Prevalence of viremia in human immunodeficiency virus-infected patients with renal disease.

BACKGROUND: The prevalence of viremia and its relationship to the pathogenesis of nephropathy in human immunodeficiency virus (HIV)-infected patients with renal disease is unknown. To assess the prevalence of plasma viremia in HIV-infected patients with chronic renal disease, we performed a cohort study in two urban university medical centers. METHODS: Samples of blood from 11 HIV-infected patients with renal failure who were treated with hemodialysis were analyzed concurrently with control samples from three non-HIV-positive patients receiving hemodialysis treatment. Samples from four HIV-infected patients with chronic renal insufficiency were evaluated concurrently. Thirty-three HIV-infected patients with serum creatinine levels of less than 132 mumol/L (1.5 mg/dL), and trace or absent dipstick proteinuria served as controls for the population with renal disease. The patients infected with HIV were staged by CD4 cell counts and the presence of opportunistic infections. Blood samples were analyzed for plasma HIV p24 antigenemia by antigen capture enzyme-linked immunosorbent assay. Blood samples were analyzed for the presence of viremia by infection of normal stimulated peripheral blood mononuclear cell cultures with plasma samples and detection of HIV p24 antigen in culture supernatants. RESULTS: Two of the 11 patients treated with hemodialysis had evidence of HIV p24 antigenemia, while seven of the 11 had evidence of plasma viremia. The proportion of hemodialysis patients with detectable antigenemia and viremia was similar to that in patients with chronic renal insufficiency. A significantly greater proportion of HIV-infected patients with renal disease had plasma viremia and antigenemia, compared with HIV-infected patients without renal disease. In logistic regression analysis, race, CD4 cell count (either on a continuous scale or dichotomized at 0.2 x 10(9)/L), and treatment with zidovudine were not significantly associated with the presence of plasma viremia, but patient age and the presence of renal disease were factors independently associated with viremia. CONCLUSIONS: The similar proportions of HIV-infected patients with viremia in groups of patients with chronic renal insufficiency and with renal disease treated with hemodialysis suggest that dialysis treatment does not increase the prevalence of plasma viremia in HIV-infected patients with renal disease. The similar proportions of HIV-infected hemodialyzed patients and patients with chronic renal insufficiency with plasma viremia, and the greater prevalence of viremia in patients with renal disease compared with HIV-infected patients without clinical renal disease suggest that plasma viremia and renal dysfunction are related. Whether this represents a cause and effect relationship is unknown. The greater prevalence of viremia in HIV-infected patients with renal disease has implications for the pathogenesis of HIV-related renal diseases and for caregivers in clinical settings and dialysis units.

Detection of a feline X-linked antigen in somatic cell hybrids. Single-cell analysis using monoclonal antibodies.

We tested the premise that monoclonal antibodies to either intracellular or membrane antigens can greatly facilitate the construction of linkage maps of mammals whose chromosomes can be introduced into rodent cells. Monoclonal antibodies against antigenic determinants of cat lymphocytes and fibroblasts were used to analyze feline antigen expression in cat-mouse somatic cell hybrid populations selected to contain the X-linked feline HPRT locus. The frequency of antigen expression as measured by fixed cell immunofluorescence (IF) assays, varied greatly within hybrid populations for all but the antigen designated as VP382. Its frequent presence in hybrid cells led to the prediction, confirmed by 8-azaguanine selection experiments, that its expression was controlled by a gene, or genes, on the feline X chromosome. The antigens identified by the rest of the antibodies segregated independently of each other in cat-mouse somatic cell hybrids and their expression appeared to be controlled by autosomal genes of the cat.

Feline oncornavirus-associated cell membrane antigen: a viral and not a cellularly coded transformation-specific antigen of cat lymphomas.

The feline oncornavirus-associated cell membrane antigen (FOCMA) was defined as a tumor antigen common to cat lymphomas and fibrosarcomas induced by feline leukemia virus (FeLV) and feline sarcoma virus (FeSV), respectively. The antigen was recognized by sera from cats thought to be resistant to leukemogenesis. We report here that a common denominator in the activity of naturally occurring viremic cat antisera to FOCMA is, in fact, their reactivity to FeLV C antigenic determinants. The cat antisera, monoclonal antibodies to FOCMA, and monoclonal antibodies to FeLV C, all reacted in immunofluorescence assays with FeLV C-infected cells and immunoprecipitated a molecule electrophoretically indistinguishable from envelope glycoprotein of FeLV. Viremic cat antisera to FOCMA bound to budding virus particles of FeLV C-infected cells, even though some of them could not be absorbed by mature virion proteins. Thus, the unusual feature of cat antibodies to FOCMA is their binding to nascent but not to mature virus particles. FOCMA-positive cat lymphomas expressed antigenic determinants of FeLV-C gp70, with or without productive infection. FeLV-negative tumors not expressing FeLV C gp70 were also FOCMA negative. Furthermore, most of the viremic cat sera and the monoclonal antibodies to FOCMA did not react with FeSV-transformed nonproducer cells. The absence of FOCMA from these cells and from FeLV-negative lymphoid tumors and its presence in FeLV-C infected fibroblasts indicated that this antigen is virus encoded and not a cellular tumor-specific antigen.

Linkage relationships and chromosome assignment of four esterase loci in the mosquito Anopheles albimanus.

Although anopheline mosquitoes are important vectors of malaria, their genetic makeup has not yet been extensively investigated. The present studies concentrate on the genetic basis of esterases in Anopheles albinomanus. Nine zones of esterase activity activity have been resolved by gel electrophoresis. Four of these esterases: EST-2, EST-4, EST-6, and EST-8 are present throughout all developmental stages and also posess allelic variation. Mass matings were carried out with homozygous males and females heterozygous for two or more loci. The analyses of the progeny from single egg batches revealed that the four esterase systems mentioned above are encoded in separate loci with codominant allels. Analyses of two-point and three-point crosses have indicated the following linkage relationships: Est-8--12%--Est-4--22%--Est-2--9%--Est-6. The assignment of this linkage group to chromosome 3 has been accomplished by the use of a Y-2 chromosome translocation.