HIV-1 can persist in latent form where the virus integrates its genetic material into the host genome and becomes virtually invisible to host-immune recognition. The persistence of CD4 T cells harboring latent HIV-1 (deemed ‘reservoir’) is the principle reason why HIV-1 infection is incurable and remains a continual public health burden. Because latent HIV-1 is silent and undergoes little to no transcription, the behaviors of latently-infected cells are essentially indistinguishable from those of uninfected cells. Mechanisms of reservoir persistence are thus largely physiologic. Our lab employs both cell-based and sequencing approaches in the NHP model to study how latently infected cells co-opt two physiologic process, (1) immuno-metabolism and (2) responses to a common co-infecting virus CMV, to maintain their survival.
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Browse the latest scientific discoveries and advances from our lab.
Nature communications · 2024-12-22
Hallmarks of primate lentiviral immunodeficiency infection recapitulate loss of innate lymphoid cells.
Read publicationClinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2024-12-22
CD8 T-Cell Expansion and Inflammation Linked to CMV Coinfection in ART-treated HIV Infection.
Read publicationBlood · 2024-12-22
Impaired T-cell responses to sphingosine-1-phosphate in HIV-1 infected lymph nodes.
Read publicationNature medicine · 2024-12-22
Inadequate T follicular cell help impairs B cell immunity during HIV infection.
Read publicationFrontiers in immunology · 2024-12-22
Similarities and Differences in the Acute-Phase Response to SARS-CoV-2 in Rhesus Macaques and African Green Monkeys.
Read publicationJCI insight · 2024-12-22
Epigenetic silencing of CD4 expression in nonpathogenic SIV infection in African green monkeys.
Read publicationBrowse the latest scientific discoveries and advances from our lab.
ORIP/NIH · $400,000
1R21OD031229-01 : "Mechanisms and therapeutic targeting of CD4 down-regulation in African green monkeys."
African green monkeys, which are natural hosts of SIV, reduce target cell number by down-regulating CD4. Our proposed studies will examine the molecular events governing this evolved phenomenon and seek to harness this mechanism in progressive hosts to render cells resistant to SIV infection. In the long-term, this project will pave the way for in vivo transfer of virus-resistant T cells, akin to similar HIV-1 cure approaches aimed at populating the host with CCR5-deficient T cells.
NIAID/NIH · $5.1 million
5R01AI167644: "Role of RhCMV in shaping the SIV proviral landscape."
Despite the profound benefit of antiretroviral therapy (ART) to patient quality of life, HIV-1 remains an incurable infection. Our proposed studies aim to examine the role of Cytomegalovirus (CMV) in promoting the proliferation of latent HIV-1 infected memory CD4 T cells. In the long-term, the proposed studies will hope to provide a rationale for current well- tolerated CMV antivirals recently approved by the FDA to accelerate clearance of the latent HIV-1 reservoir.
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