Dr. Ronald S. Veazey

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Academic Career Length

29Years (1998-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

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21 September 2022 in Nature

Journal Article

Long-primed germinal centres with enduring affinity maturation and clonal migration

Jeong Hyun Lee

Henry J. Sutton

Christopher A. Cottrell

Ivy Phung

Gabriel Ozorowski

Shane Crotty

+32

1 December 2000 in Journal of Virology

Journal Article

Dynamics of CCR5 Expression by CD4⁺T Cells in Lymphoid Tissues during Simian Immunodeficiency Virus Infection

Ronald S. Veazey

Keith G. Mansfield

Irene C. Tham

Angela C. Carville

Daniel E. Shvetz

Andrew A. Lackner

Early viral replication and profound CD4⁺T-cell depletion occur preferentially in intestinal tissues of macaques infected with simian immunodeficiency virus (SIV). Here we show that a much higher percentage of CD4⁺T cells in the intestine express CCR5 compared with those found in the peripheral blood, spleen, or lymph nodes. In addition, the selectivity and extent of the CD4⁺T-cell loss in SIV infection may depend upon these cells coexpressing CCR5 and having a “memory” phenotype (CD45RA⁻). Following intravenous infection with SIVmac251, memory CD4⁺CCR5⁺T cells were selectively eliminated within 14 days in all major lymphoid tissues (intestine, spleen, and lymph nodes). However, the effect on CD4⁺T-cell numbers was most profound in the intestine, where cells of this phenotype predominate. The CD4⁺T cells that remain after 14 days of infection lacked CCR5 and/or were naive (CD45RA⁺). Furthermore, when animals in the terminal stages of SIV infection (with AIDS) were examined, virtually no CCR5-expressing CD4⁺T cells were found in lymphoid tissues, and all of the remaining CD4⁺T cells were naive and coexpressed CXCR4. These findings suggest that chemokine receptor usage determines which cells are targeted for SIV infection and elimination in vivo.

1 March 2003 in The Journal of Infectious Diseases

Journal Article

Vaginal CD4⁺T Cells Express High Levels of CCR5 and Are Rapidly Depleted in Simian Immunodeficiency Virus Infection

Ronald S. Veazey

Preston A. Marx

Andrew A. Lackner

Worldwide, the majority of human immunodeficiency virus–1 cases occur through heterosexual transmission, yet little is known regarding the phenotype of CD4⁺ T cells in the vaginal mucosa. In the present study, lymphocytes were compared from the lymph nodes, blood, and vagina from uninfected and simian immunodeficiency virus (SIV)–infected macaques. In mature female macaques, 54%–67% of the vaginal CD4⁺ T cells expressed C chemokine receptor 5 (CCR5), whereas 84%–99% coexpressed CXC chemokine receptor 4. In contrast, only 4.4%–14.8% of peripheral blood and 2.4%–13% of lymph-node CD4⁺ T cells coexpressed CCR5. Moreover, CCR5 mean channel fluorescence was significantly higher on CD4 cells from the vagina, compared with those from blood. In macaques intravenously infected with SIV, rapid depletion of CD4⁺ T cells was observed in the vagina, particularly among the CCR5⁺CD4⁺ subset. This demonstrates that large numbers of CD4⁺ T cells expressing high levels of CCR5 reside within the vagina and that these cells are preferentially targeted for elimination by SIV infection

6 June 2012 in Mucosal Immunology

Journal Article

IL-17-producing innate lymphoid cells are restricted to mucosal tissues and are depleted in SIV-infected macaques

H Xu

X Wang

D X Liu

T Moroney-Rasmussen

A A Lackner

Ronald S. Veazey

Innate lymphoid cells (ILCs) are an emerging subset of lymphocytes involved in surveillance against virally infected cells. Here, we show CD3⁻CD8^high lymphocytes in macaque blood include major subsets of ILCs including natural killer (NK) cells expressing CD16, NKp46, and NKG2A, but also populations of ILCs in mucosal tissues having different properties. One ILC subset secreted interleukin (IL)-17 (ILC17), but these were restricted to mucosal tissues. Some mucosal ILC17 cells expressed classical NK-cell markers, but little NKG2A or NKG2D. Some ILC17 cells secreted IL-22 and tumor necrosis factor-α, but few produced interferon (IFN)-γ or contained granzyme B. IL-17 production by ILCs was induced by IL-6, transforming growth factor-β, and IL-23. Further, simian immunodeficiency virus (SIV) infection resulted in a significant loss of ILC17 cells, especially in the jejunum, which persisted throughout SIV infection. These findings indicate that ILC17 cells may be involved in innate mucosal immune responses, and their loss may contribute to loss of intestinal mucosal integrity and disease progression in human immunodeficiency virus (HIV)/SIV infection.

1 November 2001 in Trends in Immunology

Journal Article

The mucosal immune system: primary target for HIV infection and AIDS

Ronald S. Veazey

Preston A Marx

Andrew A Lackner

1 May 2005 in Nature Medicine

Journal Article

HIV swiftly guts the immune system

Ronald S. Veazey

Andrew A Lackner

About Me

Ronald S Veazey is a Professor in the Department of Pathology and Laboratory Medicine at the Tulane University School of Medicine and has been Chair of the Division of Comparative Pathology at the Tulane National Primate Research Center since 2003. He is a recognized expert on SIV and HIV infection and pathogenesis, a specialist in mucosal immunology, and in examining the earliest events in SIV transmission, immunology, and pathogenesis. As a veterinary pathologist, he has extensive training and experience in the comparative anatomy, histology, immunology, and pathophysiology of disease in both human and non-human primates. His research program has focused on the pathogenesis and immunology of AIDS since 1994, and he has developed an extensive HIV prevention research program to test the safety and efficacy of topical and systemic prevention and vaccine strategies using nonhuman primate models of HIV transmission. He is a member of the TNPRC Executive Committee, the TNPRC Pilot Research Program Committee, the Mucosal Immunology Working Group of the HIV Vaccine Trials Network (HVTN), the American Foundation for AIDS Research (AmFAR), the European Combined Highly Active Anti-Retroviral Microbicides Program (CHAARM), the Center for HIV and Vaccine Immunology (CHAVI). He has served as a permanent member of the NIH AIDS Immunology and Pathogenesis (AIP) Grant Review Study Section, and as Chairperson of the NIH Vaccine Study Section (VACC).

Dr. Ronald S. Veazey

Dr. Ronald S. Veazey

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About Me