PubMed Health⌕ Search

Biomedical subjects

D L Lodmell

Publications and source records attributed to D L Lodmell.

At least 37 records · Page 2Linked to original sources
PubMed1990

Impaired phagocytosis by the mononuclear phagocytic system in sapphire mink affected with Aleutian disease.

The phagocytic function of the mononuclear phagocytic system (MPS) in normal sapphire mink and in sapphire mink affected with experimental Aleutian disease was compared. Clearance from blood of carbon particles or 125I-labeled microaggregated human serum albumin, and subsequent measurement of radioactivity in phagocytic organs indicated profound MPS blockade in mink affected with advanced Aleutian disease. In contrast, MPS activity in mink in the early stage of the disease was comparable to that of normal mink. It is suggested that the MPS blockade may be responsible for some pathologic changes in Aleutian disease.

Aleutian Mink Disease↗
PubMed1989

Interferon induced within the central nervous system during infection is inconsequential as a mechanism responsible for murine resistance to street rabies virus.

SJL/J mice are resistant, whereas A/WySnJ mice are susceptible to intraperitoneally (i.p.) inoculated street rabies virus (SRV). In this report we determine whether interferon (IFN) induced within the central nervous system (CNS) of these mice during infection is associated with resistance. We show that the high concentration of type 1 interferon (IFN-alpha/beta) within the CNS of A/WySnJ mice is ineffective in inhibiting SRV replication in these tissues, and is unimportant in ameliorating disease. More importantly, the 100% survival of SRV-infected SJL/J mice following neutralization of IFN within the CNS with anti-IFN-alpha/beta suggests that protection of target cells by this minimal amount of IFN is not the mechanism responsible for the innate resistance of SJL/J mice to i.p. inoculated SRV.

Animals↗
PubMed1987

Immune sera and antiglycoprotein monoclonal antibodies inhibit in vitro cell-to-cell spread of pathogenic rabies viruses.

Although the cell-to-cell spread of many viruses in vitro is inhibited by antibody, the effect of antibody on such spread of rabies viruses is uncertain. Thus, we examined the effects of anti-rabies virus immune sera and monoclonal antibodies (MAbs) on the in vitro spread of pathogenic rabies viruses in neuronal and nonneuronal cells. Both anti-rabies virus immune sera and neutralizing antiglycoprotein MAbs inhibited the cell-to-cell spread of street rabies virus, challenge virus standard, and ERA rabies viruses in cultures of neuroblastoma cells and of nonneuronal BHK-21 and chicken embryo-related cells. Furthermore, the cell-to-cell spread of virus was inhibited by greater than or equal to 75% with less than 1 IU/ml of human antirabies immunoglobulin. Nonneutralizing antinucleocapsid MAbs did not inhibit viral spread. After the immune serum was removed from the monolayers, virus spread rapidly to uninfected cells. Thus, antibody controlled the cell-to-cell spread of the virus but did not eliminate it from the cultures. Because antibody was more effective in inhibiting viral spread in fibroblast and epithelioid cells than in neuroblastoma cells infected at a high multiplicity of infection, we suggest that the inhibition of viral cell-to-cell spread by antibody in vivo would more likely occur at an initial site of exposure and before nerves are infected.

Animals↗
PubMed1986

Interferon response in normal and Aleutian disease virus-infected mink.

Studies were done to determine whether differences in interferon production are responsible for the resistance of pastel mink to Aleutian disease. The abilities of normal pastel and sapphire mink to produce interferon when inoculated with either Newcastle disease virus or a synthetic polyribonucleotide, poly (I):poly (C), were identical, even to the production of a novel, acid-labile interferon. The resistance of pastel mink to Aleutian disease did not correlate with interferon production, because neither sapphire nor pastel mink produced detectable amounts of interferon when infected with either the Pullman strain of Aleutian disease virus (ADV) or the highly virulent Utah I strain. Sapphire mink infected with the Pullman strain responded normally to poly (I):poly (C) early in the course of the disease, but interferon production was impaired late, when the mink were hypergammaglobulinemic and had renal, vascular, and hepatic lesions. These data suggest that ADV Pullman neither stimulates nor interferes with interferon production in infected mink and may represent a mechanism whereby ADV can more readily establish infection.

Aleutian Mink Disease↗
PubMed1986

Mink parvoviruses and interferons: in vitro studies.

