Laboratory Studies on Rubella and the Rubella Syndrome

Plotkin, Stanley А.; Dudgeon, J. A.; Ramsay, A. Melvin

doi:10.1136/bmj.2.5368.1296

Cited by 83 publications

(24 citation statements)

References 5 publications

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“…The virus used for this study was the 8th or 9th RK 13 passage of the West Point strain (5). It titered 105.0 plaque forming units/ml on RK 13 plates.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of rubella virus by amantadine

Plotkin

1965

Archiv f Virusforschung

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“…The virus used for this study was the 8th or 9th RK 13 passage of the West Point strain (5). It titered 105.0 plaque forming units/ml on RK 13 plates.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of rubella virus by amantadine

Plotkin

1965

Archiv f Virusforschung

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“…In those animal models, both natural and experimental, previously thought to represent examples of immunologic tolerance, it is now apparent that specific antibody to virus occurs, i.e., LCM virus (11,12) and lactic dehydrogenase virus (28-31), Moloney sarcoma virus (32) infection of mice, Aleutian disease of mink (33,34), and equine infectious anemia (35). Furthermore, the observations made on human infants infected with rubella or cytomegalic virus in fetal life indicate that these babies too are not immunologically tolerant in spite of persistent infection (36)(37)(38)(39) …”

Section: A;mentioning

confidence: 99%

The Antibody Response of Mice to Murine Leukemia Virus in Spontaneous Infection: Absence of Classical Immunologic Tolerance

Oldstone

Aoki

Dixon

1972

Proc. Natl. Acad. Sci. U.S.A.

118

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Gross murine leukemia virus is the etiologic agent of spontaneous leukemias of AKR mice. Despite the persistence of the Gross virus throughout their life, these mice are not immunologically tolerant to the virus. Specific antibodies to Gross antigens can be detected in the kidney where they have been deposited in the glomeruli, apparently in the form of Gross antigenantibody complexes.To explain the life-long persistence of certain viruses in infected animals, Burnet and Fenner (1) proposed the hypothesis of immunologic tolerance. They suggested that after a generalized nonfatal infection of the embryo, the animal, after birth, would be incapable of producing antibody to the same infecting agent. Observations with lymphocytic choriomeningitis (LCM; refs. 2-6) and tumor viruses (7-10) provided the main support for this concept. In both of these infections, virus is transmitted vertically and a permanent viral carrier state ensues. Characteristically, virus is detectable in blood and organs throughout life, while free circulating antibody to viral antigen (s) is not.Previously we reported that mice infected with LCM virus either in utero or in the newborn period were not "immunologically tolerant", as they were capable of making an immune response to the virus (11-13). Now we report that neither immunologic nor clinical tolerance to Gross murine leukemia virus-(GMuLV-) related antigens occurs in AKR mice. Such mice are naturally infected in utero with GMuLV and carry large amounts of virus throughout their life (14)(15)(16)

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“…Specific antibodies of both fetal and maternal origin are present in the sera of the infants at birth. These antibodies have activity detectable by a number of methods, including viral neutralization (6,30,37). RV can be isolated from almost any organ of a full-term infant and infectious virus or viral genome may be recovered for 1 year or more in many surviving congenital rubella infants (20,39).…”

Section: Introductionmentioning

confidence: 99%

Rubella Virus Does Not Induce Apoptosis in Primary Human Embryo Fibroblast Cultures: A Possible Way of Viral Persistence in Congenital Infection

et al. 2004

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Congenital rubella is a persistent infection that contrasts with acute postnatal infection. Basis of the Rubella virus (RV) persistence still remain unknown, though several hypotheses have been postulated. RV induces apoptosis in cell lines, maybe as a way of cell-autonomous defense mechanism against virus. Considering the pattern of c-oncogenes expression during embryogenesis, which promotes proliferation while it inhibits apoptosis in specific cells, at certain times, it can be proposed that when RV infection establishes early in gestation, embryo cells that are proliferating have their apoptotic pathways shut down; then infected proliferating embryo cells cannot execute their apoptotic death program. We here report that RV induces apoptosis in human normal-term placenta chorionic villi explants (CVE) and in monolayers of cytotrophoblasts (CTB), but does not induce apoptosis in primary human embryo fibroblasts (HEF) cultures. These results suggest distinct responses to RV infection when comparing differentiated cells, as CTB, to cells with high proliferating potential, as HEF. RV shoots apoptosis in the former, whereas in fibroblastic dividing cells derived from embryo, RV appears not to be enough stimulus to activate the genetic program of cell death.

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Laboratory Studies on Rubella and the Rubella Syndrome

Cited by 83 publications

References 5 publications

Inhibition of rubella virus by amantadine

Inhibition of rubella virus by amantadine

The Antibody Response of Mice to Murine Leukemia Virus in Spontaneous Infection: Absence of Classical Immunologic Tolerance

Rubella Virus Does Not Induce Apoptosis in Primary Human Embryo Fibroblast Cultures: A Possible Way of Viral Persistence in Congenital Infection

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