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Biomedical subjects

A Simmons

Publications and source records attributed to A Simmons.

10 recordsLinked to original sources
PubMed1992

Anti-CD8 impairs clearance of herpes simplex virus from the nervous system: implications for the fate of virally infected neurons.

The role of CD8+ T cells in resistance to herpes simplex virus (HSV) was examined. After cutaneous inoculation, HSV spreads to the peripheral nervous system (PNS) where it replicates in ganglionic neurons. In normal mice, replication of virus in the PNS was rapidly terminated and evidence of neuronal destruction, assessed by a quantitative histological assay, was sparse. Clearance of infectious virus was impaired, and a strikingly high proportion of ganglionic neurons was killed, in mice treated with an antibody that depleted them of CD8+ T cells. These results suggest that CD8+ T cells play an important role in maintaining the integrity of the sensory nervous system during primary infection with HSV. Therefore, viral epitopes recognized by CD8+ T cells and restricting class I major histocompatibility complex genes are, in principle, implicated as interacting genetic determinants of neurovirulence.

Animals↗
PubMed1992

Replication of human herpesvirus 6 in epithelial cells in vitro.

Mink lung epithelial (NBL-7) cells were shown to be permissive for human herpesvirus 6 (HHV-6) by four independent methods of analysis: detection of infectious virus, viral antigens, viral DNA sequences, and herpesvirus particles. Infection was serially passaged, with minimal cytopathology, for several months demonstrating for the first time that a cell of epithelial origin can support HHV-6 replication.

Animals↗
PubMed1992

Synchronous appearance of antigen-positive and latently infected neurons in spinal ganglia of mice infected with a virulent strain of herpes simplex virus.

Studies with replication-defective mutants of herpes simplex virus (HSV) have defined the minimum requirements for establishment of latency, but their behaviour may not reflect the course of events following infection by wild-type HSV, in which ability to express viral genes has not been precluded by a genetic lesion. To address this issue we devised a strategy for studying establishment of latency by a virulent strain of HSV, based on the distinctive molecular characteristics of latently infected neurons. By combining in situ hybridization for detection of latency-associated transcripts with immunohistochemical analysis of viral proteins we demonstrate here that antigen-positive and latently infected neurons appear synchronously in spinal ganglia during the earliest stages of acute ganglionic infection. This is consistent with early divergence of the molecular pathways leading to productive and latent infection, supporting and extending the results obtained with viral mutants.

Animals↗
PubMed1992

Two patterns of persistence of herpes simplex virus DNA sequences in the nervous systems of latently infected mice.

The number of herpes simplex virus (HSV) genome equivalents recovered from latently infected mouse spinal ganglia was compared with the proportion of neurons containing latency-associated transcripts (LATs). Two distinct patterns of HSV persistence were observed, depending on the anatomical location of ganglia with respect to the site of cutaneous inoculation. The location of the bulk of latent viral DNA did not correspond with the highest prevalence of LAT+ neurons. Viral DNA was most abundant in spinal ganglia directly innervating the inoculation site and the amount recovered, which was similar to that found previously in human trigeminal ganglia, suggested that LAT+ neurons each contain hundreds of copies of HSV DNA. In stark contrast, although LAT+ neurons were most abundant in neighbouring ganglia, viral DNA was scarce (approx. 20 copies/LAT+ cell). These data indicate that amplification of HSV DNA sequences is greatest in ganglia previously shown to be associated with viral antigen expression during the productive phase of primary infection.

Animals↗
PubMed1979

Specific absorption of human serum albumin, immunoglobulin A, and immunoglobulin G with selected strains of group A and G streptococci.

Five gram-positive bacterial strains were selected for absorption studies of human serum samples. Strain AR1 (group A, M-type 1) and G148 (group G), with strong immunoglobulin G (IgG) binding capacities, and strain AW43 (group A, M-type 60), binding both IgA1 and IgA2, were compared with Staphylococcus aureus Cowan I and with Staphylococcus epidermidis L603. Both AR1 and G148 were capable of completely absorbing out serum IgG. In contrast, S. aureus Cowan I left a fraction unabsorbed, as expected from its known lack of IgG3 binding. Strain AW43 absorbed out all serum IgA, using a 10-microliter bacterial pellet for 20 microliter of serum. Serum IgM levels were slightly reduced by S. aureus Cowan I absorption. On the basis of the experiments, a bacterial mixture was designed consisting of S. aureus Cowan I and group A streptococcus strains AR1 and AW43, with absorption characteristics suitable for use in discriminating between early IgM and late IgG and IgA immune responses in routine serological work. A new type of bacteria-mammalian protein binding was discovered. Human serum albumin was completely absorbed out by strain G148 and to a lesser extent by strain AR1 and AW43. S. aureus Cowan I and S. epidermidis were negative. The binding capacity of G148 for albumin equalled that of Cowan I for IgG. The binding pattern of albumin to the strains was different from those of IgG, IgA, IgM, fibrinogen, haptoglobin, or aggregated beta 2-microglobulin and therefore seems to represent another type of bacterial-mammalian interaction with a specific albumin receptor on the surface of streptococci.

Absorption↗
PubMed1978

A pesticide (dieldrin)-induced immunohemolytic anemia.

The unusual presentation of a factory worker with severe hemolytic anemia which remitted following splenectomy prompted a search for an environmental cause for red cell injury. The investigation showed the presence of an immunoglobulin in the patient's serum and on the red cells and small amounts of complement on red cells. The patient's serum caused agglutination of a normal person's red cells only when dieldrin-coated, a reaction blocked by first reacting the serum with dieldrin. The spleen of the patient had a greater than normal concentration of dieldrin, the source of dieldrin being dietary. It is concluded that dieldrin became immunogenic and provoked a chemical immunohemolytic anemia. The spleen played a major role in destruction of red cells injured by the immunopathic process and in accumulation of the antigenic substance dieldrin.

Anemia, Hemolytic↗
PubMedDate not supplied

Another example of a B variant.

A family in which five members has a weak B variant and one member had a normal A and weak B reaction is reported. It appears that these phenotypes arise by the inheritance of a variant allele of the ABO locus. Their cells react weakly when added to anti-B sera, and they have normal anti-A activity and an absence of anti-B in their sera. Additionally, all of the members tested had increased levels of cellular H substance and all of the affected secretor members of the family secreted normal amounts of both B and H substance. Transferase activity of the sera of these individuals confirmed the presence of the B-gene specific transferase.

ABO Blood-Group System↗
PubMedDate not supplied

Detection of HBsAg in coagulation Factor IX concentrates.

HBsAg was detected in two commercial clotting factor concentrates: Proplex (Hyland) and Konyne (Cutter). HBsAg was positive by RIA in samples of Proplex but not Konyne. Immune-electron microscopy, however, demonstrated clumped small spheres of HBsAg in both preparations, and lamellar-type strands were seen in several preparations.

Blood Transfusion↗