Although interferons can inhibit the replication of a number of viruses, little is known about their ability to inhibit parvovirus replication. Therefore, in vitro experiments were done to determine if Aleutian disease virus and mink enteritis virus, two autonomously replicating mink parvoviruses, induced interferon, were sensitive to the effects of interferon, or inhibited the production of interferon. The results indicated that these parvoviruses neither induced nor were sensitive to the effects of interferon. Furthermore, preexisting parvovirus infections did not inhibit poly(I).poly(C)-induced interferon production. This independence from the interferon system may, therefore, be a general property of the autonomously replicating parvoviruses.

Animals↗
PubMed1985

Pathogenesis of street rabies virus infections in resistant and susceptible strains of mice.

Seven strains of mice were examined to determine why susceptibility differences and variations in clinical central nervous system (CNS) disease occurred among these animals after intraperitoneal inoculation of street rabies virus (SRV). Trace experiments for infectious virus indicated that these differences were associated with restriction of virus replication within the CNS. Limitation of viral replication appeared to correlate with the antibody response in that prominent serum anti-SRV neutralizing antibody titers were detected in resistant strains, whereas susceptible strains produced minimal amounts of antibody until their death. The importance of the immune response was reaffirmed with cyclophosphamide studies in that all resistant SJL/J mice died after immunosuppressive treatment. In contrast, cyclophosphamide-treated SJL/J mice whose immune systems were reconstituted with either unfractionated immune spleen cells or with sera 24 h after SRV inoculation survived a lethal dose of SRV. More importantly, immunosuppressed SJL/J and immunodeficient athymic mice were protected when reconstituted with immune serum 72 h after SRV inoculation, a time in which infectious virus was detected in the spinal cords of some mice but was not present in the peritoneal cavity. Additional studies showed that antibody in the cerebrospinal fluid was unimportant in the resistance of mouse strains which remained clinically asymptomatic, but it appeared to be associated with the survival of mice which developed clinical CNS disease. Furthermore, CNS resistance to intranasal or intracerebral inoculation with challenge virus standard rabies virus developed as early as 5 days post-intraperitoneal inoculation of SRV.

Animals↗
PubMed1984

Murine resistance to street rabies virus: genetic analysis by testing second-backcross progeny and verification of allelic resistance genes in SJL/J and CBA/J mice.

Intraperitoneal challenge with street rabies virus of second-backcross offspring produced from susceptible females mated with either randomly selected or rabies-resistant first-backcross males indicated that murine resistance is under the influence of the concurrent presence of each of two segregating genes. Furthermore, the greater than or equal to 96% resistance of offspring produced from (SJL X CBA)F1 and (CBA X SJL)F1 hybrids crossed to susceptible A.SW or A/WySn mice demonstrated that resistance genes of SJL/J and CBA/J mice are allelic.

Alleles↗
PubMed1983

Genetic control of resistance to street rabies virus in mice.

Resistance to intraperitoneally inoculated street rabies virus (SRV) in mice was shown to be under genetic control. SJL/J, CBA/J, DBA/2J, and BALB/cAn mice were resistant, whereas A/WySn/J and A.SW/SnJ mice were susceptible. In addition, female mice of the resistant BALB/cAn and DBA/2J strains were more resistant than their male counterparts. Resistance was not controlled solely by the major histocompatibility locus because susceptible A.SW/SnJ and resistant SJL/J mice have the same H-2S haplotype. Challenge of F1 hybrids produced by crossing resistant and susceptible strains indicated resistance was dominant (97% survivors). Inoculation of backcross mice produced by mating F1 hybrids with susceptible parents showed that one and/or two genes controlled susceptibility. Furthermore, inoculation of SRV obtained from six different animals indicated that differences in strain susceptibilities were not dependent on the SRV isolate. Genetic control of resistance to SRV was, however, abrogated by intracerebral inoculation of virus. Resistant strains of mice were detected that either remained asymptomatic or, in contrast, developed signs of clinical disease, but disease failed to progress and they survived. The recognition of resistant and susceptible strains of mice, differences in female-male resistance within the same resistant strain, as well as dissimilar clinical responses in different resistant mouse strains to intraperitoneally inoculated SRV provide promising probes for investigation of host resistance and mechanisms for survival after onset of clinical rabies.

