Cellular immune responses to HIV

By A. McMichael, S. Rowland-Jones. Nature, 2001

700 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Virology

View Paper: https://www.semanticscholar.org/paper/a24bec9bd2e6ae4889889a4a6e5354cc30c708b0

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In Epidemiology

1. Rafi Ahmed
2. D. Masopust

In Immunology

1. Rafi Ahmed
2. D. Masopust
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Citations in the corpus

• Dominant influence of HLA-B in mediating the potential co-evolution of HIV and HLA (2004, methodology): “We performed a comprehensive analysis of the class I restricted CD8 p T-cell responses against human immunodeficiency virus (HIV-1), immune control of which is dependent upon virus-specific CD8 p T-cell activit”
• Comprehensive Epitope Analysis of Human Immunodeficiency Virus Type 1 (HIV-1)-Specific T-Cell Responses Directed against the Entire Expressed HIV-1 Genome Demonstrate Broadly Directed Responses, but No Correlation to Viral Load (2003, background): “Accumulating data indicate a central role of human immunodeficiency virus type 1 (HIV-1)-specific T-cell responses in controlling viral replication (13, 29, 31, 35, 37, 38, 41, 47).”
• Human effector and memory CD8+ T cell responses to smallpox and yellow fever vaccines. (2008, background): “tensively analyzed in the context of chronic infections, such as human immunodeficiency virus (HIV), cytomegalovirus (CMV), hepatitis C virus (HCV), and Epstein-Barr virus (EBV) (Barouch and Letvin, 2001; Callan et al., 1998; Hamann et al., 1997; Lauer et al., 2002; Lechner et al., 2000; McMichael ”
• Evidence of HIV-1 Adaptation to HLA-Restricted Immune Responses at a Population Level (2002, background): “HLA binding, reduce T-cell receptor recognition or generate antagonistic CTL responses.(1) Mutations affecting proteasome cleavage sites flanking CTL epitopes may also disrupt cellular processing of the epitope.”
• HIV-specific CD8+ T cell proliferation is coupled to perforin expression and is maintained in nonprogressors (2002, background): “Virus-specific CD8 + T cells are important in restricting lentiviral replication and probably determine the rate of disease progression in nonhuman primate models and in human”