The work presented in this dissertation is divided into the following individual but related topics. In Chapter 1, subcellular localization sites of Brome mosaic virus (BMV) replication and coat protein (CP) were studied in Nicotiana benthamiana leaves using the immunofluorescence confocal microscopy. This study revealed that the BMV CP localizes to the endoplasmic reticulum (ER) membranes and replicase resides at the same location as the CP in the ER. Analysis of ultrastructural modifications by transmission electron microscopy revealed that modified ER membrane incorporate large assemblies of ER-derived vesicles during BMV infection in N. benthamiana leaves. These vesicles were encased into a vesicle pockets and three distinct types of vesicles were found in these pockets. For the first time we identified an additional function of BMV CP by ectopic expression experiments followed by TEM analysis. BMV CP itself is capable of modifying the ER membrane and induces vesicles similar to those present in BMV infection. Chapter 2 describes the analysis of functional domain of CP responsible for producing CP-induced vesicles in BMV virus infection cycle. A study analyzing the effect of mutations engineered into CP ORF on ER-rearrangement TEM microscopy in N. benthamiana leaves revealed that, assembly defective mutations encompassing either N-proximal arginine-rich RNA-binding motif (ARM; deletion from amino acid 2-20) or C-proximal 184F→A substitution in BMV CP led to abolish the membrane rearrangement. This data suggested that encapsidation competent CP is required for the vesicle induction. Chapter 3 unfolds the implication of membrane rearrangements induced by BMV infection in susceptible and resistant hosts to viral replication and biology. Combination of Northern blot analysis, virion extraction and virion RNA extraction assays exposed that BMV causes a subliminal infection in Nicotiana clevelandii resistant host and that BMV replication efficiency in these tissues is similar to that of the Nicotiana benthamiana susceptible host. A hallmark feature of BMV CP is its inability to induce any membrane modifications in resistant host, despite efficient replication and assembly. Additional studies involving co-infection of BMV and cucumber mosaic virus (CMV) further revealed that BMV CP is more specific in genome packaging compared to that of CMV.