Effect of Mycobacterial Infection on Virus Loads and Disease Progression in Simian Immunodeficiency Virus-Infected Rhesus Monkeys

Croix, Denise A.; Capuano, Saverio; Simpson, Laura J.; Fallert, Beth A.; Fuller, Craig L.; Klein, Edwin; Reinhart, Todd A.; Murphey‐Corb, Michael; Flynn, JoAnne L.

doi:10.1089/08892220050195856

Cited by 22 publications

(15 citation statements)

References 54 publications

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“…Moreover, a high degree of viral replication in early SIV mac -infected macaques appears to be required for successful induction of the fatal BCG disease. This requirement may indeed provide an explanation for why SIV-BCG coinfection cannot uniformly induce the tuberculosis-like disease in nonhuman primates (7,9). Modeling virus-mycobacterium coinfection for HIV-related tuberculosis in macaques certainly remains challenging.…”

Section: Discussionmentioning

confidence: 99%

Induction of an AIDS Virus-Related Tuberculosis-Like Disease in Macaques: a Model of Simian Immunodeficiency Virus- Mycobacterium Coinfection

Shen¹,

Zhou²,

Chalifoux

et al. 2002

Infect Immun

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Section: Discussionmentioning

confidence: 99%

Induction of an AIDS Virus-Related Tuberculosis-Like Disease in Macaques: a Model of Simian Immunodeficiency Virus- Mycobacterium Coinfection

Shen¹,

Zhou²,

Chalifoux

et al. 2002

Infect Immun

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“…tuberculosis coinfection have been developed (19,23,83,(92)(93)(94)112). SIV-infected rhesus macaques have been inoculated with BCG (19,(92)(93)(94) or M. tuberculosis (83). These models have recapitulated the decrease in peripheral mycobacterium-specific T cell responses observed in HIV/M.…”

Section: Animal Models: Their Potential To Address Gaps In the Human mentioning

confidence: 99%

HIV-1/Mycobacterium tuberculosisCoinfection Immunology: How Does HIV-1 Exacerbate Tuberculosis?

2011

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Human immunodeficiency virus type 1 (HIV) and Mycobacterium tuberculosis have become intertwined over the past few decades in a "syndemic" that exacerbates the morbidity and mortality associated with each pathogen alone. The severity of the coinfection has been extensively examined in clinical studies. The extrapolation of peripheral evidence from clinical studies has increased our basic understanding of how HIV increases susceptibility to TB. These studies have resulted in multiple hypotheses of how HIV exacerbates TB pathology through the manipulation of granulomas. Granulomas can be located in many tissues, most prominently the lungs and associated lymph nodes, and are made up of multiple immune cells that can actively contain M. tuberculosis. Granuloma-based research involving both animal models and clinical studies is needed to confirm these hypotheses, which will further our understanding of this coinfection and may lead to better treatment options. This review examines the data that support each hypothesis of how HIV manipulates TB pathology while emphasizing a need for more tissue-based experiments.

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“…Cell numbers were determined by trypan blue exclusion in single-cell suspensions from tissues. Flow cytometry was performed on lung, granuloma, and lymph node cell preparations at necropsy to determine the composition of the tissues, as previously described (67,69). Abs used were anti-CD3 (clone SP34), anti-CD14 (clone MOP9), anti-CD4 (clone SK3), antiCD11b (clone ICRF44), anti-CD16 (clone 3G8), anti-CD8 (clone SK1), and anti-HLA-DR (clone TU36), all from BD Biosciences (Mountain View, CA).…”

Section: Nhp Modelmentioning

confidence: 99%

Dendritic Cell Trafficking and Antigen Presentation in the Human Immune Response toMycobacterium tuberculosis

Marino

Pawar

Fuller

et al. 2004

The Journal of Immunology

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116

100

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Mycobacterium tuberculosis (Mtb) is an extraordinarily successful human pathogen, one of the major causes of death by infectious disease worldwide. A key issue for the study of tuberculosis is to understand why individuals infected with Mtb experience different clinical outcomes. To better understand the dynamics of Mtb infection and immunity, we coupled nonhuman primate experiments with a mathematical model we previously developed that qualitatively and quantitatively captures important processes of cellular priming and activation. These processes occur between the lung and the nearest draining lymph node where the key cells mediating this process are the dendritic cells (DC). The nonhuman primate experiments consist of bacteria and cell numbers from tissues of 17 adult cynomolgus macaques (Macaca fascicularis) that were infected with Mtb strain Erdman (∼25 CFU/animal via bronchoscope). The main result of this work is that delays in either DC migration to the draining lymph node or T cell trafficking to the site of infection can alter the outcome of Mtb infection, defining progression to primary disease or latent infection and reactivated tuberculosis. Our results also support the idea that the development of a new generation of treatment against Mtb should optimally elicit a fast DC turnover at the site of infection, as well as strong activation of DCs for maximal Ag presentation and production of key cytokines. This will induce the most protective T cell response.

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Effect of Mycobacterial Infection on Virus Loads and Disease Progression in Simian Immunodeficiency Virus-Infected Rhesus Monkeys

Cited by 22 publications

References 54 publications

Induction of an AIDS Virus-Related Tuberculosis-Like Disease in Macaques: a Model of Simian Immunodeficiency Virus- Mycobacterium Coinfection

Induction of an AIDS Virus-Related Tuberculosis-Like Disease in Macaques: a Model of Simian Immunodeficiency Virus- Mycobacterium Coinfection

HIV-1/Mycobacterium tuberculosisCoinfection Immunology: How Does HIV-1 Exacerbate Tuberculosis?

Dendritic Cell Trafficking and Antigen Presentation in the Human Immune Response toMycobacterium tuberculosis

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