Interferon Production by Macrophages from Adult and Newborn Rabbits Bearing Fibroma Virus-Induced Tumors

Pathak, P. N.; Tompkins, W. A. F.

doi:10.1128/iai.9.4.669-673.1974

Cited by 10 publications

(5 citation statements)

References 13 publications

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“…Although cultures of immune macrophages contain no infectious fowlpox virus, the possibility of virus antigens cannot be excluded since macrophages were recovered from chickens with active fowlpox lesions known to contain virus antigen (11). However, studies by Pathak and Tompkins (16) suggest that nonspecific immunity to fibroma virus in rabbits is not due to virus antigens in the cultures. Unstimulated macrophage cultures from normal and fibroma-immune rabbits failed to produce significant levels of interferon in vitro and only immune macrophage cultures responded to subsequent challenge.…”

Section: Discussionmentioning

confidence: 98%

In Vitro Cellular Immunity to Unrelated Pathogens in Chickens Infected with Fowlpox Virus

1974

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Peritoneal macrophages recovered from chickens 15 to 20 days after inoculation with fowlpox virus and showing a delayed hypersensitivity reaction against fowlpox antigens demonstrated an enhanced antimicrobial effect against fowlpox virus as well as unrelated viruses and bacteria. Inoculation of normal chicken macrophage cultures with fowlpox virus resulted in approximately a 200-fold increase in virus titer by 96 h, whereas the virus showed less than a fourfold increase in macrophage cultures from fowlpox-immune chickens. Similarly, the titer of Newcastle disease virus increased by more than 1 log in cultures of normal macrophages, whereas the titer decreased by approximately 1 log after infection of fowlpox-immune macrophages. Vaccinia, vesicular stomatitis, and herpes simplex viruses, which are not natural pathogens of chickens, failed to replicate in cultures of either normal or fowlpox-immune macrophages. By using Salmonella gallinarum , it was further demonstrated that the antimicrobial activity of fowlpox-immune macrophages encompassed not only nonspecific viruses but also bacteria. Infection of normal macrophages with Salmonella resulted in intracellular replication of the organism between 0 and 24 h as determined by microscope examination and viable bacteria counts. In contrast, cultures of fowlpox-immune macrophages failed to show an increase in intracellular organisms and showed a marked decrease in viable bacteria. In conclusion, these studies clearly showed that cellular immunity, previously demonstrated in mammalian species, develops in chickens after infection with fowlpox virus.

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Section: Discussionmentioning

confidence: 98%

In Vitro Cellular Immunity to Unrelated Pathogens in Chickens Infected with Fowlpox Virus

1974

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“…Experiments from other laboratories also have shown that leukocytes from animals immune to a specific antigen (viral or nonviral) produced more interferon when exposed to that antigen than leukocytes from nonimmune animals (11)(12)(13)(14)(15)(16)(17)(18)(19). Recently, Youngner and Salvin (17) reported that immunologically induced interferon differs in its physical properties from nonimmunologically induced interferon; at pH 2.0 the interferon was inactivated.…”

Section: Discussionmentioning

confidence: 99%

“…This might be one of the explanations for the lower amount of interferon produced in our experiments by splenic as compared to peritoneal leukocytes. The specific cell type(s) producing interferon in our system also remains to be determined, but evidence from other laboratories indicates that both immune lymphocytes and macrophages can produce interferon (12,15,18).…”

