Purpose of Review: Interactions between microorganisms can alter subsequent disease outcomes. Human papilloma virus (HPV) and Chlamydia trachomatis (CT) establish human genital co-infections, and CT infection is a co-factor for HPV-induced cervical cancer. This review focuses upon (i) data indicating that clinically significant interactions occur and (ii) proposed mechanisms underlying these outcomes. Recent Findings: Epidemiological surveys indicate that (i) simultaneous HPV/CT genital co-infections are common; (ii) CT co-infection accelerates HPV-induced cytopathology; and (iii) HPV infection facilitates CT infection. Single-infection studies suggest specific molecular mechanisms by which co-infection alters clinical outcomes, including (i) HPV E6/E7 protein modification of host cell pathways enhances CT replication or immune evasion and (ii) CT-mediated host cell or neutrophil dysfunctions promote HPV-mediated neoplasia. Summary: There are multiple avenues for future dissection of HPV/CT interactions. Moreover, the known and potential health consequences of co-infection highlight the need for improving current HPV vaccines and developing an effective CT vaccine.
| Identifer | oai:union.ndltd.org:ETSU/oai:dc.etsu.edu:etsu-works-11412 |
| Date | 15 June 2019 |
| Creators | Slade, Jessica A., Schoborg, Robert V. |
| Publisher | Digital Commons @ East Tennessee State University |
| Source Sets | East Tennessee State University |
| Detected Language | English |
| Type | text |
| Source | ETSU Faculty Works |
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