After treatment for primary or secondary syphilis, the HIV-infected patients responded less well serologically than the patients without HIV infection, but clinically defined failure was uncommon in both groups. Enhanced treatment with amoxicillin and probenecid did not improve the outcomes. Although T. pallidum was detected in cerebrospinal fluid before therapy in a quarter of the patients tested, such a finding did not predict treatment failure. The current recommendations for treating early syphilis appear adequate for most patients, whether or not they have HIV infection.

Phase I studies of volunteers not infected with human immunodeficiency virus type 1 (HIV-1) have shown that immunization with envelope subunit vaccine products elicits antibodies that neutralize laboratory-adapted (prototype) HIV-1 strains in vitro. Prototype strains are adapted to grow in continuous (neoplastic) cell lines and are more susceptible to neutralization than are primary isolates cultured in human peripheral blood mononuclear cells. In this study, 50 sera from nine phase I vaccine trials and 16 from HIV-1-infected persons were evaluated for neutralizing antibody activity against 3 laboratory-adapted and 5 primary HIV-1 isolates. Of 50 sera, 49 neutralized at least 1 of the prototype strains; however, none displayed neutralizing activity against primary isolates of HIV-1. Serum from most HIV-1-infected persons neutralized both laboratory-adapted and primary HIV-1 isolates. These data demonstrate a qualitative, or large quantitative, difference in the neutralizing antibody response induced by envelope subunit vaccination and natural HIV-1 infection.

Because stimulation of CD4+ lymphocytes leads to activation of human immunodeficiency virus-type 1 (HIV-1) replication, viral spread, and cell death, adoptive CD4+ T cell therapy has not been possible. When antigen and CD28 receptors on cultured T cells were stimulated by monoclonal antibodies (mAbs) to CD3 and CD28 that had been immobilized, there was an increase in the number of polyclonal CD4+ T cells from HIV-infected donors. Activated cells predominantly secreted cytokines associated with T helper cell type 1 function. The HIV-1 viral load declined in the absence of antiretroviral agents. Moreover, CD28 stimulation of CD4+ T cells from uninfected donors rendered these cells highly resistant to HIV-1 infection. Immobilization of CD28 mAb was crucial to the development of HIV resistance, as cells stimulated with soluble CD28 mAb were highly susceptible to HIV infection. The CD28-mediated antiviral effect occurred early in the viral life cycle, before HIV-1 DNA integration. These data may facilitate immune reconstitution and gene therapy approaches in persons with HIV infection.

To determine the cause of the acute urethral syndrome, we studied 59 women with dysuria and frequent urination without "significant bacteriuria" (defined as greater than or equal to 10(5) organisms per milliliter), 35 women with typical cystitis and 66 women with no symptoms of urinary-tract infection. Although none of the 59 women with urethral syndrome had greater than 3.4 x 10(4) bacteria per milliliter in either of two successive midstream urine specimens, samples of bladder urine obtained by suprapubic aspiration or catheterization from 24 women contained coliforms, and samples from three contained Staphylococcus saprophyticus; all but one of these 27 women also had pyuria. Of the 32 women with sterile bladder urine, 10 of 16 with pyuria and one of 16 without pyuria were infected with Chlamydia trachomatis (P = 0.002). Chlamydial infection was found in 11 of 42 women with urethral syndrome and pyuria, in three of 66 without symptoms, and in one of 35 with cystitis (P less than 0.01 when the group with urethral syndrome is compared with either of the other groups). Thus, 42 of 59 women with urethral syndrome had abnormal pyuria and 37 of these 42 were infected with coliforms, S. saprophyticus, or C. trachomatis, whereas few women without pyuria had demonstrable infection. Bacteriuria of greater than or equal to 10(5) per milliliter may be an insensitive diagnostic criterion when applied to symptomatic lower-urinary-tract infection.