Lipopolysaccharide Induces Immune Activation and SIV Replication in Rhesus Macaques of Chinese Origin

Bao, Rong; Zhuang, Ke; Liu, Jinbiao; Wu, Jianguo; Li, Jieliang; Wang, Xu; Ho, Wen‐Zhe

doi:10.1371/journal.pone.0098636

Cited by 11 publications

(14 citation statements)

References 24 publications

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“…M.tb H37Rv strain was obtained from the Research Institute of Tuberculosis (Tokyo, Japan). Six animals were intravenously inoculated with 0.5 mL of SIVmac239 (1.5 × 10 3 TCID50) (Bao et al, 2014). Six weeks after SIV infection, three SIV mono-infected animals and three SIV uninfected animals were inoculated with M.tb H37Rv at the dose of 34 colony forming unit (CFU) by bronchoscopic instillation as described (Zhang et al, 2011).…”

Section: Methodsmentioning

confidence: 99%

“…Six weeks after SIV infection, three SIV mono-infected animals and three SIV uninfected animals were inoculated with M.tb H37Rv at the dose of 34 colony forming unit (CFU) by bronchoscopic instillation as described (Zhang et al, 2011). The plasma SIV RNAs were quantified by real-time PCR with the primers of SIV GAG gene as described (Bao et al, 2014; Liu et al, 2016). …”

Section: Methodsmentioning

confidence: 99%

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SIV Infection Facilitates Mycobacterium tuberculosis Infection of Rhesus Macaques

et al. 2017

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Tuberculosis (TB) is a common opportunistic infection and the leading cause of death for human immunodeficiency virus (HIV)-infected patients. Thus, it is necessary to understand the pathogenetic interactions between M.tb and HIV infection. In this study, we examined M.tb and/or simian immunodeficiency virus (SIV) infection of Chinese rhesus macaques. While there was little evidence that M.tb enhanced SIV infection of macaques, SIV could facilitate M.tb infection as demonstrated by X-rays, pathological and microbiological findings. Chest X-rays showed that co-infected animals had disseminated lesions in both left and right lungs, while M.tb mono-infected animals displayed the lesions only in right lungs. Necropsy of co-infected animals revealed a disseminated M.tb infection not only in the lungs but also in the extrapulmonary organs including spleen, pancreas, liver, kidney, and heart. The bacterial counts in the lungs, the bronchial lymph nodes, and the extrapulmonary organs of co-infected animals were significantly higher than those of M.tb mono-infected animals. The mechanistic studies demonstrated that two of three co-infected animals had lower levels of M.tb specific IFN-γ and IL-22 in PBMCs than M.tb mono-infected animals. These findings suggest that Chinese rhesus macaque is a suitable and alternative non-human primate model for SIV/M.tb coinfection studies. The impairment of the specific anti-TB immunity is likely to be a contributor of SIV-mediated enhancement M.tb infection.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

SIV Infection Facilitates Mycobacterium tuberculosis Infection of Rhesus Macaques

et al. 2017

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“…Firstly, high levels of immune activation is also seen in CD8 T cells in HIV infected patients but the loss is largely limited to CD4 cells [ 10 ]. Secondly, experimental induction of immune activation in vivo in rhesus macaques using LPS [ 177 ] and in humanized mice [ 178 ] fails to cause a specific loss of CD4 T cells or alter the CD4:CD8 ratio. At the same time, induction of immune activation in natural SIV infection in AGMs can lead to partial CD4 loss in an otherwise non-pathogenic infection [ 179 ].…”

Section: Immune Activationmentioning

confidence: 99%

Host and Viral Factors in HIV-Mediated Bystander Apoptosis

Garg

Joshi

2017

Viruses

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Human immunodeficiency virus (HIV) infections lead to a progressive loss of CD4 T cells primarily via the process of apoptosis. With a limited number of infected cells and vastly disproportionate apoptosis in HIV infected patients, it is believed that apoptosis of uninfected bystander cells plays a significant role in this process. Disease progression in HIV infected individuals is highly variable suggesting that both host and viral factors may influence HIV mediated apoptosis. Amongst the viral factors, the role of Envelope (Env) glycoprotein in bystander apoptosis is well documented. Recent evidence on the variability in apoptosis induction by primary patient derived Envs underscores the role of Env glycoprotein in HIV disease. Amongst the host factors, the role of C-C Chemokine Receptor type 5 (CCR5), a coreceptor for HIV Env, is also becoming increasingly evident. Polymorphisms in the CCR5 gene and promoter affect CCR5 cell surface expression and correlate with both apoptosis and CD4 loss. Finally, chronic immune activation in HIV infections induces multiple defects in the immune system and has recently been shown to accelerate HIV Env mediated CD4 apoptosis. Consequently, those factors that affect CCR5 expression and/or immune activation in turn indirectly regulate HIV mediated apoptosis making this phenomenon both complex and multifactorial. This review explores the complex role of various host and viral factors in determining HIV mediated bystander apoptosis.

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“…In vitro stimulation of normal PBMCs failed to induce a specific CD4+ decline although the cells exhibited CD38+HLADR+ upregulation similar to that seen in HIV infections. In other more relevant in vivo models, experimental induction of immune activation failed to induce a specific CD4+ decline in both humanized mice (42) and Macaques (61) in the absence of HIV infection. Hence, we hypothesized that presence of virus/Env glycoprotein in the cultures would be essential for mediating specific CD4+ loss.…”

Section: Discussionmentioning

confidence: 99%

HIV-1 Env Glycoprotein Phenotype along with Immune Activation Determines CD4 T Cell Loss in HIV Patients

Joshi

Sedano

Beauchamp

et al. 2016

The Journal of Immunology

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The mechanism behind the selective depletion of CD4+ cells in HIV infections remains undetermined. Although HIV selectively infects CD4+ cells, the relatively few infected cells in vivo cannot account for the extent of CD4+ T cell depletion suggesting indirect or bystander mechanisms. The role of virus replication, Env glycoprotein phenotype and immune activation (IA) in this bystander phenomenon remains controversial. Using samples derived from HIV-infected patients; we demonstrate that while IA in both CD4+ and CD8+ subsets correlates with CD4 decline, apoptosis in CD4+ and not CD8+ cells is associated with disease progression. As HIV-1 Env glycoprotein has been implicated in bystander apoptosis, we cloned full length Envs from plasma of viremic patients and tested their Apoptosis Inducing Potential (AIP). Interestingly, AIP of HIV-1 Env glycoproteins were found to correlate inversely with CD4:CD8 ratios suggesting a role of Env phenotype in disease progression. In vitro mitogenic stimulation of PBMCs resulted in upregulation of IA markers but failed to alter the CD4:CD8 ratio. However, co-culture of normal PBMCs with Env expressing cells resulted in selective CD4 loss that was significantly enhanced by IA. Our study demonstrates that AIP of HIV-1 Env and IA collectively determine CD4 loss in HIV infection.

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Lipopolysaccharide Induces Immune Activation and SIV Replication in Rhesus Macaques of Chinese Origin

Cited by 11 publications

References 24 publications

SIV Infection Facilitates Mycobacterium tuberculosis Infection of Rhesus Macaques

SIV Infection Facilitates Mycobacterium tuberculosis Infection of Rhesus Macaques

Host and Viral Factors in HIV-Mediated Bystander Apoptosis

HIV-1 Env Glycoprotein Phenotype along with Immune Activation Determines CD4 T Cell Loss in HIV Patients

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