Journal
INFECTION AND IMMUNITY
Volume 74, Issue 3, Pages 1795-1799Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.74.3.1795-1799.2006
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Funding
- NIAID NIH HHS [R01 AI042156, R01 AI032943, AI32943, AI42156] Funding Source: Medline
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The hypothesis that host cell surface heparan sulfate is required to promote chlamydial infection was tested using a cell line (CHO-18.4) containing a single retroviral insertion and the concomitant loss of heparan sulfate biosynthesis. Tests of chlamydial infectivity of heparan sulfate-deficient CHO-18.4 cells and parental cells, CHO-22, demonstrated that both were equally sensitive to infection by Chlamydia trachomatis serovars L2 and D. These data do not support the hypothesis and demonstrate that host cell surface heparan sulfate does not serve an essential functional role in chlamydial infectivity.
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