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Human herpesvirus-6 (HHV-6) and human immunodeficiency virus (HIV) are both tropic for CD4+ lymphocytes. To determine whether HHV-6 infection affects the susceptibility to or the course of HIV infection, HHV-6 titers were measured by an anticomplement immunofluorescence assay in serum of three groups of homosexual or bisexual men: (1) those with AIDS (n = 78), (2) those with HIV-associated lymphadenopathy (LAS; n = 81), and (3) those who were HIV-seronegative (n = 55). Early and late serum samples were available for 45 men with LAS (median interval 49 months). Men with early LAS did not differ from HIV-seronegative men in either the percentage that were HHV-6-seropositive or in the distribution of titers. There was a significantly lower percentage of seropositives in AIDS patients than in the other two groups (P less than .01). LAS patients who progressed to AIDS did not differ in percentage seropositivity or distribution of titers from nonprogressors. HHV-6 titers tended to decrease over time. HHV-6 titers late in LAS were similar to those in AIDS patients. These findings suggest that it is unlikely that previous exposure to HHV-6 either predisposes to or affects the course of HIV infection.

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Changes in immunologic parameters were followed in members of a cohort of human immunodeficiency virus (HIV)-positive homosexual or bisexual men with lymphadenopathy and were analyzed for differences between those who have and those who have not progressed to the acquired immunodeficiency syndrome (AIDS) (progressors, nonprogressors). T helpers and the Th/Ts ratio were lower in progressors than in nonprogressors both at entry into the study and at the latest visit. T suppressors were not different in the two groups at entry but were higher in nonprogressors at the latest visit. Evaluation of the patterns of change over time showed that T helpers and Th/Ts ratios tended to decrease over time in both nonprogressors and progressors, while T suppressors increased in nonprogressors and decreased in progressors. Although progressors had a greater deterioration in immunologic parameters over time, nonprogressors also had significant deterioration when compared with controls. Based on the respective percentages of men with abnormal or normal T helpers or Th/Ts ratio at entry who have already progressed to AIDS, we would conservatively estimate, considering their latest T helpers and Th/Ts ratio, that at least an additional 16 (32%) of our nonprogressors will develop AIDS in the next 5 years.

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Seventy-five homosexual men with generalized lymphadenopathy for at least three months (lymphadenopathy syndrome [LAS]), subsequently shown to be seropositive for antibody against human immunodeficiency virus, were enrolled in a prospective study in Atlanta in 1982 and 1983. As of Nov 30, 1987, twenty-two (29%) of the 75 were known to have developed acquired immunodeficiency syndrome (AIDS) three to 60 months after enrollment and five to 69 months after onset of LAS. The six-year cumulative incidence of AIDS, by Kaplan-Meier survival analysis, was 38%. The cumulative incidence in years 4, 5, and 6 (30%) was significantly higher than in years 1, 2, and 3 (11%), suggesting that the risk for AIDS increases after the third year of LAS and that many more study participants will eventually develop AIDS. A precipitous decline in the T-helper cell count frequently heralds the diagnosis of AIDS; this decrease appears to occur at different times after the onset of LAS in different persons. The four-year cumulative incidence of AIDS following observations of T-helper cell counts less than 200/mm3, 200 to 299/mm3, 300 to 399/mm3, and 400/mm3 or greater was 84%, 41%, 25%, and 18%, respectively; these data are important for determining prognosis in the individual patient as well as for determining the suitability of candidates and baseline data for drug trials.

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A micromethod for assaying the reverse transcriptase enzyme of human T-cell lymphotropic virus type III/lymphadenopathy-associated virus in cocultures of clinical specimens for viral isolation was developed and compared with the macromethod in use. Ultracentrifuged, pelleted, and solubilized viral culture supernatants were transferred into either tubes (macromethod) or microtiter plates (micromethod) and incubated with tritiated enzyme substrate. Trichloroacetic acid-precipitated DNA was collected on individual filter papers with a Millipore filtration manifold (macromethod) or on filter sheets using a semiautomated cell harvester (micromethod). Filters were then placed in scintillation fluid and counted on a beta scintillation counter. Results of the micromethod significantly correlated to those of the macromethod, with a linear relationship between the two. The cutoffs for positivity based on the mean + 2 standard deviations for a set of known negative specimens (n = 19) was 4,973 cpm for the micromethod compared with 5,336 for the macromethod. The intrarun and interrun variations were comparable for both methods. There was a 67% increase in the maximal daily number of specimens which could be run (100 versus 60) as well as a reduction in reagent use. In summary, the micromethod utilizing a semiautomated cell harvester is comparable to the existing macromethod in accuracy and is an improvement due to savings in time and reagents.

