To determine the incidence of B19 infection in patients with AIDS who were being treated with dideoxyinosine, serial sera (n = 28) taken over a 2-year period from 14 individuals were analyzed with respect to anti-B19 serology and the presence of B19 DNA. All 14 individuals were anti-B19 IgM negative. Nine of 14 had B19 viremia by Southern analysis of polymerase chain reaction product. Five of 9 with B19 viremia had > or = 1 anti-B19 IgG-positive sample; none of 5 without viremia had anti-B19 IgG. Four of 9 viremic individuals had serially positive samples. All 4 had severe anemia (hemoglobin < 8.5 g/dL) while taking zidovudine. A fifth individual whose severe anemia resolved after zidovudine was discontinued did not have B19 viremia. Therefore, a significant proportion of this group of patients with AIDS who developed severe anemia while receiving zidovudine had persistent B19 infection. These results suggest that B19 infection should be considered in anemic patients with AIDS.

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Serum specimens which originally exhibited a narrow (indeterminate) 24-kilodalton core protein (p24) or p24/p55 pattern of reactivity with human immunodeficiency virus (HIV) in the Western blot (immunoblot) test were studied to gather information on antibody specificity. A total of 12 specimens were initially reevaluated with an indirect immunofluorescence assay (IFA), three enzyme-linked immunosorbent assays (ELISAs), and Western blot analyses. Five of the specimens were IFA positive and contained anti-gp160/gp120 antibodies which were observed only when an HIV Western blot antigen rich in gp160 and gp120 was used. The remaining seven serum specimens were nonreactive by IFA and showed variable reactivity in HIV antibody ELISAs. The specimens did not cross-react with core antigens for human T-cell leukemia virus types 1 and 2 or contain detectable levels of HIV p24 antigen. The p24/p55 reactivity of six of the seven indeterminate specimens could be reduced or eliminated by preincubating the specimens with disrupted, HIV-infected H9 cells but not with uninfected H9 cells. The six specimens also exhibited discernible reactivity with recombinant HIV p24 antigen. When an additional 23 indeterminate specimens were assayed, all of the serum specimens were nonreactive by IFA while 65% (15 of 23) showed various degrees of reactivity with the recombinant p24 protein. There was no indication that any of the HIV core antibody reactivity was caused by HIV infection. Indeterminate results for five patients with specific p24 reactivity, who were retested after a period of weeks or months, remained indeterminate for HIV antibody with no significant change in ELISA or Western blot reactivity.

Human cytomegalovirus induced beta interferon in cultures of human foreskin cells. The inhibitor was first released between 8 and 16 hours after infection, about 48 hours before progeny virus. In cultures infected with low concentrations of virus, interferon was produced as the infection spread, and then in amounts larger than expected. After infection with cytomegalovirus, cells which had been primed for 48 hours with purified beta interferon produced significantly more interferon than unprimed cells, and the interferon was produced earlier, between 2 and 8 hours after infection. CMV-induced interferon also was able to prime cells. The data suggest that the relatively large quantities of interferon detected in cultures infected with low concentrations of cytomegalovirus result from endogenous priming: those cells infected early first produce interferon which primes uninfected cells, then virus which induces the primed cells to produce interferon in relatively high concentrations.

The presence of immunoglobulin G receptors in human fibroblasts infected with human cytomegalovirus (CMV) resulted in a nonspecific cytoplasmic reaction in the indirect fluorescent-antibody test. Both CMV antibody-positive and antibody-negative sera from human or other animal species produced the cytoplasmic reaction. The substitution of a simian CMV strain for the human virus successfully eliminated this cytoplasmic reaction and, thus, allowed for the observation of virus-induced fluorescent intranuclear inclusions. With the latter system, CMV antibody titers in human sera were equivalent to those obtained by using the human virus and, in addition, allowed for the detection of relatively low-titered serum samples in which antibody measurement was difficult when human CMV-infected cells were used in the indirect fluorescent-antibody test.

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An evaluation of selected commonly used procedures for the recovery of endogenous viral contaminants in bovine serum was undertaken. Low speed centrifugation (25,000 x g) was found to be efficient for the recovery of bovine herpesvirus type 1 (BHV-1) and parainfluenza virus type 3 (PI-3) in bovine serum. Decreased infectivity titers were obtained when parainfluenza virus type 3, and to a lesser extent bovine herpesvirus type 1, were concentrated using high speed centrifugation (100,000 x g) for extended time periods. In neither case could infectious virus be recovered from serum containing sufficient titers of homologous neutralizing antibody, although electron microscopy examination revealed the presence of the viruses previously added. In the presence of homologous antibody, virus particles appeared to have a diffuse, poorly defined outer membrane. Neutralizing antibody titers to bovine herpesvirus type 1 and parainfluenza virus types were found in fetal, calf, and adult bovine sera. The prevalence and magnitude of the antibody titers to these viruses increased with the age of the animals examined.