Animals↗
PubMed1981

Influence of cell type and virus upon lysis of rabies virus-infected cells by antibody and complement.

Mouse neuroblastoma (MNB) cells infected with ERA virus were specifically lysed in the presence of rabbit complement by antisera produced in mice to challenge virus standard (CVS), ERA, Flury HEP or street virus (SV) strains of rabies. MNB or EL-4 cells persistently infected with ERA, MNB cells infected with CVS, and BHK-21/S13 cells infected with ERA or Flury HEP also were suitable targets. CER cells infected with either ERA, CVS or Flury HEP, BHK-21/S13 cells infected with CVS and MNB cells infected with Flury HEP were not suitable targets. Two unusual findings indicated that 1. some cells which were greater than 80 percent positive for rabies viral membrane antigen(s) were poorly lysed, and 2. some cells that expressed cytoplasmic antigen lacked detectable membrane antigens.

Animals↗
PubMed1980

Nonspecific inhibition of encephalomyocarditis virus replication by a type II interferon released from unstimulated cells of Mycobacterium tuberculosis-sensitized mice.

Unstimulated peritoneal cells (PC) from mice sensitized with nonviable Mycobacterium tuberculosis in an oil-droplet emulsion inhibit encephalomyocarditis virus (EMCV) replication in mouse embryo fibroblast monolayers. Concentrations of mycobacteria ranging from 50 to 500 microgram elicit PC that inhibit EMCV replication greater than 99%. PC collected 2 to 6 weeks post-inoculation of mycobacteria are most effective (greater than 99% inhibition), although cells harvested from mice 7 through 10 weeks inhibit viral replication greater than 90%. Inhibition of replication is not detected unless PC are in contact with infected monolayers for a minimum of 8 to 10 hr; nonviable PC are not effective. Optimal inhibition occurs in cultures infected with a low multiplicity of EMCV that are incubated at 37 degrees C. Inhibition of replication is not due to pH changes or depletion of nutrients in cultures, adsorption and/or inactivation of EMCV by macrophages, or killing of monolayers by the PC. Inhibition of viral replication by the unstimulated PC appears to be due to an interferon that is similar but not identical to classical mouse Type II interferon.

Animals↗
PubMed1978

Enhanced resistance against encephalomyocarditis virus infection in mice, induced by a nonviable Mycobacterium tuberculosis oil-droplet vaccine.

Female C57B1/10 mice injected intravenously (i.v.) with nonviable Mycobacterium tuberculosis Jamaica cells associated with oil-droplet emulsions (WCV) were highly resistant to the i.v. injection of encephalomyocarditis virus (EMCV). Resistance to infection (87% survival) was detected from 1 week to at least 12 weeks after injection of WCV. Mice vaccinated i.v. also were resistant to intraperitoneal, subcutaneous, or intramuscular virus challenge, but were not resistant to intracranial challenge. Mice vaccinated intraperitoneally also were resistant to virus infection, whereas WCV administered intramuscularly or subcutaneously did not protect mice from virus injected by any route. Less than 50% of WCV mice that survived virus challenge possessed serum anti-EMCV-neutralizing antibody (less than 1:10), and none had detectable (less than 1:10) serum interferon. Interferon was not detected in sera of WCV mice from 4 to 144 h after i.v. injection of EMCV. Studies concerning the effects of WCV on EMCV infection suggest that mice may be protected by mechanisms that inhibit early viral replication and spread of virus to the central nervous system.

Animals↗
PubMed1978

Induction of enhanced resistance against encephalomyocarditis virus infection of mice by nonviable Mycobacterium tuberculosis: mechanisms of protection.

Nonviable Mycobacterium tuberculosis strain Jamaica suspended in oil-droplet emulsions was used to enhance resistance of mice against encephalomyocarditis virus (EMCV). The mycobacteria-injected mice were significantly resistant to 50,000 50% lethal doses of EMCV. Similar concentrations of virus in plasma of normal and mycobacteria-injected mice from 1 to 120 min after injection of EMCV showed that resistance was not a result of rapid elimination of virus from the circulation. Furthermore, survival of viremic mice indicated protective mechanisms were operative after EMCV had escaped primary surveillance. Resistance did not appear to be associated with the mouse major histocompatibility gene complex. The spleen was intimately associated with protection, and the thymus was nonessential for enhanced resistance to EMCV. Protection was significantly diminished by cyclophosphamide injected intraperitoneally from 3 days before to the day of virus challenge. Finally, silica given intraperitoneally 24 h before virus completely abrogated resistance of mycobacteria-injected mice to EMCV. These results suggest that macrophages functioning independently of T-lymphocytes are important effector cells in resistance to EMCV of mice injected with nonviable mycobacteria.

