Viruses and the Versatile Macrophage

Morahan, P.S.; Connor, J.T.H.; Leary, Kathryn

doi:10.1093/oxfordjournals.bmb.a072017

Cited by 117 publications

(50 citation statements)

References 83 publications

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“…These M~b most closely resemble inflammatory M~b, and both are probably less differentiated than the steady-state Res M~b Van der Meer et al, 1983). The current data with TG Mq~ extend the early reports that TG Mq~ produce more infectious HSV than do Res Mq~ (reviewed in Morahan, 1984;Morahan et al, 1985). Our results establish that TG M~b are very susceptible to the c.p.e, of HSV, and emphasize that there is heterogeneous expression of viral antigens and virus replication among the TG M~b population.…”

Section: Discussionsupporting

confidence: 86%

“…Macrophages (MS) play a highly significant role in non-specific resistance to virus infection, due in part to non-permissiveness of M~b for replication of many viruses (intrinsic resistance), and inhibition of virus replication in infected permissive cells (extrinsic resistance) (for reviews, see Morahan & Murasko, 1988;Morahan, 1984;Morahan et al, 1985). MS, however, display considerable heterogeneity in immune functions including anti-tumour activity, antimicrobial (Johnson, 1964;Stevens & Cook, 1971), but the molecular mechanisms by which Res Mq~ prevent infectious virus from being produced have yet to be defined .…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of Macrophage Activation on Resistance of Mouse Peritoneal Macrophages to Infection with Herpes Simplex Virus Types 1 and 2

Sit

Tenney

Rothstein

et al. 1988

Journal of General Virology

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SUMMARYTo define the effect of heterogeneity of murine peritoneal macrophages (MS) on intrinsic resistance to herpes simplex virus (HSV) infection, several MS populations were characterized for their response to infection with HSV type 1 (HSV-1) and HSV-2. Steady-state resident MS (Res MS) were compared in parallel with MS activated with Corynebacterium parvum (now designated Propionibacterium acnes) (CP MS) and thioglycollate-elicited inflammatory MS (TG M~b). Res MS were completely nonpermissive for productive virus infection and showed no c.p.e. The intrinsic resistance of CP MS to HSV infection was similar to that of Res MS, in that the infection was non-productive for infectious virus, but CP MS showed marked c.p.e. TG MS showed semi-permissiveness, with virus yields at least 10-fold higher than those in Res MS and CP MS, and marked c.p.e. The three distinct intrinsic response patterns were maintained regardless of whether MS were derived from CD-1 or B6C3F1 mice, or whether the infecting virus was HSV-1 or HSV-2. To define the level at which M S restrict HSV replication, immunofluorescence assays for viral antigens and hybridization analyses for viral DNA were performed. All MS populations showed immediate early and early virus polypeptides. Res MS and CP MS showed no viral DNA replication, but TG MS showed moderate levels of viral DNA synthesis that paralleled the infectious virus titres produced. Investigation of the mechanism for the heterogeneous intrinsic antiviral response among the M S revealed that interferon was not involved, because antiserum to mouse ot/fl interferon did not alter the intrinsic resistance patterns. Induction of c.p.e, in M~b required live, replication-competent HSV. The involvement of tumour necrosis factor (TNF) in c.p.e, was found to be unlikely; no significant amounts of TNF were detected in the culture medium of the MS, and inclusion of anti-TNF antibody did not inhibit c.p.e. INTRODUCTION Macrophages (MS) play a highly significant role in non-specific resistance to virus infection, due in part to non-permissiveness of M~b for replication of many viruses (intrinsic resistance), and inhibition of virus replication in infected permissive cells (extrinsic resistance) (for reviews,

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Section: Discussionsupporting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Effect of Macrophage Activation on Resistance of Mouse Peritoneal Macrophages to Infection with Herpes Simplex Virus Types 1 and 2

Sit

Tenney

Rothstein

et al. 1988

Journal of General Virology

View full text Add to dashboard Cite

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“…The other one is the ability of macrophages to phagocytose and digest virus particles or to inhibit virus growth inside the macrophages themselves, defined as intrinsic resistance (42). First, the antiviral activity of macrophages against other permissive cells (21,22,36) was demonstrated in vitro. Macrophages from naive and infected mice showed 61 and 71% inhibition of virus replication in surrounding BALB/c-3T3 fibroblasts, respectively (Fig.…”

