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Title: TRANSCRIPTIONAL ANALYSIS OF RICKETTSIA PROWAZEKII INVASION GENE HOMOLOG (INVA) DURING HOST CELL INFECTION

Author
item GAYWEE, JARIYANART - U.OF MD,SCHL OF MDCN
item RADULOVIC, SUZANA - U.OF MD,SCHL OF MDCN
item HIGGINS, JAMES
item AZAD, ABDU - U.OF MD,SCHL OF MDCN

Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/8/2002
Publication Date: 11/2/2002
Citation: Gaywee, J., Radulovic, S., Higgins, J.A., Azad, A.F. 2002. Transcriptional analysis of rickettsia prowazekii invasion gene homolog (inva) during host cell infection. Infection and Immunity. pp.6346-6354.

Interpretive Summary: As part of their participation in this project, USDA-ARS scientists provided expertise in real time RT-PCR for the detection of the Rickettsia bacteria gene invA. The protein expressed by this gene may play a role in mediating the invasion of host cells by this intracellular pathogen. Using a cultured cell line from which ribonucleic acid (RNA) was extracted at various time points post-infection (p.i.), Rickettsia invA expression was found to peak at approximately 24 hrs p.i. This increase in invA expression does not apear to be a consequence of increased reproduction of the Rickettsia bacteria , but may in fact represent invasion of other cells adjacent to those first infected. The invA gene and its expressed protein may represent targets for chemotherapy or potential immunizing agents to ameliorate the morbidity and mortality associated with Rickettsia infection.

Technical Abstract: An invasion gene homolog, invA, of Rickettsia prowazekii has recently been identified to encode a member of Nudix hydrolase subfamily which acts specifically on dinucleoside oligophosphates (NpnN, n³ 5), a group of cellular signaling molecules known as "alarmones". InvA is thought to enhance intracellular survival by regulating stress-induced toxic nucleotide levels during rickettsial infection. To further characterize the physiological function of InvA, the gene expression pattern during various stages of rickettsial intracellular growth was investigated. Using semi-quantitative RT-PCR and real time fluorescent probe-based quantitative RT-PCR, a differential expression profile of invA during rickettsial host cell infection was examined. The invA transcript temporarily increased at the early period of infection, 24 h and 8 days post-infection. Expression of rickettsial groEL, a molecular indicator of cellular stresses, was also shown to be upregulated during the early period of infection. Furthermore, invA was co-transcribed in a polycistronic message with rrp, a gene encoding the response regulator protein homolog, which is a part of a two-component signal transduction system. These results support our earlier findings that under such stress conditions dinucleoside oligophosphate pyrophosphatase may function as a buffer enhancing rickettsial survival within the cytoplasm of eukaryotic cell. The expression of rickettsial dinucleoside oligophosphate pyrophosphatase may be regulated by the part of two-component signal transduction system similar to that described for response regulators in other bacterial systems.