Oral bacteria induce a differential activation of human immunodeficiency virus-1 promoter in T cells, macrophages and dendritic cells.
BACKGROUND
The human immunodeficiency virus (HIV) can integrate into T cells, macrophages and dendritic cells resulting in a latent infection. Reports have also demonstrated that various microbial and host cell factors can trigger HIV reactivation leading to HIV recrudescence, potentially undermining highly active antiretroviral therapies.


METHODS
This study evaluated the capacity of oral bacteria associated with chronic periodontal infections to stimulate HIV promoter activation in various cell models of HIV latency.


RESULTS
T cells (1G5) challenged with oral bacteria demonstrated a dose-response of HIV promoter activation with a subset of the bacteria, as well as kinetics that were generally similar irrespective of the stimuli. Direct bacterial challenge of the T cells resulted in increased activation of approximately 1.5- to 7-fold over controls. Challenge of macrophages (BF24) indicated different kinetics for individual bacteria and resulted in consistent increases in promoter activation of five fold to six fold over basal levels for all bacteria except Streptococcus mutans. Dendritic cells showed increases in HIV reactivation of 7- to 34-fold specific for individual species of bacteria.


CONCLUSIONS
These results suggested that oral bacteria have the capability to reactivate HIV from latently infected cells, showing a relationship of mature dendritic cells > immature dendritic cells > macrophages > or = T cells. Expression of various pattern recognition receptors on these various cell types may provide insight into the primary receptors/signaling pathways used for reactivation by the bacteria.
Huang
C B
CB
Center for Oral Health Research, College of Dentistry, University of Kentucky, Lexington, KY 40536, USA. chuan2@uky.edu
Emerson
K A
KA
Gonzalez
O A
OA
Ebersole
J L
JL
D016924:Actinomyces viscosus / Q000502:physiology; D016976:Aggregatibacter actinomycetemcomitans / Q000502:physiology; D001439:Bacteroides / Q000502:physiology; D044883:Campylobacter rectus / Q000502:physiology; D002460:Cell Line; D055113:Chronic Periodontitis / Q000382:microbiology*; D003713:Dendritic Cells / Q000821:virology*; D016967:Fusobacterium nucleatum / Q000502:physiology; D006090:Gram-Negative Bacteria / Q000502:physiology*; D006094:Gram-Positive Bacteria / Q000502:physiology*; D015658:HIV Infections / Q000821:virology; D016325:HIV Long Terminal Repeat / Q000502:physiology; D015497:HIV-1 / Q000235:genetics / Q000502:physiology*; D006801:Humans; D008070:Lipopolysaccharides / Q000502:physiology; D008264:Macrophages / Q000821:virology*; D009055:Mouth / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000502:physiology; D018713:Prevotella intermedia / Q000502:physiology; D011401:Promoter Regions, Genetic / Q000502:physiology; D013295:Streptococcus mutans / Q000502:physiology; D013601:T-Lymphocytes / Q000821:virology*; D014162:Transfection; D014775:Virus Activation / Q000502:physiology*; D017735:Virus Latency / Q000502:physiology
D008070:Lipopolysaccharides
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