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Viruses are the simplest organisms comprising only DNA or RNA genomes wrapped in protective shells of proteins or proteins and lipids. Their reproduction is only possible after they successfully enter a host cell, where they depend on the cellular apparatus for a variety of vital steps in their life cycles. Depending on the nature of viral genomes, these steps can include transcription of viral genes to synthesize viral mRNA, translation of viral proteins, and ultimately replication (multiplication) of viral genomes. The replicated viral genomes are then reassembled into virus particles, completing the life cycle of a typical virus. Throughout the entire process viruses interact intimately with the cellular environment, and must not only coerce the host cells for collaboration, but also counteract the hazard of host defense. As a result, viruses, despite their simple genomes, evolved to encode a vast array of regulative capacities that fine tune their gene expression and genome replication based on their surroundings and the progression of their life cycles. My thesis research focused on examining some of the virus-encoded regulative strategies. This dissertation contains four chapters. The first chapter reviewed the relevant literature, providing the background information and the current status of related research. The second chapter examined the impact of several cis-acting RNA elements on the replication of a virus with a single-stranded (ss), positive sense (+) RNA genome. The third chapter adopted a virus model with a genome of circular ssDNA, and investigated how a transcription factor encoded by this virus activates the transcription of late genes of the same virus. Finally, the last chapter sought to determine how a virus-encoded replication protein executes two opposite functions in the same infected cell. I used Turnip crinkle virus (TCV) as a small (+) RNA virus model for the research presented in Chapters two and four. Chapter two investigated how cis-acting RNA elements that are located in the coding region of TCV RNA-dependent-RNA polymerase (RdRp) influence the replication of this virus. Previous studies of these structures were limited to synonymous mutations that did not alter the amino acid sequence of RdRp, because the impact of nonsynonymous changes would be compounded by possible interference with the RdRp activity. Furthermore, those previous studies also could not determine whether certain cis-acting elements play multiple roles. For example, mutations within cis-acting elements important for RdRp translation could not be further tested to see if they are also important for the replication itself, because the latter step requires RdRp translation to be optimal. I have developed a new approach that decouples the translation and replication steps. This new approach allowed me to introduce a variety of mutations, including deletions of up to 1,000 nucleotides (nt), in the RdRp coding region. Using this approach, I was able to identify several new cis-acting elements that are important for the replication of TCV. In Chapter three, I studied a common phenomenon in a group of ssDNA viruses in the family Geminiviridae, known as bipartite begomoviruses. I used Mungbean yellow mosaic virus (MYMV) as a model to study the transcriptional activation of the late gene BV1 by AC2, an early expressing transcriptional activator protein of this virus. Previous research by others showed that AC2 bound to DNA but nonspecifically. I hence hypothesized that the transcriptional activation of BV1 gene required interactions between AC2 and transcription factors of the host plants, the latter binding to the promoter DNA of BV1 gene (PBV1) through specific promoter motifs. Therefore, my goal was to identify the specific motifs located in PBV1 that could be bound by potential AC2-interacting transcription factors of host plants. I was able to identify three ABA-responsive elements (ABREs) within the first 73 nt of PBV1 that collaboratively mediated the transcriptional activation of this promoter by the AC2 protein. Therefore, plant transcription factors involved in the ABA signaling pathways are likely candidates recruited by MYMV AC2 to mediate the activation of BV1 expression.In Chapter four, I investigated how p28, a TCV-encoded auxiliary replication protein (ARP), exerts two opposite functions in the same infected cell. My colleagues and I have established earlier that p28 plays two opposite roles in TCV replication: it supports TCV replication as an ARP, and represses TCV replication by eliciting superinfection exclusion (SIE). A p28 derivative with a C-terminal green fluorescent protein (GFP) tag, designated p28-GFP, exerted strong repression on the replication of a TCV replicon. However, p28-GFP failed to recapitulate the replication function of p28 because it was unable to complement the replication of a p28-defective TCV replicon. The focus of the Chapter four was to resolve why the p28-GFP, and other C-terminally tagged p28 variants, exhibited a strong repressive activity but lacked the replication activity. I initially hypothesized that the C-terminal tags stabilized the p28 protein, resulting in a higher p28 concentration in host cells, favoring p28 polymerization to form repressive protein aggregates. I first tested if the tendency of GFP to dimerize enhanced polymerization of p28-GFP, by replacing GFP with the non-dimerizing mNeonGreen (mNG). I found that the resulting p28-mNG still formed intracellular aggregates and exerted strong repressive activity to TCV replication. Simultaneously, I tested if the TCV RNA sequence encoding p28 was important for the formation of p28 protein aggregates using a codon shuffled (CS) p28, and found that the RNA sequence of p28 was not important for protein aggregation. Subsequently, I tested if I could abolish the repressive activity of C-terminally tagged p28 variants, and restore the replication-complementation activity to them, by diminishing their expression levels with weaker promoters. I found that very low expression of p28-mNG, as well as another p28 variant with a C-terminal duplicated HA tag (p28-2XHA), indeed abrogated their repressive activity. Surprisingly, even at very low expression levels, these C-terminally tagged p28 variants remained incapable of complementing the replication of a TCV mutant that did not encode its own p28. These results prompted the alternative hypothesis that an intact C-terminus free of any modifications is needed for the replication function of p28. Since our previous studies showed that HA-p28, a p28 derivative with an N-terminal, single-copy HA tag, did not significantly change the replication function of p28, I used it as the template to make small modifications at the C terminus of p28. I found that while deleting or mutating the last two amino acid (aa) residues substantially weakened the replication function of p28, a two-aa addition at this end had a relatively minor effect. These findings thus rejected my alternative hypothesis, suggesting that fusion of a C-terminal tag does not necessarily abolish the replication function of p28. Rather, there appears to be an upper limit on the size of the C-terminal tags. In summary, this dissertation examined three types of virus-encoded mechanisms that bolster the reproduction of viruses in infected cells. My research findings are expected to lay the foundation for additional investigations by fellow plant virologists, and contribute to the knowledge-based control and management of plant virus diseases.