{'fraction_non_alphanumeric': 0.031799729364005415, 'fraction_numerical': 0.02435723951285521, 'mean_word_length': 5.573333333333333, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Transcription of seven genes in a model of interferon‑γ-induced persistent Chlamydia psittaci infection.

The obligate intracellular bacterium Chlamydia psittaci is the causative agent of psittacosis in birds and humans. The capability of this zoonotic pathogen to develop a persistent phase may serve a role in the chronicity of infections, in addition to the failure of antibiotic therapy or immunoprophylaxis. In the present study, a C. psittaci strain 6BC persistent infection cell model was induced using interferon (IFN)‑γ, alterations in the infectivity and morphology of the pathogen were analyzed, and the transcript profile of seven selected genes was analyzed. Following treatment with IFN‑γ, the infectivity of C. psittaci 6BC was decreased, the inclusion bodies appeared to be smaller, reticulate bodies were larger and the number of infectious elementary bodies was decreased compared with acute infection. In IFN‑γ‑induced persistently infected cells, the relative mRNA expression levels of the genes CPSIT‑0208, CPSIT‑0310, CPSIT‑0846, CPSIT‑0844 and CPSIT‑0594 were upregulated at 2‑48 h post‑infection (p.i.). The genes CPSIT‑0959 and CPSIT‑0057 were downregulated at 2‑36 h p.i. The results of the present study advanced the understanding of C. psittaci persistent infection and demonstrated a number of previously unknown alterations in chlamydial gene expression, which may provide novel targets to further analyze this particular host‑pathogen interaction.