C Rochat1, B S Polla, C P Herbort. 1. Department of Ophthalmology, Hôpital Jules Gonin, University of Lausanne, Switzerland.
Abstract
PURPOSE: Acute retinal necrosis (ARN) is a newly recognized disease caused by human commensal viruses of the herpes family (herpes simplex virus, varicella-zoster virus and cytomegalovirus) occurring in apparently immunocompetent patients. As at least three viruses can cause ARN, the modification in the host-virus interaction at the origin of the disease most probably comes from the host. A review of 216 reported cases of ARN showed that there were signs of impaired cellular immunity in 16% of these cases. The purpose of this study was to investigate immune parameters in ARN. METHODS: In nine HIV-negative ARN patients who were not under steroid or immunosuppressive therapy, the following prospective immunological investigations were performed: (1) skin testing for delayed-type hypersensitivity to seven common antigens (Candida, diphtheria, purified protein derivative tuberculin Proteus, Streptococcus, tetanus, Trichophyton); (2) lymphocytic proliferative responses in vitro to these antigens and to three mitogens; (3) determination of blood lymphocyte sub-populations by flow cytometry. RESULTS: Cutaneous anergy was found in five of seven tested cases. The lymphocyte proliferative index was less than 20% of the index of a control group for all antigens in three of nine cases, and for three or more antigens in eight of nine cases. In eight of nine cases there was a relative increase of B-lymphocytes, and in seven of nine cases B-lymphocytes were also increased in absolute numbers. In all nine cases one or more of these parameters were abnormal. CONCLUSION: Our findings suggest that ARN may develop in association with an imbalance of the immune system characterized by an impaired cellular response and/or a maintained or increased humoral response.
PURPOSE:Acute retinal necrosis (ARN) is a newly recognized disease caused by human commensal viruses of the herpes family (herpes simplex virus, varicella-zoster virus and cytomegalovirus) occurring in apparently immunocompetent patients. As at least three viruses can cause ARN, the modification in the host-virus interaction at the origin of the disease most probably comes from the host. A review of 216 reported cases of ARN showed that there were signs of impaired cellular immunity in 16% of these cases. The purpose of this study was to investigate immune parameters in ARN. METHODS: In nine HIV-negative ARN patients who were not under steroid or immunosuppressive therapy, the following prospective immunological investigations were performed: (1) skin testing for delayed-type hypersensitivity to seven common antigens (Candida, diphtheria, purified protein derivative tuberculin Proteus, Streptococcus, tetanus, Trichophyton); (2) lymphocytic proliferative responses in vitro to these antigens and to three mitogens; (3) determination of blood lymphocyte sub-populations by flow cytometry. RESULTS:Cutaneous anergy was found in five of seven tested cases. The lymphocyte proliferative index was less than 20% of the index of a control group for all antigens in three of nine cases, and for three or more antigens in eight of nine cases. In eight of nine cases there was a relative increase of B-lymphocytes, and in seven of nine cases B-lymphocytes were also increased in absolute numbers. In all nine cases one or more of these parameters were abnormal. CONCLUSION: Our findings suggest that ARN may develop in association with an imbalance of the immune system characterized by an impaired cellular response and/or a maintained or increased humoral response.