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Alicja Trocha

Researcher at Ragon Institute of MGH, MIT and Harvard

Publications -  48
Citations -  6535

Alicja Trocha is an academic researcher from Ragon Institute of MGH, MIT and Harvard. The author has contributed to research in topics: CTL* & Epitope. The author has an hindex of 38, co-authored 48 publications receiving 6402 citations. Previous affiliations of Alicja Trocha include Harvard University & University of California, Los Angeles.

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Evolution and transmission of stable CTL escape mutations in HIV infection

TL;DR: Investigation of mother–child transmission in the setting of HLA-B27 expression suggests that CTL escape mutations in epitopes associated with suppression of viraemia will accumulate as the epidemic progresses, and therefore have important implications for vaccine design.
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Association between virus-specific cytotoxic T-lymphocyte and helper responses in human immunodeficiency virus type 1 infection.

TL;DR: Analysis of functional human immunodeficiency virus type 1 (HIV-1)-specific memory CTL precursor frequencies and p24-specific proliferative responses in a cohort of infected untreated persons provides cellular immunologic parameters to guide therapeutic and prophylactic vaccine development.
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Suppression of human immunodeficiency virus type 1 replication by CD8+ cells: evidence for HLA class I-restricted triggering of cytolytic and noncytolytic mechanisms.

TL;DR: It is demonstrated that HIV-1-specific cytotoxic T lymphocytes (CTL) mediate antiviral suppression by both cytolytic and noncy tolytic mechanisms and suggest that CTL play an important role in the observed antiviral activity of CD8+ cells from infected individuals.
Journal Article

Cytotoxic T lymphocytes in asymptomatic long-term nonprogressing HIV-1 infection. Breadth and specificity of the response and relation to in vivo viral quasispecies in a person with prolonged infection and low viral load.

TL;DR: It is demonstrated that HIV-1-specific CTL can be highly activated and broadly directed in the setting of an extremely low viral load, and that neither high viral load nor antigenic diversity is required for the generation of a multispecific CTL response.