Introduction: At the Public Health Center of Chiba City, HIV/AIDS counseling by a clinical psychologist has been conducted since 1993. The contents of counseling are divided into such categories as antibody test counseling (pre-test and post-test), telephone counseling of the general public, HIV carrier/AIDS patient counseling (including family of patients), and local community sponsored psychological education to promote precaution. In this study, we tried to evaluate the necessity and effectiveness of counseling conducted by a clinical psychologist at the antibody test phase.
Methods: The characteristics of 346 counseling cases at the health center were analyzed. In addition, we tried to verify the effectiveness of counseling through interviews.
Results: About 20% of the clients had an exceedingly high level of anxiety. The level declined after counseling on the test day.
Conclusion: It was proved that counseling conducted by a clinical psychologist at the health center has the following effectiveness: (1) Reduces the anxiety level of highly anxious clients, (2) Deals with clients with psychological problems and/or AIDS related neurosis, and (3) Counseling Facilitates a behavioral change in less critical clients.
In the future, it is recommended that clinical psychologists be assigned to public health centers located around the metropolitan areas, so they can conduct counseling.

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Objective: Opportunistic infections which occur in HIV-infected patients are also seen in hematological disorders such as multiple myeloma and malignant lymphoma. To assess the difference in perturbation in T-cell subsets, we evaluated CD4 subsets in both diseases. In addition, changes in increased CD4 T-cell subsets by anti-retroviral therapy in HIV-infected patients were analyzed.
Method: PBMCs of 17 HIV-infected patients, 10 multiple myeloma (MM) patients and 9 malignant lymphoma (ML) patients were FACS scanned by two-color immunofluorescence analysis with monoclonal antibodies against CD4, CD8, CD45 RA, CD45 RO, CD 25 and HLA-DR.
Results: In HIV-infected patients, memory cells (CD4+ CD45 RO+) and naive cells (CD4+ CD45 RA+) were well preserved except in the patients with extremely low CD4 cells. On the contrary, in MM and ML patients, memory CD4 cells were well preserved while naive CD4 cells were obviously depleted even in patients with high CD4 cell counts. CD8 cell numbers were correlated with CD4 cell numbers more strongly in MM and ML patients than in HIV-infected patients. Other CD4 subset patterns were not different in among patients. After anti-retroviral therapy, a rise in CD4 cells observed in 8 HIVinfected patients was found to reflect a rise in memory CD4 cells. The increase in naive CD4 cells was very slow, or was not found in some cases.
Conclusion: Decreased naive CD4 cells and reciprocally high memory CD4 cells in MM and ML patients were observed. In HIV-infected patients, both memory and naive CD4 cells were equally impaired but early restoration of memory CD4 cells might be expected by anti-retroviral therapy. An increase in naive CD4 cells seemed to play an important role in the remission of opportunistic infections.

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Objective: To examine if the intracellular HIV-1 envelope protein (Env) can be trapped by an intracellular chimeric CD4.
Material & Methods: We previously reported a mutant Friend murine leukemia virus Env, FCR, whose intracellular transport was inhibited. Here, a chimera consisting of a surface domain of CD4 and a C-terminal two-thirds of FCR was constructed. HeLa cells expressing the CD4-FCR were transfected with an infectious HIV-1 clone DNA, pNL4-3, and the processing of HIV-1 Env was examined.
Results: Intracellular transport of the CD4-FCR chimera to the cell surface was inhibited as was FCR. When the CD4-FCR-expressing HeLa cells were transfected with pNL4-3, the processing of HIV-1 Env and the infectious HIV-1 production were inhibited. Immunoprecipitation analysis showed binding of the CD4-FCR to the unprocessed HIV-1 Env.
Conclusion: These results suggest that HIV-1 Env could be trapped by the intracellular CD4 in the chimera.

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Introduction: A male patient with high fever and respiratory distress visited a town clinic and was diagnosed to be suffering from AIDS (by CDC criteria).
Case presentation: He was 28yr old and had donated blood 3yr earlier, when an anti-HIV test was negative. His chest XP showed interstitial pneumonia. His WBC was 22, 500/μl and CD4 was 35/μl. He had normocytic anemia (Hb 10.5g/dl). Anti HIV test was positive and his HIVRNA level was 1.6×10⁵ copies/liter. He was transferred to the Hokkaido University Hospital and treated with AZT, ddI and IDV for AIDS and many drugs for pneumonia, but treatment was in vain, and he died 6 months later. An autopsy revealed desquamative interstitial pneumonia, cerebral hemorrhage, fatty liver and pericarditits.
Discussion: It was shown that this patient progressed to AIDS in a short period of time. There are several factors relating to disease progression. In this case, the subtype of HIV was B and E, and the virus load was rather large.
Conclusion: This case report suggests the importance of recognition that there could be AIDS patients in ordinary clinic settings. On the other hand, it has been shown that donor interviews at blood centers to prevent window-phase infection of HIV is very important, although actual window-phase infection has been reported only once so far.

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