Section: Discussionmentioning

confidence: 99%

Cellular Immunity to Herpes Simplex Virus Mediated by Interferon

Lodmell

Notkins

1974

The Journal of Experimental Medicine

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Several lines of evidence suggest that cellular immunity plays an important role in the defense against herpes simplex virus (HSV) l infections. First, HSV can persist both in vivo and in vitro despite the presence of high concentrations of neutralizing antibody (1). Second, HSV infections are more severe in patients with deficiencies in cellular immunity (2-4). Third, experimental suppression of the cellular immune response makes animals more susceptible to HSV infection (2, 4). The precise way by which cell-mediated immunity operates to protect the host against HSV is far from clear; but recent studies suggest that different immunological mechanisms are required to control different modes of viral spread (5). For example, in the typical lytic infection, HSV can spread by either the extracellular route (Type I spread) or directly from cell-to-contiguous-cell (Type II spread) presumably as a result of cell fusion. Type I spread is readily stopped by antiviral antibody that neutralizes extraceUular virus. Type II spread is not stopped by antiviral antibody because the intracellular location of the virus protects it from neutralization.Little is still known about how the host combats Type II spread, but theoretically, the immune response could stop Type II spread by acting on one or more of three different sites. First, it could act by destroying virus-infected cells. Second, it could break cell-to-cell contact or prevent cell fusion; if this happens the virus would have to travel by the extracellular route to infect adjacent cells and the virus could then be neutralized by antiviral antibody. Third, if the host's immune response leads to the destruction of the surrounding uninfected cells or inhibits viral replication in these cells, the spread of virus would be halted.Evidence that the immune response of the host can directly or indirectly act at each of these sites is beginning to accumulate. It is known that HSV can induce new antigens on the surface of infected cells and that antiviral antibody and complement can react I A bbrevlations used in this paper: C FA, complete Freund's adjuvant; GM, growth medium; HSV, herpes simplex virus; IFA, incomplete Freund's adjuvant; MEM, minimum essential medium; PBS, phosphate-buffered saline; PEC, peritoneal exudate cells; PFU, plaque-forming units; PPD, purified protein derivative; RK, rabbit kidney; VSV, vesicular stomatitis virus.

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“…control animals, a process thought to be mediated by inter- have been examined directly for the production of interferon in the host, and increases in the levels of interferon can be detected in serum, peritoneal exudate cells, spleen, liver, and lymph node and in extracts of lesions (174,191,362,390,436,466,496). The recovery of interferon from the site of vaccinia virus inoculations of guinea pigs prompted Friedman et al (174) to suggest that interferon was the protective element in guinea pigs that were immunocompromised by treatment with methotrexate and X rays (no detectable neutralizing antibody or DTH reaction).…”

Section: Interferonsmentioning

confidence: 99%

“…Human peripheral blood lymphocytes (PBL) from immune individuals make gamma interferon following stimulation in vitro with viral antigen(141). Additionally, perito-2 y ., neal exudate cells isolated from adult rabbits with tumors 0 q , D , induced by SFV (Patuxent strain) produced more interferon upon challenge with virus than did cells obtained from either g0 t E vnonimmune or neonatal rabbits(362).In vivo influence of interferon and interferon inducers on = Q 8 poxvirus pathogenesis. The effects of interferon on poxvirus r 5areplication in vivo have been examined by correlating inter-= z eX feron levels with the severity of disease or by measuring = nr QQ disease parameters in animals treated with interferon, inter-o°Z <^> t 3 > feron inducers, and immunomodulators.…”

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confidence: 97%

Poxvirus pathogenesis.

Buller

Palumbo

1991

Microbiological Reviews

293

163

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Marchal (285) and Downie (126) bodies, respectively. Because of the ambiguity associated with describing structures solely on the basis of their reaction with various histochemical stains, Kato et al. (253) carefully examined the virusspecific cytoplasmic structures of a large number of poxvirus species and, using a criterion based on morphologic observations, histochemical staining, and immunochemical reactivity, suggested that the acidophilic and basophilic inclusion bodies be referred to as A-and B-type inclusion bodies, respectively. Under the auspices of a Poxvirus Subcommittee created at the Sixth International Congress for Microbiology in 1953, Fenner and Burnet (161) wrote a review which summarized the characteristics of the poxvirus group. This article remains the basis for the subsequent classification of poxviruses. The poxvirus family is divided into two subfamilies: Entomopoxvirinae (poxviruses of the insects) and Chordopoxvirinae (poxviruses of the vertebrates); the latter group of viruses is the focus of this review (Table 1). The vertebrate poxviruses share a group-specific NP antigen (511) and are able, in a reciprocal fashion, to participate in nongenetic reactivation (160, 168). This is a process whereby an infectious poxvirus is able to reactivate a second, heatinactivated poxvirus, as indicated by the production of progeny virus. Poxviruses were further classified into genera by comparing cross-protection in animal studies, crossneutralization of infectivity in tissue culture, and crosshybridization of genomic DNA from virions. This latter criterion is now the method of choice for preliminary classification of poxvirus isolates. In general, members of the same genera have similar morphology and biological properties. Virion Morphology Poxviruses are the largest of all animal viruses and can be visualized by light microscopy, although the details of the

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Interferon Production by Macrophages from Adult and Newborn Rabbits Bearing Fibroma Virus-Induced Tumors

Cited by 10 publications

References 13 publications

In Vitro Cellular Immunity to Unrelated Pathogens in Chickens Infected with Fowlpox Virus

In Vitro Cellular Immunity to Unrelated Pathogens in Chickens Infected with Fowlpox Virus

Cellular Immunity to Herpes Simplex Virus Mediated by Interferon

Poxvirus pathogenesis.

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