Location

Philadelphia

Start Date

13-5-2015 1:00 PM

Description

Background: Chlamydia pneumoniae (Cpn) and Herpes simplex virus type 1 (HSV-1) have been studied as pathogens contributing to neurodegenerative diseases. Cpn and HSV-1 are both ubiquitous, thus many individuals presumably are exposed to both pathogens during their life time. Since Cpn can establish persistence under adverse environmental conditions, we speculate that productive HSV infection might induce Cpn persistence in cells infected with both pathogens. Intermittent reactivation of either or both pathogens might contribute to progressive pathology associated with neurodegenerative diseases. Objectives: Determine whether Cpn and HSV-1 can co-infect cells and whether the presence of one pathogen alters replication of the other. Methods: The ability of Cpn and HSV-1 to co-infect an astrocyte cell line (STTG-1) was analyzed by immunofluorescence (IF) labeling using antibodies specific for HSV and Cpn, and RT-PCR using primers specific for each pathogen. Cells were infected with HSV or Cpn alone, or co infected with both pathogens for 24 or 48 hours. Results: IF revealed that cells could be simultaneously infected with both pathogens. Gene expression data support the observation that HSV replication is somewhat diminished in the presence of Cpn; similarly, the developmental cycle of Cpn appears to be disrupted by HSV. Conclusions: IF and gene expression data suggest both HSV-1 and Cpn inhibit, but do not prevent, infection by the second pathogen, possibly by competing for the same cellular receptors. Moreover, disruption of host cell transcription by HSV-1 may modify normal Cpn development

Included in

Life Sciences Commons

COinS
 
May 13th, 1:00 PM

Herpes simplex virus type 1 and Chlamydia pneumoniae infection of astrocytes: the effects of co-infection on pathogen replication

Philadelphia

Background: Chlamydia pneumoniae (Cpn) and Herpes simplex virus type 1 (HSV-1) have been studied as pathogens contributing to neurodegenerative diseases. Cpn and HSV-1 are both ubiquitous, thus many individuals presumably are exposed to both pathogens during their life time. Since Cpn can establish persistence under adverse environmental conditions, we speculate that productive HSV infection might induce Cpn persistence in cells infected with both pathogens. Intermittent reactivation of either or both pathogens might contribute to progressive pathology associated with neurodegenerative diseases. Objectives: Determine whether Cpn and HSV-1 can co-infect cells and whether the presence of one pathogen alters replication of the other. Methods: The ability of Cpn and HSV-1 to co-infect an astrocyte cell line (STTG-1) was analyzed by immunofluorescence (IF) labeling using antibodies specific for HSV and Cpn, and RT-PCR using primers specific for each pathogen. Cells were infected with HSV or Cpn alone, or co infected with both pathogens for 24 or 48 hours. Results: IF revealed that cells could be simultaneously infected with both pathogens. Gene expression data support the observation that HSV replication is somewhat diminished in the presence of Cpn; similarly, the developmental cycle of Cpn appears to be disrupted by HSV. Conclusions: IF and gene expression data suggest both HSV-1 and Cpn inhibit, but do not prevent, infection by the second pathogen, possibly by competing for the same cellular receptors. Moreover, disruption of host cell transcription by HSV-1 may modify normal Cpn development