CCR2-64I polymorphism, syncytium-inducing human immunodeficiency virus strains, and disease progression.

NOTE. Numerical values are numbers of individuals. NSI, non–syncytium inducing; SFMHS, San Francisco Men’s Health Study; SI, syncytium inducing. a Fisher’s exact P value. does not predict the ability of an assay to detect C. pneumoniae in tissues. We agree with Valassina et al. [1] that the presence of C. pneumoniae DNA alone in arterial specimens is insufficient proof of the presence of viable organisms in vascular tissue; however, cultural isolation of the bacterium from atherosclerotic plaques has been reported repeatedly [5, 6]. Furthermore, culture-derived data are in accordance with the results of our study on C. pneumoniae RNA in carotid plaques. Regarding the suggestion that inflammatory mechanisms such as molecular mimicry or induction of metabolic mechanisms are responsible for atheroma formation, rather than the presence of viable bacteria, we believe this to be partially true. However, the results of studies in animal models indicate that the presence of viable bacteria in vascular tissues is an essential element in the association between C. pneumoniae and development of atherosclerotic lesions [7].