns6, Pns11 and Pns12 are matrix proteins of viroplasm, which is the putative site of viral replication . Pns4 is a phosphoprotein and is localized around the viroplasm matrix in insect cells . Several proteins of RDV have been shown to play specific roles in RDV-rice interaction. For example, Pns6 was identified as a viral movement protein and Pns10 as a RNA silencing suppressor of RDV [28, 29]. P2 interacts with ent-kaurene oxidases of rice, which leads to reduced biosynthesis of gibberellins and rice dwarf symptoms .
In this study, the transcriptome of the indica subspecies of rice, namely Oryza sativa L. ssp. indica cv Yixiang2292, in response to RDV infection was profiled using Affymetrix GeneChips, which contains probes representing the entire genome of rice  (http://www.affymetrix.com). Our results further confirm the notion that induction of defense related genes is common for rice infected with RDV and there are correlations between transcriptional changes and symptom development in RDV-infected rice.