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We compared recipients of eight lots of factors VIII and IX voluntarily withdrawn from distribution because one donor was known to have subsequently developed the acquired immunodeficiency syndrome with a nonexposed cohort matched by age, sex, and factor use. The factor VIII recipient cohorts did not differ in prevalence of antibody to human immunodeficiency virus (HIV) (exposed, 75%; nonexposed, 86%), T-cell subset numbers (median: exposed, 619 T-helper cells per cubic millimeter; nonexposed, 659 T-helper cells per cubic millimeter), T-helper to T-suppressor ratios, or immunoglobulin levels. Exposed individuals had higher levels of immune complexes by C1q binding and staphylococcal binding assays and lower responses to phytohemagglutinin and concanavalin A. However, only the staphylococcal binding assay values were outside the normal range for our laboratory. Factor IX recipient cohorts did not differ in HIV antibody prevalence (exposed, 30%; nonexposed, 40%) or any immune tests. Although exposed and nonexposed individuals did not differ from each other in a clinically meaningful fashion at initial testing, both the exposed and nonexposed cohorts had high rates of HIV seroprevalence. Market withdrawals were clearly insufficient means of limiting the spread of HIV in hemophilic patients; however, the currently available methods of donor screening and viral inactivation of blood products will prevent continued exposure within this population.

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The DNA of a papovavirus associated with budgerigar fledgling disease was purified and cloned into plasmid pBR322. The genome was circular and approximately 5.1 kilobases long. Physical mapping of the genome with restriction endonucleases revealed little similarity to simian virus 40 or polyomavirus DNA. Transformation trials using murine 3T3 cells were negative. Attempts to characterize proteins were unsuccessful due to the apparent close association of the virus and host cell components.

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An upper respiratory condition that resulted in 20% mortality in a flock of yellow-naped Amazon parrots was apparently caused by a concomitant infection of mycoplasmas and bacteria. Mycoplasma gallisepticum (MG), M. iowae, and an unidentified mycoplasma were isolated from the affected parrots. Budgerigars were experimentally infected with a parrot strain of MG designated MG(P) 1669 as well as with the R strain of MG and the F10-2 strain of M. synoviae (MS). Air-sac lesions were evident in all groups of challenged budgerigars, and MS and MG were cultured from the tracheas, air sacs, and lungs of the budgerigars up to 5 weeks postexposure. Serological findings were ambiguous and therefore considered unreliable. White leghorn and commercial broiler chickens challenged with the MG(P) 1669 isolate did not exhibit any significant air-sac lesions relative to the controls. However, MG was cultured from both groups of experimentally infected birds. Eight weeks after exposure, the white leghorns were seropositive to all MG antigens used in the agglutination test.

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Morphological changes induced by a newly described avian virus in budgerigar (Melopsittacus undulatus) tissues were examined with light and electron microscopes. Infected cells viewed with the light microscope were found to have enlarged nuclei containing marginated chromatin. Cytoplasmic contents were frequently clear in appearance. Tissues affected included skin, feather, follicle, kidney, uropygial gland, crop, lung, liver, heart, bone marrow, spleen and brain. Serum from infected birds contained viral particles. No tumours were found in affected birds. Electron microscopy demonstrated viral particles that were naked, predominantly icosehedral, and 42-49 nm in diameter. Occasional elongate forms of the virions were seen in kidney tissue. Small groups of virions were occasionally enclosed within nuclear and cytoplasmic membranes. Viral particles were observed in chicken embryo fibroblast cultures 18 hours post-inoculation. The particles first appeared in swollen nuclei and subsequently were found in the cytoplasm of more senescent cells. Cytoplasmic disruption and swollen rough endoplasmic reticulum were also observed in infected cells. Negatively stained preparations of the fluid from infected chicken embryo fibroblast cultures contained typical cubic viral particles as well as elongate forms similar to those seen in excised tissue preparations.

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A virus suspected of causing high death rates in fledgling budgerigars in Georgia and Texas aviaries was isolated in budgerigar embryo fibroblasts inoculated with tissue homogenates from affected birds. Virus was most easily recovered from tissues containing many intranuclear inclusion bodies. Cytopathic effect on fibroblasts of all four isolates was characterized by a swollen nucleus followed by rounding and detachment of the affected cell from the monolayer. Properties suggesting the B-931 isolate belongs to the papovaviridae family are (1) presence of DNA; (2) insensitivity to treatment with CHCl3; and (3) presence of cubic viral particles 42 to 49 nm in diameter in the nucleus of infected chicken embryo fibroblasts. The isolate did not hemagglutinate erythrocytes of chickens, turkeys, budgerigars, guinea pigs, or type O humans and was basically stable against heating and freeze-thawing. An examination of fledgling budgerigars from infected aviaries demonstrated that sick birds carried more virus than healthy birds.

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Fledgling budgerigars from aviaries in Georgia and Texas were reported to have high rates of mortality. Affected birds died acutely and exhibited abdominal distention and reddening of the skin. Postmortem lesions were hydropericardium, enlarged heart and liver with areas of necrosis, and swollen, congested kidneys. Histologic examination of a variety of tissues revealed cells with enlarged nuclei containing inclusions. Electron micrographs revealed the presence of viral particles 42 to 49 nm in diameter in the nuclei of epithelial cells of the renal tubule.

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