2000 Fiscal Year Final Research Report Summary
Studies on apoptosis induced in the virus-infected cells
| Project/Area Number |
11670298
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KOYAMA Hajime The University of Tokushima, School of Medicine, Associate Professor, 医学部, 助教授 (80109074)
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| Co-Investigator(Kenkyū-buntansha) |
ADACHI Akio The University of Tokushima, School of Medicine, Professor, 医学部, 教授 (90127043)
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| Project Period (FY) |
1999 – 2000
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| Keywords | apoptosis / antiapoptosis / sorbitol / virus / phagocytosis / defense mechanism |
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| Research Abstract |
To understand the biological significance of virus-induced apoptosis in animal virus infection, we quantitatively characterized apoptosis and virus multiplication in the virus-infected cells. Based on the observation that the multiplication of the insect virus was abolished when the infected cells induced apoptosis, virus-induced apoptosis has been considered to be one of the host defense mechanism against virus invasion. However, in contrast to the infection with insect viruses, influenza virus and some RNA animal viruses can grow rapidly under the conditions that the infected cells induced apoptosis. The progeny virus yield reached the maximum level at the time when these infected cells induced apoptosis, indicating influenza virus is able to overcome apoptosis of the infected cells by a rapid multiplication.
On the other hand, we found that HEp-2 cells induced massive apoptosis immediately after the treatment with sorbitol, one of the polyhydric alcohol. By the use of sorbitol-treatment, we showed that (1) animal viruses are able to grow in the apoptotic cells, (2) large DNA viruses, such as herpes simplex virus type one (HSV-1) and type 2 (HSV-2), overcome apoptosis by multiple antiapoptosis genes of the viruses which allow the viruses to suppress the induction of apoptosis in the infected cells, and (3) one of antiapoptosis genes of HSV-2 is US3 gene.
These results indicate that the biological significance of apoptosis in the animal virus infection is not the abortion of virus multiplication by premature death of the infected cells and suggest that apoptosis works as a host defense mechanism by converting the virus-infected cells to the target of phagocytotic activity of macrophages in the infected animal.
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