Replication and immunosuppressive effects of Pseudorabies virus on swine peripheral blood mononuclear cells

Chinsakchai, Sudarat; Molitor, Thomas W.

doi:10.1016/0165-2427(92)90142-d

Cited by 27 publications

(16 citation statements)

References 13 publications

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“…Regarding PRV, it is known that it infects monocytes and activated T lymphocytes, although viral replication in these cells is clearly restricted (28). The death of some infected monocytes and lymphocytes has also been reported after an in vitro inoculation with PRV (7,43), but the precise mechanisms of cell death were not investigated. The results of our in vivo study show the occurrence of PRV-induced apoptosis in mononuclear immune cells that infiltrate the TG and suggest that it may account for suppression of cell-mediated immunity following infection of swine.…”

Section: Discussionmentioning

confidence: 99%

“…Regarding PRV, several authors have focused on the interactions between this virus and peripheral blood mononuclear cells. The occurrence of cell-associated viremia after experimental infection of pigs has been reported (4,29,33), and both in vivo and in vitro studies have shown that monocytes are the porcine mononuclear cells most susceptible to PRV infection, followed by stimulated T lymphocytes (7,28,29,43). Although some monocytes and T lymphocytes die due to infection after an in vitro inoculation with PRV (7,43), it has not been established whether it occurs through an apoptotic pathway and, if so, what could be the role of immune cell apoptosis in PRV pathogenesis during productive infection of swine.…”

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confidence: 99%

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Induction and Inhibition of Apoptosis by Pseudorabies Virus in the Trigeminal Ganglion during Acute Infection of Swine

Alemañ¹,

Quiroga

López-Peña

et al. 2001

J Virol

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We examined the ability of pseudorabies virus (PRV) to induce and suppress apoptosis in the trigeminal ganglion during acute infection of its natural host. Eight pigs were intranasally inoculated with a virulent field strain of PRV, and at various early times after inoculation, the trigeminal ganglia were assessed histologically. PRV-infected cells were detected by use of immunohistochemistry and in situ hybridization, and apoptosis was identified by in situ terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling. Light and electron microscopy was also used for morphological studies. Apoptosis was readily detected among infiltrating immune cells that were located surrounding PRV-infected neurons. The majority of PRV-infected neurons did not show morphological or histochemical evidence of apoptosis, even including those neurons that were surrounded by numerous inflammatory cells and exhibited profound pathological changes. However, neuronal virus-induced apoptosis also occurred but at a sporadic low level. These findings suggest that PRV is able to block apoptosis of infected trigeminal ganglionic neurons during acute infection of swine. Furthermore, our results also suggest that apoptosis of infiltrating inflammatory cells may represent an important viral mechanism of immune evasion.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Induction and Inhibition of Apoptosis by Pseudorabies Virus in the Trigeminal Ganglion during Acute Infection of Swine

Alemañ¹,

Quiroga

López-Peña

et al. 2001

J Virol

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“…In the studies of Wang et aI. [-13] and Chinsakchai and Molitor [2], monocytes were indicated as the most susceptible subpopulation, followed by mitogen-stimulated T-lymphocytes. Forty to seventy per cent of monocytes that were isolated by means of adhesion to glass or polystyrene celt culture dishes, were found to be infected with a progeny titer of 107 TC1Ds0 PRV per 106 inoculated monocytes.…”

Section: Introductionmentioning

confidence: 98%

“…In this paper, the susceptibility of mononuclear cells to PRV infection was determined in vitro in the different PBMC subpopulations, obtained by two separation techniques different from that described by Chinsakchai and Molitor [2]. In the most susceptible subpopulation, the kinetics of viral antigen expression and virus production were studied.…”

Section: Introductionmentioning

confidence: 99%

Virus production and viral antigen expression in porcine blood monocytes inoculated with pseudorabies virus

