ABSTRACT
UNLABELLED: The purpose of the study is to determine the role of certain clinical and immunological factors of the onset and development of age-related macular degeneration (AMD). MATERIALS AND METHODS: Retrospective analysis of patients records; determination of IFNalpha IFNgamma, IL-1beta, and TNFalpha cytokines levels as well as extracellular peroxidase activity (EPA) in blood serum and tear; measuring frequency of occurrence of intraocular infectious antigens with predominantly intracellular localization, such as Herpesviridae spp. (Herpes simplex, Cytomegalovirus, Epstein-Barr virus) and Chlamydiaceae spp. (Chlamydia pneumoniae, Chlamydia trachomatis) in lens matter and aqueous humor by means of polymerase chain reaction (PCR). The new evidence strongly suggests a relationship between AMD development and hypertension (p < 0.001; r = +0.30, P < 95%) as well as between AMD progression and hypertension accompanied by chronic inflammation with predominantly intracellular localization of the infectious agent (p < 0.05 for the predisciform stage, p < 0.001 for the disciform and cicatrical stages; r = +0.30, P < 95%). "Dry" AMD is characterized by hypertension-associated systemic and then local increase of EPA. In "wet" AMD it is the interferon response that is impaired: IFNalpha and IFNgamma are systemically decreased, while local level of IFNalpha is increased. Intraocular Herpes simplex infection is pathogenically significant for AMD development (18.8% in the study group vs 0% in the control group). CONCLUSION: AMD progression is associated with hypertension accompanied by chronic inflammation with predominantly intracellular localization of the infectious agent as well as impairment of the interferon response (systemic decrease of IFNalpha and IFNgamma with local increase of IFNalpha). Moreover, the presence of intraocular Herpes simplex infection leads to activation of the first line antiviral immunity (IFNgalpha) with decompensation of the local interferon response (IFNgamma).
