<span style="font-size:11.0pt;font-family: "Times New Roman";mso-fareast-font-family:"Times New Roman";mso-bidi-font-family: Mangal;mso-ansi-language:EN-GB;mso-fareast-language:EN-US;mso-bidi-language: HI" lang="EN-GB">Analyzing time course microarray data of <i style="mso-bidi-font-style: normal">Toxoplasma gondii</i> and study the impact on host transcript levels using Bioconductor</span>

Abstract

46-51Toxoplasma gondii is an obligate, intracellular, apicomplexan parasite that can infect a wide range of warm-blooded animals including humans. In humans and other intermediate hosts, Toxoplasma develops into chronic infection that cannot be eliminated by host’s immune response or by currently used drugs. The ability of the parasite to convert to the bradyzoite stage and to live inside slow-growing cysts that can go unnoticed by the host immune system allows for the persistence of parasite throughout the life of the infected host. Little is known, however, about how bradyzoites manipulate their host cell. Large scale microarray experiments are becoming increasingly routine, particularly those which track a number of different cell lines through time. This time course information provides valuable insight into dynamics of various biological processes. The proper statistical analysis, however, requires the use of more sophisticated tools and complex statistical models. In the current study, the open-source R programming environment in conjunction with the open-source Bioconductor software was used to analyze microarray data of T. gondii. Several statistical analysis procedures like (log) fold changes in conjunction with ordinary and moderated t-statistics were used to determine differentially expressed genes. The differentially expressed genes were subjected to cluster analysis, followed by the annotation of the up and down regulated genes based on the gene ontology. The findings in the present study suggest the overall effect of the gene expression changes is to modulate the key metabolic pathways leading to compromised host immune response, enhancement in programmed cell death, depression in cell proliferation process and induction of various diseases

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