Variation in susceptibility of different cell types to temperature-sensitive host range mutants of herpes simplex virus type 2

Koment, Roger W.; Rapp, Fred

doi:10.1016/0042-6822(75)90088-4

Cited by 16 publications

(9 citation statements)

References 4 publications

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“…These mutants will replicate to parental virus levels in both rabbit kidney and human embryo lung cells at 39°, indicating that these are host range mutants [4], It is not unusual that these mutants are attenuated in their neurovirulence for experimental animals. Isolates of small-plaque variants of HSV-I [2] and other variants or mutated viruses generally tend to be less virulent than their large-plaque counterparts [I].…”

Section: Discussionmentioning

confidence: 99%

“…Previous reports from our laboratory [3,4] have detailed the isolation of four small-plaque is mutants of HSV-2 strain 333 which do not replicate in HEF cells at 39°. These mutants will replicate to parental virus levels in both rabbit kidney and human embryo lung cells at 39°, indicating that these are host range mutants [4], It is not unusual that these mutants are attenuated in their neurovirulence for experimental animals.…”

Section: Discussionmentioning

confidence: 99%

“…Although these mutants fail to induce virus CPE or replicate in HEF or mouse embryo fibroblast cells in vitro at 39 v they are capable of lytic replication in rabbit kidney and rabbit lung cells at the nonpermissive temperature [4], It was, therefore, of interest to determine whether these mutants were as virulent as parental virus when inoculated into rabbits. To resolve this question, 100,000 PFU of parental virus 333 or a mutant were inoculated onto the scarified cornea of both eyes of weanling rabbits.…”

Section: Days After Subcutaneous Injectionmentioning

confidence: 99%

“…In several virus systems, plaque variants or mutants have been character ized by comparing plaque size with virulence in animals, as reviewed by T akemoto [1], Using large and small plaque variants of herpes simplex virus type 1 (HSV-1), R app and Falk [2] observed that small plaque variants were generally less virulent for rabbits and mice than large plaque variants. We have previously described the isolation and preliminary characterization of four host range temperature-sensitive (ts) mutants of herpes simplex virus type 2 (HSV-2) which neither induce cytopathic effect (CPE) nor replicate in hamster embryo fibroblast (HEF) cells at 39° [3,4], Each of these mutants retained the …”

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confidence: 99%

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<i>In vivo </i>Characteristics of Temperature-Sensitive Host Range Mutants of Herpes Simplex Virus Type 2

Koment¹,

Rapp²

1975

Intervirology

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The in vivo properties of four host range temperature-sensitive (ts) mutants of herpes simplex virus type 2 (HSV-2) were correlated with known in vitro characteristics. Mutants and parental virus were inoculated into newborn and weanling mice and weanling hamsters by intracranial and subcutaneous routes, and into weanling rabbits by corneal scarification. In all cases the pattern of attenuation of mutants in vivo correlated with their stability in vitro at 39°. The most attenuated mutant (mutant 69) was also the most consistent in its inability to induce cytopathic effects (CPE) in vitro or to replicate under nonpermissive conditions. Conversely, the most virulent mutant (mutant 41) was the least stable under nonpermissive conditions.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Days After Subcutaneous Injectionmentioning

confidence: 99%

mentioning

confidence: 99%

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<i>In vivo </i>Characteristics of Temperature-Sensitive Host Range Mutants of Herpes Simplex Virus Type 2

Koment¹,

Rapp²

1975

Intervirology

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“…HVJ was restricted in its replication in C 6 cells but not in LLCMK 2 and chick embryo fibroblast cells at the non-permissive temperature of 39 ° C. This ts effect of HVJ in C 6 cells was associated with reduced synthesis of M protein. Temperaturedependent host-range mutants isolated from mutagenized population have been described for a variety of viruses (5,6,14,20,24), while only a few reports have described host-dependent temperature-sensitive replication of wild-type virus (3). A study of this phenomenon would be useful for an understanding of the relationship of viral and host factors during infection.…”

Section: Introductionmentioning

confidence: 99%

Host-dependent temperature-sensitive growth of HVJ (Sendai virus) wild-type in rat glioma C 6 cells

Ogura

Sato

Hatano

1987

Archives of Virology

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At non-permissive temperature viral specific RNA synthesis was not restricted in rat glioma (C 6) cells infected with HVJ (Sendai virus) wild-type. However, as has previously been shown (J Gen Virol [1984] 65: 639-643), the synthesis of M protein was reduced at non-permissive temperature, in contrast to the L, P, HN, Fo and NP proteins which were synthesized in comparable amounts at permissive and non-permissive temperatures. In this report we show additionally that viral nucleocapsids (NC), which consist of L, P and NP proteins, were formed within the infected cells at both temperatures. Hemagglutinin and neuraminidase activities were also detected in samples incubated at non-permissive temperature. By membrane immunofluorescence and cell-surface immunoprecipitation it was shown that migration of HN and Fo proteins to the cell surface occurred normally at non-permissive temperature. Additionally, the L, P and NP proteins, which were associated with the plasma membrane isolated from the infected cells maintained at permissive temperature, were absent from the membrane of cells incubated at non-permissive temperature. These results suggest that NC and glycoproteins synthesized at non-permissive temperature could not assemble effectively at the plasma membrane because of a lack of M protein. Thus, the host-dependent ts lesion of HVJ in C 6 cells was considered to be mainly in M protein synthesis.

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A nonlytic transforming mutant of herpes simplex virus type 2

Howett

Rapp

1978

Journal of Medical Virology

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A small-plaque mutant (NO.69) of herpes simplex virus type 2 (HSV-2) strain 333 has been previously isolated and characterized in this laboratory. This mutant was shown to produce a high ratio of noninfectious to infectious particles when grown at the nonpermissive temperature in hamster embryo fibroblasts [Westmoreland D. and Rapp F. (1976). Journal of Virology [8:92--102]. In this study, we have demonstrated that it is possible to obtain noninfectious stocks of this virus which retain transforming ability in a biochemical transformation assay specific for detection of the HSV gene for thymidine kinase. This mutant contains a DNA genome that has a density identical to the DNA of wild-type virus. Virus and cell DNA synthesis after infection with the mutant at both the permissive and nonpermissive temperature are similar to that observed in cultures infected with the parental virus. Clones of mouse cells biochemically transformed by this virus contain HSV antigens and are presently being examined for oncogenicity.

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Variation in susceptibility of different cell types to temperature-sensitive host range mutants of herpes simplex virus type 2

Cited by 16 publications

References 4 publications

<i>In vivo </i>Characteristics of Temperature-Sensitive Host Range Mutants of Herpes Simplex Virus Type 2

<i>In vivo </i>Characteristics of Temperature-Sensitive Host Range Mutants of Herpes Simplex Virus Type 2

Host-dependent temperature-sensitive growth of HVJ (Sendai virus) wild-type in rat glioma C 6 cells

A nonlytic transforming mutant of herpes simplex virus type 2

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