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. 1984 Feb;3(2):267–277. doi: 10.1002/j.1460-2075.1984.tb01796.x

Herpes simplex virus infection causes the accumulation of a heat-shock protein.

N B LaThangue, K Shriver, C Dawson, W L Chan
PMCID: PMC557334  PMID: 6325164

Abstract

A monoclonal antibody, produced from mice immunized with a herpes simplex virus (HSV)-infected cell extract, reacts with a molecule which is present in uninfected cells and which accumulates in large amounts during HSV 2 infection. In uninfected cells this molecule is growth regulated, in that exponentially growing cells have intense nuclear immunofluorescence, whereas confluent quiescent cells have little. It has a mol. wt. of 57 000 (p57) in exponential cells, and one of 61 000 (p61) in quiescent cells. In HSV 2-infected cells, p57 accumulates and nuclear and cytoplasmic immunofluorescence increases. In uninfected cells, p57 also accumulates during heat-shock treatment, and this is associated with a new immunofluorescence throughout the cytoplasm. We suggest that HSV 2 infection induces a cellular stress response which is involved in the shut-off of host cell polypeptide synthesis.

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Selected References

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