Abstract:MAASSAB, H. F. (University of Michigan, Ann Arbor), AND J. A. VERONELLI. Characteristics of serially propagated monkey kidney cell cultures with persistent rubella infection. J. Bacteriol. 91:436-441. 1966.-A persistent infection of LLC-MK2 cells with rubella virus has been established and maintained for over 3 years. This "carrier culture," designated as LLC-MK2-RAL, possesses distinct morphological and biological characteristics when compared with the original uninfected LLC-MK2 line. The mechanism of viral … Show more
“…Although it has been suggested that interferon may play a role in maintaining the persistent infection of cells by rubella virus in vitro (6,12,29), there are several reports of rubella viral persistence in the absence of detectable interferon (8,14,19,20). Our data indicated that neither the initiation nor maintenance of rubella viral persistence was due to the presence of interferon.…”
Section: Resultscontrasting
confidence: 69%
“…Persistent infections with rubella virus have been reported previously for several cell lines (11,12,14,23,24,29). Because of experimental variations among laboratories, many of the data are either inconclusive or contradictory regarding the function of interferon in rubella viral persistence and interference against superinfection with heterologous viruses.…”
MATERIALS AND METHODS Cell lines. Primary African green monkey kidney cells and cell lines of baby hamster kidney-21, clone 13 (BHK), BSC-1, HeLa, human amnion, RK-13, and Vero were obtained from Grand Island Biological Co., Grand Island, N.Y. The rabbit embryo chondrocyte culture was supplied by E. M.
“…Although it has been suggested that interferon may play a role in maintaining the persistent infection of cells by rubella virus in vitro (6,12,29), there are several reports of rubella viral persistence in the absence of detectable interferon (8,14,19,20). Our data indicated that neither the initiation nor maintenance of rubella viral persistence was due to the presence of interferon.…”
Section: Resultscontrasting
confidence: 69%
“…Persistent infections with rubella virus have been reported previously for several cell lines (11,12,14,23,24,29). Because of experimental variations among laboratories, many of the data are either inconclusive or contradictory regarding the function of interferon in rubella viral persistence and interference against superinfection with heterologous viruses.…”
MATERIALS AND METHODS Cell lines. Primary African green monkey kidney cells and cell lines of baby hamster kidney-21, clone 13 (BHK), BSC-1, HeLa, human amnion, RK-13, and Vero were obtained from Grand Island Biological Co., Grand Island, N.Y. The rabbit embryo chondrocyte culture was supplied by E. M.
“…Even the impairment induced by live virus could be prevented if the virus and its neutralizing antibody were added simultaneously to the lymphocytes (13). However, lymphocytes have been shown to allow replication of virus within the cell and to transmit the virus to daughter cells during cell division without the virus going through a surface transmission (6,53). Such daughter cells also appeared unresponsive to PHA stimulation.…”
In vitro rubella virus infections of lymphocytes from normal adult humans impaired their responsiveness to phytohemagglutinin (PHA) stimulations; a situation which seemed analogous to the PHA unresponsiveness of peripheral lymphocytes from babies with the congenital rubella syndrome. Such in vitro viral infection of normal cells also decreased the synthesis of normal nucleic acids and structural proteins, and abrogated the enhanced DNA synthesis induced by pokeweed and specific antigen stimulations. Furthermore, it was shown that live rubella virus, but not ultraviolet-irradiated virus, was necessary for the impaired mitogenic responses of normal leukocytes.
These observations are interpreted to favor the view that the virus achieves its inhibitory effect on the action of mitogens by interference either directly or indirectly at an intracellular site. Such an action could reduce the functional potential of lymphocytes and impair their effectiveness as immunologically competent cells or as effectors in immunologic reactions.
“…Rubella virus carrier cultures have been induced in stable cell lines (37)(38)(39). Cell strains derived from certain tissues (skin and pharyngeal mucosa) of human embryos were also found to survive in a carrier state when experimentally infected with rubella virus (40).…”
Spontaneous rubella carrier cultures derived from tissues of infants with congenital rubella were studied in an attempt to elucidate a possible mechanism for viral persistence observed in these infants. Chronically infected cells were found to have a reduced growth rate and the cultures appeared to have a shortened life span. The rubella carrier state was not dependent on serum inhibitors or rubella antibodies. Virtually every cell in the carrier population was found to be producing virus. The carrier cultures could not be cured by rubella antibodies. The rubella-infected cells were resistant to superinfection with vesicular stomatitis virus and herpes simplex virus but were susceptible to infection with echovirus 11. The replication of vesicular stomatitis virus was apparently blocked at an intracellular site, for the virus readily adsorbed to the chronically infected cells and entered into an eclipse phase; however no infectious virus developed. No evidence of interferon production by these cells could be obtained. It is postulated that clones of rubella-infected cells in vivo, with properties similar to those in carrier cultures developed in vitro from tissues of in utero infected infants, might explain the observed viral persistence noted in congenital rubella.
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