Novel strategies for characterizing T Cell responses in SIV-infected rhesus monkeys

Human Immunodeficiency Virus (HIV) is the cause of Acquired Immune Deficiency Syndrome (AIDS) and has killed over 25 million people since the disease was first recognized in 1981. As of 2007, 33 million people globally are infected with HIV and this number is growing. HIV infects and depletes CD4+ helper T cells, affecting the ability of the immune system to defend the host against common infections. While anti-retroviral therapy has decreased morbidity and mortality, these drugs are not curative. In addition, they are beyond the financial reach of many HIV infected patients. Thus, the development of strategies to control HIV spread is a high priority. The most relevant animal model for studying HIV is the Simian Immunodeficiency Virus (SIV) - infected rhesus monkey. While HIV research has focused on studying peripheral blood specimens, mucosal sites have recently been identified as a focal point for HIV replication and tissue destruction. They are usually the sites of primary infection in the setting of sexual transmission and they are also important sites of immune depletion. If methods for controlling the replication of the virus early after infection in mucosal sites are available, it may be possible to eliminate the virus prior to systemic spread. While strategies for generating strong neutralizing antibody responses have not yet been developed, emerging data suggest that CD8+ cytotoxic T cells can contribute substantially to early virus control. It is important to study CD8+ T cells in the setting of SIV infection in rhesus monkeys, particularly in mucosal sites, using functional as well as transcriptional assays.

Department dc:contributor.department

Harvard University--MIT Division of Health Sciences and Technology.

Grantor dc:publisher

Massachusetts Institute of Technology

Year dc:date.issued

2009

Author dc:creator

• Shi, Amy (Amy J.)

Advisor dc:contributor.advisor

• Norman L. Letvin.

• Harvard University--MIT Division of Health Sciences and Technology.

Statement dc:rights

• M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.

Licence dc:rights.uri

• http://dspace.mit.edu/handle/1721.1/7582

Language dc:language.iso

eng

Handle dc:identifier.uri

http://hdl.handle.net/1721.1/54675

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/54675