Animals↗
PubMed1976

Inhibition of vaccinia virus replication in skin of tuberculin-sensitized animals challenged with PPD.

Induction of a celayed-type hypersensitivity reaction in tuberculin-sensitized animals by tuberculin purified protein derivative (PPD) at the site of dermal vaccinia virus (VV) infection markedly accelerated elimination of VV and led to clinical recovery. Viral titers were depressed by over 99.9% in the skin of animals given PPD as compared to animals given phosphate-buffered saline or nonspecific irritants. Low concentrations of acid labile interferon were found in the skin of uninfected tuberculin-sensitized animals challenged with PPD. High concentrations of acid stable interferon were found in skin of tuberculin-sensitized animals infected with VV and challenged with either PPD or PBS. The time of appearance of the acid stable interferon was markedly accelerated, however, in the animals challenged with PPD as compared with PBS. It is concluded that recovery from dermal vaccinia infection can be enhanced by induction of a local delayed-type hypersensitivity reaction with an antigen untelated to the infecting virus.

Animals↗
PubMed1974

Cellular immunity to herpes simplex virus mediated by interferon.

Rabbit kidney cell monolayers infected with herpes simplex virus (HSV) were incubated with leukocytes from rabbits immunized with complete Freund's adjuvant. When the leukocytes were exposed to tuberculin purified protein derivative (PPD), viral replication and plaque formation were markedly inhibited. Similarly, when leukocytes from animals immunized with HSV were exposed to UV-inactivated HSV, viral replication was markedly inhibited. Exposure of leukocytes from unimmunized animals or animals immunized with incomplete Freund's adjuvant to UV-inactivated virus or PPD produced relatively little inhibition of viral replication. Examination of supernatant fluids from stimulated cultures revealed a soluble mediator that had the properties of interferon. Interferon production was detected within several hours after exposure of sensitized leukocytes to antigen. Supernatant fluids from as few as one sensitized leukocyte per 200 rabbit kidney cells inhibited HSV replication by over 90%. These findings support the concept that the cellular immune response to HSV consists of two phases: an immunologically specific antigen recognition phase, and a nonspecific effector phase that stops HSV spread by generating interferon.

Animals↗
PubMed1973

Prevention of cell-to-cell spread of herpes simplex virus by leukocytes.

Antibody to herpes simplex virus (HSV) plus complement destroyed HSV-infected cells but did not stop the spread of the infection. Studies on the relationship between the time of appearance of viral antigens on the cell surface, immunological destruction of the cells by antiviral antibody and complement, and transfer of the virus to adjacent cells showed that the virus spread from infected to uninfected cells before the infected cells were susceptible to immunological destruction. Incubation of infected monolayers with leukocytes, however, stopped the spread of the virus by nonspecifically damaging both infected and uninfected cells and by presumably breaking intercellular bridges. When leukocytes were removed from infected monolayers, viral plaques developed. If, however, antiviral antibody and complement were added to monolayers before the leukocytes were removed, the development of plaques was prevented. These findings suggest that both antibody and leukocytes are needed to cure HSV infections.

Animals↗
PubMed1973

Antibody-forming cells and serum hemolysin responses of pastel and sapphire mink inoculated with Aleutian disease virus.

The effect of Aleutian disease virus (ADV) on serum hemolysin titers and antibody-forming cells in lymph nodes and spleens of sapphire and pastel mink inoculated with goat erythrocytes (G-RBC) was investigated. ADV injected 1 day after primary antigenic stimulation with G-RBC did not depress the immune responses of either color phase for a period of 26 days. However, when G-RBC were injected 47 days after ADV, both the number of antibody-forming cells and hemolysin titers were more markedly depressed in sapphire than in pastel mink. The results are discussed in relation to the greater susceptibility of sapphire mink and the variable susceptibility of pastel mink to the Pullman isolate of ADV.

Aleutian Mink Disease↗