Nauwynck

Pensaert

1994

Archives of Virology

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Interactions of pseudorabies virus (PRV) with peripheral blood mononuclear cells (PBMC) were studied. T-lymphocytes, B-lymphocytes and monocytes were selected or depleted from the PBMC fraction by means of several separation techniques. After inoculation with virulent PRV in vitro, the percentage of cells that expressed viral antigens was determined in the different subpopulations by immunofluorescence. The susceptibility of monocytes depended on the method of isolation. When plasma-coated polystyrene culture grade dishes were used, 17 to 26% of the monocytes showed expression of viral antigens. However, PRV antigens were detected in only 2% of the monocytes when the cells had first been labelled with monoclonal antibodies against a monocyte marker and subsequently separated on polystyrene bacteriological Petri disches coated with anti-mouse monoclonal antibodies. In subpopulations of unstimulated T- and B-lymphocytes only 0.4 to 0.7% of the cells were found positive by immunofluorescence. Viral antigens appeared in the cytoplasm and on the cell membrane of monocytes isolated on plasma-coated dishes starting 5 h after inoculation and the expression was found in a maximal number of monocytes, 7 to 8 h after inoculation. The intracellular and extracellular virus progeny titers obtained in monocyte cultures were low, ranging from 10(4.3) to 10(5.2) TClD50 per 10(6) inoculated monocytes. The percentage of inoculated monocytes which produced infectious PRV was 0.1% in two experiments and less than 0.01% in one experiment. The results indicate that although monocytes are the most susceptible subpopulation of unstimulated PBMC to a PRV infection in vitro, replication is clearly restricted. Only a subset of monocytes expresses viral antigens and an even smaller fraction produces infectious virus.

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“…IFN-γ may protect the host's APC compartment from an extensive viral infection. This is because the PrV infects monocytes and alveolar macrophages resulting in a reduced lymphocyte proliferation responsiveness of peripheral blood mononuclear cells to Con-A stimulation, and IFN-γ can inhibit PrV replication in certain cell types (6,36). However, it is possible that an antibody may play a role in protecting the APCs, possibly by neutralizing the virus or by protecting the infected APCs from lysis by reducing the expression level of the viral glycoproteins and MHC class I molecule on the cell surface (15).…”

Section: Discussionmentioning

confidence: 99%

Cytokine GM‐CSF Genetic Adjuvant Facilitates Prophylactic DNA Vaccine against Pseudorabies Virus through Enhanced Immune Responses

Yoon

Aleyas

George

et al. 2006

Microbiology and Immunology

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Granulocyte/macrophage colony‐stimulatory factor (GM‐CSF) is an attractive adjuvant for a DNA vaccine on account of its ability to recruit antigen‐presenting cells (APCs) to the site of antigen synthesis as well as its ability to stimulate the maturation of dendritic cells (DCs). This study evaluated the utility of GM‐CSF cDNA as a DNA vaccine adjuvant for glycoprotein B (gB) of pseudorabies virus (PrV) in a murine model. The co‐injection of GM‐CSF DNA enhanced the levels of serum PrV‐specific IgG with a 1.5‐ to 2‐fold increase. Moreover, GM‐CSF co‐injection inhibited the production of IgG2a isotype. However, it enhanced production of an IgG1 isotype resulting in humoral responses biased to the Th2‐type against PrV antigen. In contrast, the co‐administration of GM‐CSF DNA enhanced the T cell‐mediated immunity biased to the Th1‐type, as judged by the significantly higher level of cytokine IL‐2 and IFN‐γ production but not IL‐4. When challenged with a lethal dose of PrV, the GM‐CSF co‐injection enhanced the resistance against a PrV infection. This suggests that co‐inoculation with a vector expressing GM‐CSF enhanced the protective immunity against a PrV infection. This immunity was caused by the induction of increased humoral and cellular immunity in response to PrV antigen.

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Replication and immunosuppressive effects of Pseudorabies virus on swine peripheral blood mononuclear cells

Cited by 27 publications

References 13 publications

Induction and Inhibition of Apoptosis by Pseudorabies Virus in the Trigeminal Ganglion during Acute Infection of Swine

Induction and Inhibition of Apoptosis by Pseudorabies Virus in the Trigeminal Ganglion during Acute Infection of Swine

Virus production and viral antigen expression in porcine blood monocytes inoculated with pseudorabies virus

Cytokine GM‐CSF Genetic Adjuvant Facilitates Prophylactic DNA Vaccine against Pseudorabies Virus through Enhanced Immune Responses

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