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Corrina L. Hale

Researcher at Harvard University

Publications -  5
Citations -  389

Corrina L. Hale is an academic researcher from Harvard University. The author has contributed to research in topics: Simian immunodeficiency virus & Viral load. The author has an hindex of 5, co-authored 5 publications receiving 380 citations.

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Vaccine Protection against Simian Immunodeficiency Virus by Recombinant Strains of Herpes Simplex Virus

TL;DR: The development and use of replication-competent and replication-defective strains of recombinant herpes simplex virus that express envelope and Nef antigens of simian immunodeficiency virus (SIV) show great promise for being able to elicit persistent immune responses and to provide durable protection against AIDS.
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Decreased Frequency of Cytomegalovirus (CMV)-Specific CD4+ T Lymphocytes in Simian Immunodeficiency Virus-Infected Rhesus Macaques: Inverse Relationship with CMV Viremia

TL;DR: The frequency of cytomegalovirus (CMV)-specific CD4+ T lymphocytes was determined in CMV-seropositive rhesus macaques with or without simian immunodeficiency virus (SIV) infection by using the sensitive assays of intracellular cytokine staining and gamma interferon ELISPOT to facilitate the study of CMV pathogenesis in AIDS.
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Differential dynamics of CD4(+) and CD8(+) T-lymphocyte proliferation and activation in acute simian immunodeficiency virus infection

TL;DR: Divergent patterns of proliferation and activation are exhibited by CD4+ and CD8+ T lymphocytes in early SIV infection and may determine how these cells are differentially affected in AIDS.
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Direct relationship between suppression of virus-specific immunity and emergence of cytomegalovirus disease in simian AIDS

TL;DR: The occurrence of CMV reactivation-associated disease in AIDS is associated with suppression of both cellular and humoral CMV-specific immune responses, and the underlying mechanism may be a dysfunction of memory B and CD8+ T lymphocytes associated with SIV-induced impairment of CMv-specific CD4+ T-cell help.
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Emergence of cytotoxic T lymphocyte escape mutations in nonpathogenic simian immunodeficiency virus infection.

TL;DR: The occurrence of CTL escape in a host that does not develop AIDS is recorded, and adds to the growing body of evidence that CTL exert significant selective pressure in SIV infection.