Tumour necrosis factor and interleukin 6 production during interaction between activated CD4+ lymphocytes and simian immunodeficiency virus-infected macrophages.

The mechanism for the gradual loss of CD4+ T lymphocytes and the development of the slowly progressive inflammatory/degenerative lesions that accompany human immunodeficiency virus infection are poorly understood. Using the Simian immunodeficiency virus (SIVmac) macaque model of AIDS, we found that persistently infected primary macrophages fuse with primary activated CD4+ lymphocytes and that this interaction results in production of tumour necrosis factor-alpha (TNF alpha) and interleukin 6 (IL-6). An earlier report had shown that SIV-infected macaque macrophages fuse with CEM174 cells (a human CD4+ cell line) and cause their lysis.

Ovine lentivirus is macrophagetropic and does not replicate productively in T lymphocytes.

The lentiviruses of sheep, goats, and horses cause chronic multiorgan disease in which macrophages are highly permissive for viral replication. Monocytes, which mature into macrophages, are thought to be latently infected with lentivirus, but the extent to which other leukocytes are infected is unknown. Dendritic cells have not been studied separately from monocytes and T-cell subsets have not been examined in previous attempts to identify infected cells in peripheral blood mononuclear cells (PBMC).

Human immunodeficiency virus infection in microglia: correlation between cells infected in the brain and cells cultured from infectious brain tissue.

In acquired immunodeficiency syndrome, the lesions of the central nervous system in association with the human immunodeficiency virus are thought to be related to an infection of microglia, although no studies are available in which cultured and physiological characteristics of microglia cells infected in vivo have been examined. In this report, we used brain tissue from a child dying of human immunodeficiency virus infection and show that microglia cells were the main cell population being infected. Moreover, isolated macrophage-like cells from fresh brain material revealed a close resemblance to peripheral blood macrophages in their content of surface and intracellular antigens.

Lentivirus induced arthritis in animals.

Retroviral arthritis in sheep and goats depends on persistent infection in the animals. Virus is latent in macrophage precursor cells and viral replication is initiated when these cells are induced to differentiate. Antiviral antibodies and cytokines modulate the efficiency of viral gene product expression.

Analysis of Borna disease virus-specific RNAs in infected cells and tissues.

Borna disease virus (BDV) is an infectious agent that causes profound disturbances in motor function and behaviour in a wide range of animal species and possibly humans. The infectious nature of BDV has long been established, but the aetiological agent has not been isolated or classified. Recently, we have reported the isolation of BDV-specific cDNA clones using subtractive libraries constructed from mRNA from infected material.

Molecular and immunopathological studies of borna disease virus infection in rats.

Borna disease virus is an agent distinct from all known viruses. Pathogenesis of its infection is also unique. This review highlights several aspects of the biology of this viral infection and the preliminary characterization of the agent.

Recovery of the simian immunodeficiency virus (SIV) and depression of colony formation in in vitro infected progenitor cell-enriched rhesus bone marrow (BM).

Rhesus progenitor-enriched BM was exposed overnight to SIV and cultured in a limiting dilution assay where the potential for progenitor interaction with lymphocytes or macrophages was low. Virus was consistently isolated late in culture, detection being aided by coculture with CEM174 lymphoblasts. Although infected cells had reduced clonogenic activity, colonies were indistinguishable from those derived from uninfected BM with respect to proliferative potential, morphology, and longevity in culture.

Rhesus monkey macrophages infected with simian immunodeficiency virus cause rapid lysis of CD4-bearing lymphocytes.

Inoculation of simian immunodeficiency virus into cultures of primary rhesus monkey macrophages or CD4-bearing transformed T lymphocytes resulted in persistent infection, with minimal virus replication in the macrophages and extensive replication in the lymphocytes. However, uninfected T cells added to infected macrophages underwent rapid fusion and lysis and were almost completely eliminated without the production of virus particles. Lysis required direct contact between the T cells and the infected macrophages, which enabled binding between CD4 on the former and viral gp120 on the latter to occur.

A borna virus cDNA encoding a protein recognized by antibodies in humans with behavioral diseases.

Borna disease virus (BDV) causes a rare neurological disease in horses and sheep. The virus has not been classified because neither an infectious particle nor a specific nucleic acid had been identified. To identify the genome of BDV, a subtractive complementary DNA expression library was constructed with polyadenylate-selected RNA from a BDV-infected MDCK cell line.

Physical studies on the membranes and lipids of plasmalogen-deficient Megasphaera elsdenii.

Membrane fluidity and thermotropic phase behavior in the wild-type and plasmalogen-deficient strains of Megasphaera elsdenii have been studied by means of diphenylhexatiene steady state fluorescence anisotropy in isolated membranes, and by 31P-NMR and X-ray diffraction of the isolated phospholipids. Compared to the wild-type plasmalogen content of greater than 75%, plasmalogen-deficient strains had less than 5% plasmalogen, consisting largely of phosphatidylethanolamine and phosphatidylserine. Steady state fluorescence anisotropy measurements yielded an order parameter which was 6% lower in the plasmalogen-deficient membranes from 10 degrees to 40 degrees C, indicating higher membrane lipid mobilities.