Section: Discussionmentioning

confidence: 99%

Role of Macrophages in Acute Murine Cytomegalovirus Infection

Hamano

Yoshida

Takimoto

et al. 1998

Microbiology and Immunology

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It has been recognized that macrophages play an important role in controlling virus infection in experimental animal models. To evaluate the role of macrophages in acute murine cytomegalovirus infection, macrophages in the spleen and the liver were eliminated by an intravenous injection of liposomes containing a cytolytic agent, dichloromethylene diphosphonate. The depletion of macrophages led to a significant increase of virus titer in the spleen and lungs in both susceptible BALB/c and resistant C57BL/6 mice during the first three days after intravenous infection. In the spleen, the increase of virus titer in macrophagedepleted BALB/c mice was much greater than that in NK cell-depleted mice. These results suggest that macrophages contribute to protection mainly by the mechanisms which are independent of NK cells during the first three days after infection. The increase of virus titer in macrophage-depleted C57BL/6 mice was as great as that in NK cell-depleted mice because of the high contribution of NK cells to protection in C57BL/6 mice. In the liver in both strains of mice, the effects of macrophage depletion on virus titer were not as much as those in the spleen and lungs. Furthermore, the local depletion of peritoneal macrophages resulted in a great increase of virus titer in the spleen at three days after intraperitoneal infection. We conclude that macrophages greatly contribute to decreasing the virus load in some organs possibly through either or both intrinsic and extrinsic mechanisms in the early phase of primary infection with murine cytomegalovirus.

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“…The alveolar macrophage has a major role in defending the lower respiratory tract against invading pathogens including viruses (Morahan et aL, 1985). Paradoxically, alveolar macrophages replicate RSV (Panuska et al, 1990a;Becker et al, 1992), other paramyxoviruses (Mills, 1979), orthomyxoviruses (Nain et al, 1990), coronavirus (Laude et al, 1984), retroviruses (Gendelman et al, 1985;Chayt et al, 1986) and DNA viruses Nash et al, 1988) which should increase viral burden.…”

Section: Introductionmentioning

confidence: 99%

“…These cytokines and mediators, following binding to their cognate receptors, affect diverse biological processes modulating gene transcription thus altering immune responsiveness, as well as cellular maturation and differentiation (Nathan, 1987;Dinarello, 1989;Braquet et al, 1989), processes known to alter cellular interactions with virus. Macrophages can also restrict viral replication by inactivation of extracellular virus, lysis of virus-infected cells, secretion of enzymes competing for virus-dependent substrates, and production of defective interfering virus (for a review see Morahan et al, 1985). We examined each of these mechanisms to define the nature of restricted RSV replication in alveolar macrophages.…”

Section: Introductionmentioning

confidence: 99%

Restricted replication of respiratory syncytial virus in human alveolar macrophages

Cirino

Panuska

Villani³

et al. 1993

Journal of General Virology

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The cellular factors that regulate infection and replication of respiratory syncytial virus (RSV) in human alveolar macrophages were examined. RSV-exposed alveolar macrophages demonstrated a time-dependent expression of viral glycoproteins, maximal by 24 h postinfection resulting in infection of approx. 38 % of the cells. Essentially all (33 %) of these freshly isolated alveolar macrophages replicated RSV as shown by infectious centre assays. This RSV-permissive subpopulation of alveolar macrophages consisted primarily of major histocompatibility class II-expressing cells as determined by fluorescence-activated cell sorting. Reinfection of alveolar macrophages did not significantly alter the number of cells infected or capable of replicating RSV. However, in vitro differentiation of alveolar macrophages prior to infection resulted in a significant (P < 0-05), time-dependent decrease (approx. sevenfold) in the number of cells that replicated virus. The mechanism by which cellular differentiation restricted RSV replication is unknown. Production of defective interfering particles did not account for this decrease. Alveolar macrophages infected with RSV produce a variety of cytokines potentially contributing to this restricted viral replication. Pretreatment with several of these cytokines did not affect viral infection or replication. However, tumour necrosis factor (TNF~) significantly (P < 0"05) decreased viral replication but only by 30 to 60 %. Thus RSV replication is reduced by in vitro differentiation of alveolar macrophages and, to a lesser degree, by pretreatment with TNF.

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Viruses and the Versatile Macrophage

Cited by 117 publications

References 83 publications

Effect of Macrophage Activation on Resistance of Mouse Peritoneal Macrophages to Infection with Herpes Simplex Virus Types 1 and 2

Effect of Macrophage Activation on Resistance of Mouse Peritoneal Macrophages to Infection with Herpes Simplex Virus Types 1 and 2

Role of Macrophages in Acute Murine Cytomegalovirus Infection

Restricted replication of respiratory syncytial virus in human alveolar macrophages

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