Chlamydia trachomatis enters a viable but non-cultivable (persistent) state within herpes simplex virus type 2 (HSV-2) co-infected host cells

Authors

  • Srilekha Deka,

    1. Department of Microbiology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.
    Search for more papers by this author
  • Jennifer Vanover,

    1. Department of Microbiology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.
    Search for more papers by this author
  • Sophie Dessus-Babus,

    1. Department of Microbiology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.
    Search for more papers by this author
  • Judy Whittimore,

    1. Department of Microbiology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.
    Search for more papers by this author
  • Mary K. Howett,

    1. Department of Bioscience and Biotechnology, Drexel University, Philadelphia, PA, USA.
    Search for more papers by this author
  • Priscilla B. Wyrick,

    1. Department of Microbiology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.
    Search for more papers by this author
  • Robert V. Schoborg

    Corresponding author
    1. Department of Microbiology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.
      *E-mail schoborg@mail.etsu.edu; Tel. (+1) 423 439 6295; Fax (+1) 423 439 8044.
    Search for more papers by this author

*E-mail schoborg@mail.etsu.edu; Tel. (+1) 423 439 6295; Fax (+1) 423 439 8044.

Summary

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 co-infected cells were swollen, aberrantly shaped and electron-lucent. In infectious titre assays, HSV-2 co-infection 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 non-cultivable 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 co-infected individuals.

Ancillary