Lentiviruses are etiological agents of chronic diseases in animals and acquired immunodeficiency syndrome in humans.

Lentiviruses are species-specific, exogenously transmitted retroviruses that have a unique ability to replicate continuously but at a restricted rate in host tissues. This property is thought to be related to the retroviral nature of the replication process (RNA to DNA to RNA) and to the ability of the viruses to do this in cells of the macrophage lineage. The viral genomes are expressed only in certain populations of macrophages and this is dependent on a number of interactive factors including the genus of the host, the age of the host, maturation/differentiation factors in macrophages, the strain of virus and regulatory factors in the virus and the regulatory factors in the virus and the macrophages.

Preliminary studies on the biology of Borna disease virus.

Borna disease virus (BDV) is an unclassified agent that causes neurological disease in a wide range of animal species and possibly in humans. The infectious nature of BDV has been long established but, despite extensive progress on the pathogenesis of the infection, the aetiological agent is still uncharacterized. Recent studies have shown that BDV replicates productively in cultures of foetal rabbit glial cells (FRG) which produce a virus-specific protein that is easily detected immunocytochemically.

Evidence for interference, coinfections, and intertypic virus enhancement of infection by ovine-caprine lentiviruses.

The ovine-caprine lentiviruses share nucleotide homology and serological properties in their gag-pol genes and gene products but constitute two distinct biological groups represented by ovine visna virus of Icelandic origin and by caprine arthritis-encephalitis and ovine progressive pneumonia viruses of U.S. origin.

Astrocytes and Schwann cells are virus-host cells in the nervous system of rats with Borna disease.

Borna disease virus (BDV) replicates only in cells in the central (CNS) and peripheral (PNS) nervous system in adult rats. Infection of the nervous system is associated with a transient, intense mononuclear meningoencephalitis and immunemediated loss of BDV-infected neurons. The identification of BDV antigen in neurons and the accompanying immunologically-specific lysis of these cells led to the prediction that the CNS would be virus-free after the animal had recovered from encephalitis.

Modulation of lentivirus replication by antibodies. Non-neutralizing antibodies to caprine arthritis-encephalitis virus enhance early stages of infection in macrophages, but do not cause increased production of virions.

Non-neutralizing antibodies to caprine arthritis-encephalitis virus (CAEV) enhance the early stages of the virus life cycle but do not potentiate enhanced production of virus particles by macrophages. In primary macrophages used for these studies, there was enhancement in binding, internalization and uncoating of virus pretreated with non-neutralizing sera in comparison to virus pretreated with a non-immune serum. However, this did not lead to enhanced production of virus particles.

Pathogenesis of ovine lentivirus-induced arthritis: phenotypic evaluation of T lymphocytes in synovial fluid, synovium, and peripheral circulation.

Sheep and goats develop a chronic, progressive arthritis reminiscent of rheumatoid arthritis, but caused by lentiviruses related to human immunodeficiency virus. The distribution of T lymphocytes in peripheral circulation of two infected sheep with arthritis, one infected sheep with interstitial pneumonia, three asymptomatic sheep, and three uninfected sheep was evaluated. Sheep with clinical disease have depressed ratios of CD4/CD8 lymphocytes in peripheral circulation compared to asymptomatic and uninfected animals.

Lentivirus-induced interferon inhibits maturation and proliferation of monocytes and restricts the replication of caprine arthritis-encephalitis virus.

In this study, we investigated the effect of a lentivirus-induced interferon (LV-IFN) on the interaction of caprine arthritis-encephalitis virus and its host cell, the monocyte-macrophage. LV-IFN was produced in culture supernatant 48 h after adding fresh goat lymphocytes to caprine arthritis-encephalitis virus-infected goat macrophages. The culture supernatant contained IFN activity at a titer of 1:360 as assayed by inhibition of vesicular stomatitis virus-induced lysis of fibroblasts.

Modulation of lentivirus replication by antibodies: Fc portion of immunoglobulin molecule is essential for enhancement of binding, internalization, and neutralization of visna virus in macrophages.

Antibodies to visna virus neutralized the virus in fibroblasts and macrophages but specifically enhanced the binding, penetration, and uncoating of the virus in the latter cells. F(ab')2 fragments of the immune antibody neutralized the virus in fibroblasts but did not enhance the early stages of the virus life cycle in macrophages. Furthermore, these fragments did not neutralize infectivity in macrophages but delayed the appearance of infectious virus in cells after the inoculation of preincubated virus-F(ab')2 complexes.

Immunopathology of lentiviral infections in ungulate animals.

The immunopathogenesis of lentiviral lesions in sheep and goats requires continuous replication of the virus in tissues of the animal. This entails escape from various defense mechanisms of the host. Viral expression occurs mainly in tissue-specific macrophage populations and viral proteins produced by the cells induce and combine with antibodies to form immune complexes.

Neurotransmitter abnormalities in Borna disease.

Borna disease (BD) agent is an infectious pathogen that causes progressive central nervous system (CNS) dysfunction in a wide range of vertebrate hosts. The course of BD in adult rats is biphasic. The acute phase is characterized by aggressive behavior and inflammatory cell infiltrates in brain.