| Autor: |
Deka, Srilekha, Vanover, Jennifer, Dessus-Babus, Sophie, Whittimore, Judy, Howett, Mary K., Wyrick, Priscilla B., Schoborg, Robert V. |
| Předmět: |
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| Zdroj: |
ETSU Faculty Works. |
| Druh dokumentu: |
Text |
| DOI: |
10.1111/j.1462-5822.2005.00608.x |
| Popis: |
Epidemiological and clinical studies have shown that double infection with herpes simplex virus type 2 (HSV-2) and Chlamydia trachomatis occurs in vivo. We hypothesized that co-infection would alter replication of these agents. To test this hypothesis, HeLa cells were infected with C. trachomatis serovar E, followed 24 h later by HSV-2 strain 333. Transmission electron microscopic (TEM) analyses indicated that, by 10 h after HSV addition, reticulate bodies (RBs) in coinfected cells were swollen, aberrantly shaped and electron-lucent. In infectious titre assays, HSV-2 coinfection abrogated production of infectious chlamydial progeny. Western blot analyses indicated that accumulation of chlamydial major outer membrane protein (MOMP) was decreased by HSV co-infection while accumulation of chlamydial heat-shock protein 60-1 (HSP60-1) was increased. Polymerase chain reaction (PCR) experiments indicated that chlamydial genome copy number was unaltered by HSV-2 superinfection. Semi-quantitative, reverse transcription PCR (RT-PCR) experiments demonstrated that levels of chlamydial groEL, ftsK, ftsW, dnaA and unprocessed 16S rRNA transcripts were not changed by HSV-2 super-infection. These data indicate that HSV-2 superinfection drives chlamydia into a viable but noncultivable state, which is the hallmark of persistence. Because chlamydial HSP60-1 has been associated with immunopathology in vivo, these results also suggest that disease severity might be increased in coinfected individuals. |
| Databáze: |
Networked Digital Library of Theses & Dissertations |
| Externí odkaz: |
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