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World J Clin Infect Dis. Aug 25, 2012; 2(4): 54-62
Published online Aug 25, 2012. doi: 10.5495/wjcid.v2.i4.54
Human immunodeficiency virus, atherosclerosis and Chlamydophila pneumoniae
Guadalupe García-Elorriaga, Guillermo del Rey-Pineda
Guadalupe García-Elorriaga, Hospital de Infectología, Centro Médico Nacional, La Raza, Mexico City 02990, Mexico
Guillermo del Rey-Pineda, Department of Infectious Diseases, Intestinal Bacteriology Laboratory, Hospital Infantil de México Federico Gómez, Mexico City 06720, Mexico
Guillermo del Rey-Pineda, Secretaría de Salud (SSA), Mexico and Central Blood Bank, Centro Médico Nacional, La Raza, Mexico City 02990, Mexico
Author contributions: Both authors made substantial contributions to this paper.
Correspondence to: Guadalupe García-Elorriaga, PhD, Researcher, Hospital de Infectología, Centro Médico Nacional, La Raza, Mexico City 02992, Mexico. gelorriaga@webtelmex.net.mx
Telephone: +52-55-57245900 Fax: +52-55-53530989
Received: August 12, 2011
Revised: April 26, 2012
Accepted: July 4, 2012
Published online: August 25, 2012

Chlamydophila pneumoniae (C. pneumoniae) is an obligate, intracellular bacterium associated with a wide variety of acute and chronic diseases. C. pneumoniae infection is characterized by persistence and immunopathological damage to host target tissues, including the lung. Over the past 20 years, a variety of studies have investigated a possible link between C. pneumoniae infection and atherosclerosis, because of its role in all stages of atherosclerosis, from initial inflammatory lesions to plaque rupture. In the current highly active antiretroviral therapy (HAART) era, many human immunodeficiency virus (HIV)-infected patients are experiencing health problems that accompany the aging process, mainly the risk of cardiovascular disease (CVD). There is renewed interest in a link between atherosclerotic CVD and as yet poorly defined environmental exposures, including infectious agents. On the one hand, the patient with HIV and lipodystrophy caused by HAART and exacerbated by C. pneumoniae infection could be a factor of risk for atherosclerosis. An assessment of the therapy against C. pneumoniae and HAART should always be conducted. It is advisable that HIV-acquired immune deficiency syndrome patients undergo a serological test to determine exposure to C. pneumoniae and to assess treatment options. On the other hand, in patients with a positive serology to C. pneumoniae, an increment of the body mass index has been found; therefore, it is probable that the recurrent infection may play an important role in creating adverse endothelial conditions allowing the infection by C. pneumoniae in its chronic form, to damage the endothelial surface. Vascular studies would be necessary for corroboration.

Keywords: Acquired immune deficiency syndrome, Atheroma, Chlamydophila pneumoniae, Immunobiology of infection, Obesity, Inflammation