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HIV-1 reverse transcriptase-specific CTL against conserved epitopes do not protect against progression to AIDS
S H van der Burg1, M R Klein, O Pontesilli
1Department of Immunohematology, Blood Bank, University Hospital, Leiden, The Netherlands.
Journal of Immunology (Baltimore, Md. : 1950)
|October 8, 1997
Summary
Long-term survivors with HIV-1 maintain strong T-cell responses against reverse transcriptase (RT). The specificity and magnitude of these responses do not explain slower disease progression in HIV-1 patients.
Area of Science:
- Immunology
- Virology
- HIV/AIDS Research
Background:
- Long-term survivors (LTS) of HIV-1 infection often exhibit sustained HIV-1-specific cytotoxic T-lymphocyte (CTL) responses.
- It is hypothesized that differences in CTL epitope recognition, possibly due to structural or functional constraints, distinguish LTS from rapid progressors.
Purpose of the Study:
- To investigate the CTL response targeting reverse transcriptase (RT) in both LTS and individuals who rapidly progressed to AIDS.
- To compare the magnitude and specificity of RT-specific CTL responses between these two groups.
Main Methods:
- Studied CTL responses to reverse transcriptase (RT) in long-term survivors (LTS) and rapid progressors (AIDS within 3-6 years).
- Established and analyzed 19 CTL lines from blood samples collected at various time points.
- Identified nine distinct RT-derived epitopes recognized by CTL.
Main Results:
- Both LTS and progressors showed comparable, vigorous RT-specific CTL responses during the asymptomatic phase.
- CTL from progressors recognized epitopes with similar amino acid conservation as those targeted by LTS.
- Five of seven analyzed epitopes were recognized by CTL from both LTS and progressors.
- One epitope recognized by progressors contained the essential YMDD motif for RT activity.
Conclusions:
- The magnitude of HIV-1-specific CTL responses against RT does not appear to be a primary factor in slower disease progression.
- The specificity of CTL responses targeting RT epitopes is unlikely to be the main reason for a more protracted course of HIV-1 disease.