| Project/Area Number |
09670660
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Neurology
|
|---|
| Research Institution | Nagasaki University |
|---|
Principal Investigator |
SHIRABE Susumu Nagasaki Univ.Sch.of Med.Hospital, Assistant, 医学部附属病院, 助手 (40264220)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Tatsufumi Nagasaki Univ.Sch.of Med.Hospital, Lecturer, 医学部附属病院, 講師 (00198219)
KATAMINE Shigeru Nagasaki Univ.Sch.of Med., Professor, 医学部, 教授 (40161062)
|
|---|
| Project Period (FY) |
1997 – 1998
|
| Project Status |
Completed (Fiscal Year 1998)
|
| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1998: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
|
|---|
| Keywords | HTLV-I / HTLV-I associated myelopathy / tax / HLA anchor motif / quasispecies / synonimous mutation / non-synonimous mutation / molecular epidemiology / 非同義置 |
|---|
| Research Abstract |
We have a case of identical twin of discordant outcome (a healthy carrier and HAM patient) of HTLV-I associated myelopathy (HAM). We investigated healthy carriers and HAM patients in this family including this twin by nucleotide sequence analysis of tax gene, viral load of HTLV-I provirus of lymphocytes, titers of serum anti-HTLV-I antibody, spontaneous proliferation of peripheral blood cells, and HLA typing.
1) twenty different molecular clones were selected randomly, then tax gene amplified by nested PCR was sequenced. Eight out of 18 showed mutations were found in clones derived from LIAM patient. All clones from carrier showed mutation.
2) Five mutations had non-synonymous mutations. One of change found in carrier may explain difference of immunological response to the HLA anchor motif.
3) HTLV-l proviral load was significant higher in HAM patients than on carrier.
4) Spontaneous proliferation was exaggerated in HAM patients.
5) Nucleotide sequence of ENV also showed mutation responsible for change of HLA anchor motif iii carrier of twin.
|
