Successful coronary artery bypass surgery in a patient with AIDS.

We report the case of a 47-year-old man with AIDS who underwent a successful quadruple coronary artery bypass operation. The improving prognosis of patients with HIV/AIDS, in addition to the reported incidence of plasma lipid abnormalities in patients receiving protease inhibitors, are laying the groundwork for a larger population in which premature coronary artery disease develops. Operative risk, immunosuppressive effect of cardiopulmonary bypass, and practical considerations in the care of these patients are discussed.

Misdiagnosis of HIV infection by HIV-1 plasma viral load testing: a case series.

BACKGROUND: The availability of sensitive assays for plasma HIV viral load and the trend toward earlier and more aggressive treatment of HIV infection has led to the inappropriate use of these assays as primary tools for the diagnosis of acute HIV infection. OBJECTIVE: To describe limitations in the use of plasma viral load testing for the diagnosis of HIV infection. DESIGN: Case series. SETTING: Academic medical centers in Providence, Rhode Island, and Worcester, Massachusetts. PATIENTS: Three persons in whom HIV infection was falsely diagnosed by plasma viral load testing. MEASUREMENTS: Laboratory measures and clinical outcomes. RESULTS: Two cases of false-positive results obtained by using branched-chain DNA plasma viral load assays and one case of a false-positive result obtained by using reverse transcriptase-polymerase chain reaction plasma viral load assay are reported. All three plasma viral load tests yielded positive results with low values (1254 copies/mL, 1574 copies/mL, and 1300 copies/mL). Infection with HIV was initially diagnosed in all three patients, but each patient subsequently tested negative by HIV-1 enzyme-linked immunosorbent assay and repeated plasma viral load testing. CONCLUSION: Physicians should exercise caution when using plasma viral load assays to detect primary HIV infection, particularly when the pretest probability of infection is low.

Acute gonococcal sepsis in an HIV-infected woman.

This is a case report of a 35-year-old woman infected with the human immunodeficiency virus who presented with acute bacterial sepsis that proved to be secondary to Neisseria gonorrhoeae. Typical skin and joint findings developed only after the acute sepsis had resolved. Patients with disseminated gonococcal infection rarely have signs of acute bacterial sepsis. This case raises the question of whether HIV-infected patients are at an increased risk of contracting severe gonococcal disease.

Poorly differentiated non-small cell carcinoma of the lung in acquired immunodeficiency syndrome.

Case of a 33-year-old female with AIDS who presented with fevers, chills, lower back pain and a large right hilar mass. Biopsy of the right paratracheal nodes revealed poorly differentiated non-small cell carcinoma with extensive necrosis. In patients infected with HIV the incidence of primary lung carcinoma is unknown. Despite these uncertainties, primary lung carcinoma must be considered in the differential diagnosis of young HIV-infected individuals presenting with intrathoracic radiographic abnormalities.

Neuraminidase augments Fc gamma receptor II-mediated antibody-dependent enhancement of dengue virus infection.

Antibody-dependent enhancement (ADE) of dengue virus infection occurs when neutralizing antibodies at sub-neutralizing concentrations or non-neutralizing antibodies form complexes with the virus. These virus-antibody complexes can then attach to a Fc gamma receptor-bearing cell, via the Fc portion of the immunoglobulin, resulting in an increased number of infected cells. ADE may be responsible in part for the most severe clinical manifestations of dengue virus infection which include haemorrhage and shock. Three classes of human Fc gamma receptors exist, Fc gamma RI, Fc gamma RII and Fc gamma RIII. In this study, we examined the effects of neuraminidase on ADE of dengue virus infection mediated by the low-affinity Fc gamma RII. K562 cells, which express only Fc gamma RII, treated with neuraminidase resulted in augmentation of ADE of dengue virus infection by human anti-dengue antibodies. This augmented ADE of infection could be blocked by anti-Fc gamma RII monoclonal antibody IV.3. Incubation of neuraminidase-treated K562 cells with IgG-coated human red blood cells resulted in an increase in the percentage of rosette formations compared with the untreated K562 cells. A bispecific antibody directed against Fc gamma RII and dengue virus (IV.3 x 2H2) enhanced virus infection. Neuraminidase also augmented ADE mediated by this antibody, but to a much lesser degree (by 50%) compared with that seen using conventional human anti-dengue antibody (by 200 to 300%). Fluorescence-activated cell sorting analysis of neuraminidase-treated K562 cells showed that the number of Fc gamma RII-specific antibodies that bind to Fc gamma RII increases by 15 to 20% after treatment with neuraminidase. These results indicate that neuraminidase augments ADE of dengue virus infection and that the augmented ADE is mediated through Fc gamma RII.

Antibody-dependent enhancement of dengue virus infection mediated by bispecific antibodies against cell surface molecules other than Fc gamma receptors.

It is known that antibodies to dengue viruses at subneutralizing concentrations enhance dengue virus infection of Fc gamma R+ cells. This phenomenon called antibody-dependent enhancement (ADE) occurs when virus-antibody complexes bind to the Fc gamma R via the Fc portion of the Ig. It has been hypothesized that ADE may be responsible for the pathogenesis of the severe manifestations of dengue virus infection including dengue hemorrhagic fever/dengue shock syndrome. To further analyze the mechanisms of ADE, we prepared bispecific antibodies by chemically cross-linking antidengue virus antibodies to antibodies specific for Fc gamma RI or Fc gamma RII and the non-Fc R molecules beta2 microglobulin, CD15 or CD33 and examined whether these bispecific antibodies could enhance infection. Bispecific antibodies targeting dengue virus to Fc gamma RI or Fc gamma RII enhanced dengue virus infection, consistent with previous reports using conventional antibodies. Furthermore, bispecific antibodies targeting dengue virus to beta2 microglobulin, CD15 or CD33 also enhanced dengue virus infection. Bispecific antibody mediated ADE was inhibited by pretreating the cells with the appropriate blocking mAb. These results indicate that cell surface molecules other than Fc gamma R can mediate ADE and suggest that the Fc gamma R does not provide a unique signal necessary for enhanced infection. We hypothesize that directing dengue virus to the cell surface by a bispecific antibody facilitates the interaction between dengue virus and its receptor, thereby increasing its infectivity.